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2017 DIRECTORY OF TRAINING
OPPORTUNITIES
The Divito Laboratory, Brigham and Women’s Hospital
BRIGHAM AND WOMEN’S HOSPITAL The Divito Laboratory
The Divito laboratory in the Department of Dermatology at Brigham and Women’s Hospital (BWH) in Boston is seeking a post-doctoral fellow in translational immunology. My laboratory investigates the immune-pathogenesis of serious cutaneous diseases including severe drug allergies and graft-versus-host disease as well as novel therapeutics for cutaneous disease. Our lab work is translational and aims to directly impact patient care. We work with both human specimens and mouse models of disease. Our research utilizes both traditional immunologic techniques (immunofluorescence/ immunohistochemistry, microscopy, flow cytometry and sorting, in situ hybridization, western blot, etc) and novel technologies (high-throughput TCR sequencing, nanostring analysis, multispectral labeling and imaging of tissue, and laser capture microscopy). The BWH Department of Dermatology is located in the Longwood Medical Area, which contains ten major institutions, including research-oriented hospitals, research institutes, Harvard Medical School, and the Harvard School of Public Health, providing a rich training environment. Co-mentorship is possible in certain cases. Highly-motivated candidates with a Ph.D. or M.D./Ph.D. in Immunology, or an M.D. with dermatology experience are strongly encouraged to apply. Applicants should possess strong laboratory, analytical, interpersonal and communication skills. Interested candidates should email a brief cover letter indicating their research interests and career goals, CV, and contact information for 3 references to: Matthew Opperman, [email protected] Sherrie Divito, M.D., Ph.D. Brigham and Women’s Hospital Department of Dermatology 77 Ave. Louis Pasteur, HIM660 Boston, MA 02115
The Warren Alpert Medical School of Brown University
BROWN UNIVERSITY Dermatoepidemiology Fellowship
Research in epidemiology and related areas of cutaneous malignancies and dysplasias (melanoma, keratinocyte carcinomas (BCC and SCC), cutaneous lymphomas, dysplastic nevi, actinic keratosis, etc), and teledermatology. One (1) year fellowship Deadline generally fall or winter Contact: Martin A. Weinstock, MD, PhD Email: [email protected] Martin A. Weinstock, MD, PhD VA Medical Center – 111D 830 Chalkstone Avenue Providence, RI 02908 401-457-3333 401-273-7100 x3627
The Warren Alpert Medical School of Brown University
BROWN UNIVERSITY Clinical and Translational Research Program
The Clinical and Translational Research Program (CTRP) comprises a multi-disciplinary research group focused on hypothesis-driven work on a wide variety of dermatologic diseases. Clinicians, epidemiologists, post-doctoral researchers, medical students, undergraduate students, and administrators make up this unique team, which gathers its strength from this rich network of experts working in an exciting and exceedingly collaborative environment. The CTRP functions under the mission of investigating an inclusive range of diseases, from common cancers to rare orphan diseases, in an effort to measurably expand our understanding, as well as to move discoveries from the conceptual world into clinical practice. Dermatoepidemiology Division, based at the Providence VA Medical Center, conducts epidemiologic research on cutaneous malignancies and dysplasias, including melanoma and other skin cancers and skin cancer precursors, as funded by the National Institutes of Health, the Department of Veteran's Affairs, and private foundations. Interested residents are encouraged to participate in the activities of the unit. We provide training in dermatoepidemiology with easy access to large and well-established cohort data as well as hospital data. DEADLINE: Flexible CONTACT Eunyoung Cho, Sc.D. Associate Professor Director of Research Department of Dermatology The Warren Alpert Medical School of Brown University 339 Eddy St, Providence, RI 02903 Email: [email protected] Website: https://www.brown.edu/academics/medical/about/departments/dermatology/about/dermatoepidemiology-division
The Chuan-Yuan Li Laboratory, Duke University Medical Center
DUKE UNIVERSITY MEDICAL CENTER
The Chuan-Yuan Li Laboratory
The laboratory of Dr. Chuan-Yuan Li in the Department of Dermatology at Duke University Medical Center is recruiting a
postdoctoral research fellow. We are seeking outstanding PhD (or equivalent) applicants with strong background in
molecular and cellular biology. Areas of interest include in vivo tumor biology, cancer or normal stem cell biology, skin
biology and wound healing. Expertise and training in bioinformatics is a plus.
The Li lab is interested in a variety of areas such as skin cancer, stem cell biology, and wound healing (Liu et al, Cell Research,
2017, doi: 10.1038/cr.2017.41; Liu et al, Mol. Cell, 58:284-296; Huang et al, Nat. Med. 2011, 17:860-66; Li et al, Cell Stem Cell 2010, 7:508-20; Li et al Science Signaling, 2010, 3; Ra13).
Please check our website:
https://scholars.duke.edu/person/chuan.li#show%20less%20content for more details.
The position will be available until filled.
Interested candidates please send a copy of CV and names and contact information of three (3) references to:
Dr. Chuan-Yuan Li, Ph.D.
Professor and Vice Chair for Research
Department of Dermatology
Duke University Medical Center
Durham, NC 27710
Email: [email protected]
The Garza Lab, Johns Hopkins School of Medicine
JOHNS HOPKINS UNIVERSITY The Garza Lab
The Garza lab is interested in regenerative medicine, reactivating the programs of embryogenesis in adults to fully rebuild damaged tissue. We use the skin as a model system. Our general goal is to promote regeneration and stem cells to improve skin appearance and function in health and disease. We try to bridge rigorous science to translational medicine in an effort to generate products that will find broad use in our patients. Our lab currently focuses on two areas, among many other less active projects: GENERAL SUMMARY 1: Appendage Regeneration Regrowing a lost limb is a long-term goal. In the short term we use the hair follicle as a proxy since the genetic pathways which control hair and limb development overlap. Recently mice were discovered to have the ability to recreate an entire hair follicle with blood vessels, nerves and stem cells after its complete destruction. We have defined novel pathways which control this and want to test their mechanism and ability to work in human subjects. This work will eventually help with scars, burns, alopecia and also skin rejuvenation. 2: Skin Identity Conversion In the short term to help amputees, we wish to convert the identity of the skin at the stump site to the thick type of skin found on the palms and soles. We are FDA approved and began human testing in Fall 2014 for the ability of fibroblast stem cells to convert skin identity. TRAINING POSITION Depending on exact timing we occasionally have spots open for graduate students, PhD postdocs, and MD-PhD dermatologists pursuing postdoc DEADLINE No deadline; rolling admissions. Contact to see exact availability CONTACT Luis Garza, MD, PhD Associate Professor Department of Dermatology Johns Hopkins School of Medicine Office: Room 204 Lab: Suite 216 Koch CRBII 1551 Orleans Street Baltimore, MD 21287 Phone: 410-955-8662 Email: [email protected] Website: http://www.hopkinsmedicine.org/dermatology/about_us/our_experts/garza_luis.html
Massachusetts General Hospital/Harvard Medical School
MASSACHUSETTS GENERAL HOSPITAL/HARVARD MEDICAL SCHOOL
Post-Doctoral Fellow Position in Angiogenesis/Immunology/Wound healing Dr. Alexander G. Marneros, Laboratory of Angiogenesis and Inflammation, Cutaneous Biology Research Center, Department of Dermatology, Massachusetts General Hospital/Harvard Medical School. Our laboratory is investigating molecular mechanisms involved in wound healing, angiogenesis and inflammation. PROJECT 1: We are investigating molecular mechanisms that control macrophage activation and the role that activated macrophages play for inflammation and pathological angiogenesis. We have established in vitro assays to identify regulators of macrophage polarization. In chemical screens we could identify pharmacologic inhibitors of alternative macrophage polarization (M2-type macrophages) and could show in vivo that these inhibitors can block macrophage-induced angiogenesis (Cell Reports, 2013; JBC, 2014; Am J Path, 2013, 2014, 2016). This project aims to define molecular pathways that are critical for macrophage polarization and that influence the ability of activated macrophages to induce pathological angiogenesis in conditions such as age-related macular degeneration, cancer or wound healing. PROJECT 2: We use human genetics approaches to discover the genes that cause congenital wound healing disorders. We have identified novel genes that cause aplasia cutis congenita and associated syndromes (PLoS Genet, 2013, Am J Hum Gen, 2013; J Invest Dermatol, 2015). These approaches revealed completely unknown mechanisms involved in skin morphogenesis. We are investigating these mechanisms now in mouse models of these diseases. PROJECT 3: We investigate the role of proangiogenic factors for wound healing and age-related diseases. We could show that the proangiogenic factor VEGF-A induces oxidative stress and NLRP3 inflammasome activation to promote age-related diseases (Cell Reports, 2013; FASEB J, 2014; EMBO Mol Med, 2016). We use a variety of in vivo and in vitro approaches to investigate a novel pathogenic link between VEGF-A and NLRP3 inflammasome activation. In summary, our laboratory uses a large number of diverse experimental approaches (human genetics, mouse genetics, chemical screens, in vitro assays, cutting-edge imaging technology) to define novel mechanisms in angiogenesis, wound healing and inflammation. All of our projects have strong translational clinical relevance. Our laboratory is embedded in a highly productive and well-equipped environment at the Cutaneous Biology Research Center of Massachusetts General Hospital/Harvard Medical School. Cutting-edge technologies are available within our Department and the MGH/Harvard research community. REQUIRED PROFILE Passionate about science and commitment for ~2 years required Ability to work independently within a dynamic team Position start date: Flexible LAB WEBSITE: http://www.massgeneral.org/research/researchlab.aspx?id=1076 Interested candidates should send the CV and references to Alexander G. Marneros, M.D., Ph.D. [email protected] or [email protected]
Massachusetts General Hospital/Harvard Medical School
MASSACHUSETTS GENERAL HOSPITAL/HARVARD MEDICAL SCHOOL
Epidemiology of Skin diseases (PORES)
The Patient-Oriented Research in the Epidemiology of Skin diseases (PORES) unit at the Massachusetts General Hospital/Harvard Medical School has an immediate opening for a postdoctoral candidate to study the genomics of non-melanoma skin cancer. Applicants must have an M.D. and/or Ph.D. degree and optimally will have experience with epidemiologic and statistical data analysis. Strong quantitative skills and practical experience working with large-scale datasets and applying epidemiologic tools are a plus. Experience in systems biology, systems genetics and genomics research is essential. Interested candidates who have previous experience in statistics, bioinformatics, epidemiology, genetic epidemiology, and genomics of complex human diseases (required for this position) should send their cover-letter, CV and the names of 3 references. The research will be done under the mentorship of faculty member Maryam Asgari, MD MPH. Starting date: July 1, 2017 (can be earlier, depending on candidate and circumstances)
Duration: The post-doctoral fellow will be funded for up to three (3) years
Post-doctoral fellow must be a US Citizen or green-card holder
MGH/HMS is a committed Equal Opportunity/Affirmative Action Employer
Minorities, women, handicapped and veterans are encouraged to apply
Job Type: Full-time
Required education: Doctorate
Required experience: 3 years of Research
Contact Information: Dr. Maryam Asgari, via [email protected] Website: www.massgeneral.org/research/researchlab.aspx?id=1681 Apply Online: https://partners.taleo.net/careersection/ghc/jobdetail.ftl?job=3032295 Application Deadline: June 30, 2017
The Tsai Lab, Moffitt Cancer Center
MOFFITT CANCER CENTER The Tsai Lab
The Tsai Lab at the Moffitt Cancer Center in Tampa, FL is looking to hire motivated, career-oriented research fellows (postdoctoral, postbaccalaureate, residents, graduate students). Our collective goal is to identify, test, and validate novel targets for the targeted chemoprevention and treatment of skin cancer. The PI, Dr. Kenneth Y. Tsai, MD, PhD, is a dermatologist, dermatopathologist, and NIH-funded investigator with extensive experience in mouse models of cancer, molecular biology, and in the diagnosis and research of skin cancer. He leads the Non-Melanoma Skin Cancer Research & Treatment Section of the Skin Cancer Center of Excellence at Moffitt. Our recent work is focused on three major areas: (1) an integrated genomic and evolutionary characterization of skin squamous cell carcinoma (cuSCC) development from normal skin to precancerous actinic keratosis to cuSCC using next generation sequencing and UV-driven mouse models; and (2) examination of the roles of microRNAs in driving cuSCC development; and (3) characterization of JNK signaling and the advent of JNK2 as a target in skin cancers (cuSCC and melanoma). Additionally, we are actively involved in technology development: we collaborate extensively with Samir Mitragotri, Ph.D. (UCSB) and Kevin Dalby, Ph.D. (UT Austin) to develop novel technologies to non-invasively sample skin for biomarker discovery and to validate additional kinase targets for cancer therapy. More information is available at www.kytsai.com. Our lab environment is highly collaborative, with regular and frequent contact with the PI, and an expectation that the best work comes from committed individuals who actively communicate. Successful applicants can expect to have intensive training in state-of-the-art research methods as well as development of presentation and writing skills with regular and frequent contact with the PI. We are seeking talented, highly motivated, and collaborative individuals with recent experience in the biological sciences, bioinformatics, or equivalent. Ideal candidates will work effectively and efficiently both individually, as well as in a team atmosphere and are detail-oriented, creative, and excited to explore novel, unexplored avenues. Projects in our laboratory employ a variety of technologies based upon cell culture, human tissue samples, and mouse models and include microscopy, next generation sequencing, proteomics, informatics, flow cytometry and mass spectrometry. Trainees will be expected to attend and present their work at international meetings, to apply for internal and external funding opportunities, and to publish extensively in order to make them competitive for the next career transition.
The laboratory is located within the Moffitt Cancer Center, which is a modern, non-profit cancer treatment and research center currently ranked as the No. 6 Cancer Hospital in the USA, and is the only National Cancer Institute-designated Comprehensive Cancer Center based in the state of Florida. Moffitt Cancer Center generously supports innovative core facilities for flow cytometry, cellular therapy, proteomics, molecular biology, structural biology, microarray, analytic microscopy, drug discovery, and biostatistics. The Center also offers a state-of-the-art vivarium, equipped with onsite advanced imaging facilities. This includes CT, MRI, ultrasound, and in-vivo bioluminescence systems. We invite you to join us. A competitive salary and benefits package will be offered to successful candidates. Interested candidates should send a single PDF file that includes a CV, a statement of research accomplishments/interests/career goals (2 pages max), and 3 references to Dr. Kenneth Y. Tsai: [email protected].
National Cancer Institute (NCI-NIH)
NATIONAL CANCER INSTITUTE Signaling Pathways in Skin Biology and Cancer
Post-Doctoral research position is available at the National Cancer Institute (NCI-NIH, Bethesda, MD, USA), in the group of Dr. Ramiro Iglesias-Bartolome at LCMB. The recently established group focuses on identifying signaling pathways that regulate skin and somatic stem cell biology. Qualified applicants will study G protein coupled receptors (GPCRs) and related signaling in stem cell fate decisions and cancer, particularly skin basal and squamous cell carcinoma. We use cell and mouse models, bioinformatics and functional genomic approaches, and we are in the process of developing novel screening strategies. The candidate will have access to state-of-the-art genomic, proteomic and imaging technologies and have opportunities to interact with experts from multidisciplinary teams. This position is a unique opportunity for self-motivated candidates to enhance their training and expand their professional horizons.
Postdoctoral applicants should have a doctoral or MD degree within the last five (5) years with a solid background in cell biology, biochemistry and/or developmental biology. Previous experience in skin biology, cell signaling, cancer biology, mouse models or bioinformatics and functional genomics would be desirable.
Submit a cover letter with a research statement indicating areas of expertise and preferred starting date, CV, and contact information for three (3) references.
Submit by email to Dr. Ramiro Iglesias-Bartolome ([email protected]).
In the email subject please indicate “Postdoc/Postbac application” to ensure proper attention.
Application deadline: 4/30/2017
https://ccr.cancer.gov/Laboratory-of-Cellular-and-Molecular-Biology/ramiro-iglesias-bartolome
Page 1 of 2 National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES (NIAMS)
Dermatology Research Fellowships at the NIH The Dermatology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health offers both laboratory-based and patient-centered postdoctoral research fellowships for interested, talented physicians and non-physicians. The Dermatology Branch Has prepared numerous individuals for careers in academic dermatology and related fields. Has many trainees who have assumed leadership positions, in the United States and overseas. Offers the Dermatology Research Scholar program for physicians interested in a translational research career. Laboratory research areas include: cutaneous immunology and inflammation, the skin microbiome, tissue stem cells, and
Merkel cell development/Merkel cell carcinoma. Clinical research areas include: chronic graft-versus-host disease (GvHD), primary immunodeficiency, autoinflammatory
skin disease, cutaneous oncology, drug hypersensitivity, and the microbiome in health and disease. Fellows consistently rank the NIH among the top 10 places in the US to work. Applications are accepted and considered on a rolling basis. Competitive salaries commensurate to experience, benefits, and travel opportunities are provided. American-trained physicians must have successfully completed dermatology residency training and be Board-eligible to be considered for the Research Scholar program. The Dermatology Branch is located at the main NIH campus in Bethesda, MD just outside Washington, DC. Additional information can be obtained by contacting any of the investigators listed below. The Dermatology Branch is particularly interested in recruiting for the following opportunities: THE CUTANEOUS DEVELOPMENT AND CARCINOGENESIS SECTION is accepting applications for a research fellowship investigating skin cancer biology with Dr. Isaac Brownell. The laboratory investigates the molecular oncogenesis of Merkel cell carcinoma and the regulation of cutaneous stem cells. Experience with cancer biology, tumor immunology, bioinformatics, mouse genetics, or tumor xenografts is a plus. Interested candidates should send a CV and cover letter to: Dr. Isaac Brownell [email protected] http://ccr.cancer.gov/staff/staff.asp?Name=brownell THE DERMATOLOGY CONSULTATION SERVICE AND CLINICAL RESEARCH SECTION offers a 3-year post-residency Fellowship (Dermatology Research Scholar) under the supervision of Dr. Edward Cowen. The Research Scholar gains comprehensive exposure to the unique clinical environment of the NIH Dermatology Consult Service, formal training in Clinical Research leading to a Master’s Degree from Duke University, and the opportunity to design and conduct cutting edge clinical research. Current areas of active investigation include chronic graft-versus-host disease (cGVHD) and autoinflammatory skin diseases. Other interests include primary immunodeficiencies, cancer-associated genodermatoses, and adverse drug reactions. Interested candidates should contact: Dr. Edward W. Cowen [email protected] https://ccr.cancer.gov/Dermatology-Branch/edward-w-cowen
Page 2 of 2 National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
THE SKIN MICROBIOME SECTION is accepting applications for a lab-based postdoctoral research fellowship or a 3-year post-residency translational research fellowship (Dermatology Research Scholar) working with Dr. Heidi Kong. The research group studies host-microbial interactions in healthy individuals and patients. Active investigations include atopic dermatitis and primary immunodeficiencies. Interested candidates should send a CV and cover letter to: Dr. Heidi Kong [email protected] http://ccr.cancer.gov/staff/staff.asp?profileid=11188 THE SKIN IMMUNITY SECTION is accepting applications for a postdoctoral research fellowship working with Keisuke (Chris) Nagao. The research group studies fundamental and pathological aspects of skin immunity by exploring cross-talks that occur between innate leukocytes, hair follicles/stroma and the microbiota by utilizing cutting-edge technology such as single-cell RNA sequencing in both mice and humans. Mouse models of atopic dermatitis and inflammatory alopecia are actively studied. Dr. Chris Nagao [email protected] https://ccr.cancer.gov/Dermatology-Branch/keisuke-chris-nagao
NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES Post-Doctoral Fellow Position in Skin Diseases
Research in the Laboratory of Skin Biology covers topics within the field of epidermal development and differentiation. In particular, we are focused on dissecting the gene regulatory networks and signaling pathways linked to human diseases, such as ectodermal dysplasias and skin inflammatory disorders. We are interested in identifying signaling pathways, and genome-wide and disease-specific molecular interaction networks linked to inflammatory human diseases, which encompass multi-scale molecule interactions, such as transcriptional regulations and protein-protein interactions. Applicants possess a Ph.D. or M.D., with receipt of the last graduate degree within the past 5 years. The candidate should have a strong background in molecular and developmental biology, documented by peer-reviewed publications. The position is in the Laboratory of Skin Biology of the National Institute of Arthritis and Musculoskeletal and Skin Diseases in Bethesda, MD and interested candidates should send CV and references to [email protected]. Lab website: https://www.niams.nih.gov/Research/Ongoing_Research/Branch_Lab/Skin_Biology/dsbs.asp The NIH is dedicated to building a diverse community in its training and employment programs.
Northwestern University, Feinberg School of Medicine Page 1 of 11
NORTHWESTERN UNIVERSITY Feinberg School of Medicine
Northwestern University’s (NU) Feinberg School of Medicine is seeking outstanding candidates for its NIH-funded (T32) Postgraduate Program in Cutaneous Biology and has opportunities as well in several laboratories outside of the T32 in Northwestern individual laboratories (contact Erica Zuniga at [email protected] for more information). The goal of the T32-funded training program is to prepare both physician-scientists (M.D. and M.D./Ph.D.) and Ph.D. scientists for careers in independent research in cutaneous biology through a mentored laboratory experience coupled with an intensive educational enrichment program. Cutaneous biology research at NU is highlighted by vibrant collaborations between the NU Skin Disease Research Center (NU-SDRC), the NU Skin Cancer Institute, the Dermatology Clinical Trials unit and a core of outstanding preceptors from seven major NU departments (Dermatology, Cell and Molecular Biology, Chemistry, Medicine, Microbiology and Immunology, Pathology, Pediatrics). Unique to this training program are major opportunities in keratinocyte biology, cutaneous oncology, regenerative medicine and nanotechnology, as well as the ability to leverage basic findings into translational research projects. Fellows can conduct research in: cell adhesion, cell motility, cell proliferation and differentiation, cutaneous immunology, epidemiology, epithelial stem cell biology, experimental carcinogenesis, extracellular matrix biology, inflammation, RNA silencing, signal transduction, wound healing and viral pathogenesis. In general, new fellows start in early July; however, we have a rolling start date for one of our slots, so applicants are encouraged to inquire at any time. To apply send your CV, a description of your research interests and career goals, and the names of three (3) references to: Robert M. Lavker, PhD Director, NU Postgraduate Program in Cutaneous Biology Northwestern University Department of Dermatology 303 E. Chicago Ave., Ward 9-124 Chicago, IL 60611 Fax: 312-503-4325 E-mail: [email protected]
Northwestern University, Feinberg School of Medicine Page 2 of 11
NORTHWESTERN UNIVERSITY RESEARCH PROFILES: Guillermo Ameer, ScD Professor of Surgery, Division of Vascular Xiaomin Bao, PhD Assistant Professor of Molecular Biosciences Paul Bryce, PhD, Associate Professor of Medicine, Division of Allergy Irina Budunova, MD, PhD Associate Professor of Dermatology Navdeep Chandel, PhD Professor of Medicine, Division of Pulmonary Jaehyuk Choi, MD, PhD Assistant Professor of Dermatology Lisa Godsel, PhD Research Assistant Professor of Pathology & Dermatology Robert Goldman, PhD Professor of Cell & Molecular Biology Cara Gottardi, PhD Associate Professor of Medicine, Division of Pulmonary Kathleen Green, PhD Professor of Pathology Alan Hauser, MD, PhD Associate Professor of Microbiology-Immunology Thomas Hope, PhD Professor of Cell & Molecular Biology Steven Kosak, PhD Assistant Professor of Cell & Molecular Biology Todd A Kuiken, M.D., Ph.D Professor of Physical Medicine and Rehabilitation Laimonis Laimins, PhD Professor of Microbiology-Immunology Robert Lavker, PhD Professor of Dermatology
Richard Longnecker, PhD Professor of Microbiology-Immunology Stephen Miller, PhD Professor of Microbiology-Immunology Chad Mirkin, PhD Professor of Chemistry Brian J. Mitchell, PhD Assistant Professor of Cell & Molecular Biology William A. Muller, MD, PhD Professor and Chair of Pathology Amy Paller, MD Professor and Chair of Dermatology John Rogers, PhD Professor of Materials Science and Engineering Robert Schleimer, PhD Professor of Medicine, Division of Allergy Jonathan Silverberg, MD, PhD, MPH, Assistant Professor of Dermatology (Epidemiology) Sergey Troyanovsky, PhD Associate Professor of Dermatology John Varga, MD Professor of Medicine, Division of Rheumatology Douglas Vaughan, MD Chair and Professor of Medicine, Division of Cardiology
Northwestern University, Feinberg School of Medicine Page 3 of 11
Guillermo Ameer, ScD, Northwestern University, Department of Surgery, Division of Vascular [email protected] / http://www.ameerlab.northwestern.edu/main.php Dr. Ameer’s research interests include biomaterials, vascular and orthopedic tissue engineering, controlled drug and gene delivery, stem cell engineering and bio/nanotechnology for improved therapeutics and diagnostics. For the in vivo approach to tissue or organ replacement, the Ameer lab is interested in developing scaffolds and techniques that will be conductive to the reconstitution or maintenance of normal tissue micro architecture. Disruption of normal tissue microarchitecture can lead to scarring or degeneration resulting in loss of or impaired function. Therefore, we are developing and studying novel biomaterials and processing techniques to produce scaffolds suitable for tissue engineering. In particular we are interested in understanding the effects of scaffold characteristics on cellular and tissue development in order to prevent deleterious processes. Moreover, we have developed an approach to harvest patient-specific endothelial progenitor cells and are investigating methods for cell-specific differentiation. Xiaomin Bao, PhD, Northwestern University, Department of Molecular Biosciences [email protected] / http://www.molbiosci.northwestern.edu/people/core-faculty/xiaomin-bao.html The Bao laboratory is interested in understanding the gene regulatory mechanism underlying human epidermal tissue homeostasis. In particular, we focus on the roles of epigenetic regulators such as the BAF chromatin remodeling complex, which use the energy from ATP to actively position nucleosomes on the DNA to facilitate transcription factor (TF) binding. Our recent studies revealed that both the regulatory subunit BAF53a and the catalytic subunits Brg1/Brm are essential for epidermal tissue homeostasis (Bao et al., Cell Stem Cell, 2013). We further demonstrated that the BAF complex cooperate with the lineage-specific TF p63 to activate epidermal terminal differentiation (Bao et al., Genome Biology, 2015). Leveraging our strengths of genetic models, proteomics and genomics, we are currently actively exploring how BAF complex crosstalk to its interacting proteins in both normal epidermal tissue homeostasis and in skin disease progression. Paul Bryce, PhD, Northwestern University, Department of Medicine, Division of Allergy [email protected] The research in the Bryce lab is focused on regulation of immune responses by mast cells. These cells are an important link between innate immune responses, through modulation of epithelial and endothelial cell responses, and the development and elicitation of adaptive immunity. The lab has been studying how mast cell-derived mediators might regulate the recruitment and development of tissue specific inflammation. In one project the lab is investigating how histamine and the histamine receptors influence migration of cells to the skin or lungs. A second project is focused on food allergy and how oral antigen can trigger a plethora of immune activation, including skin, intestinal, and lung responses. A third project being actively pursued focuses on the role of mast cells as a source of IL-33, a newly described cytokine that appears important in allergic immunity and which we have shown is expressed by these cells during activation. Irina Budunova, MD, PhD, Northwestern University, Department of Dermatology [email protected] / http://www.feinberg.northwestern.edu/faculty-profiles/az/profile.html?xid=15774 The research interests in Dr. Budunova’s laboratory have been centered on the role of the glucocorticoid receptor (GR) signaling in skin stem cell maintenance and carcinogenesis. We are also very much interested in translational aspects of the GR biology, and the development of novel approaches to the GR– targeting therapies with reduced side effects. This is important as glucocorticoids remain the most commonly used anti-inflammatory drugs in dermatology. However, their use is limited by the development of detrimental side effects, particularly skin atrophy. Our laboratory has been involved in the search for novel selective GR activators (SEGRA) that preserve therapeutic potential of glucocorticoids but have fewer metabolic and atrophic side effects. Our other goal is to develop GR molecular signature in skin. Our current projects use integrative informatics approach to understand the complex molecular networks underlying glucocorticoid-induced skin atrophy, to identify novel targets (atrophogenes) and to use drug repurposing to reveal anti-atrophogenic compounds among FDA-approved drugs. We also study tye sexual dimorhic effects of topical steroids. We found recently that REDD1 (regulated in development and DNA damage responses 1) is one of the central drivers of steroid – induced skin atrophy, and discovered that REDD1 inhibition may allow to dissociate therapeutic and side effects of glucocorticoids in skin. Dr. Budunova and her laboratory actively participate in the drug repurposing programs at NU Center for Molecular Innovation and Drug Discovery. Dr. Budunova trained seventeen postdoctoral fellows during the last 10 years. Most of her previous trainees have published research papers summarizing their research in peer reviewed journals, several trainees became independent researchers at the rank of Associate/Assistant professor. Postdoctoral position supported by the NIH grant “Integrative informatics approach to develop safe glucocorticoid therapies” is available.
Northwestern University, Feinberg School of Medicine Page 4 of 11
Navdeep Chandel, PhD, Northwestern University, Department of Medicine, Division of Pulmonary [email protected]
The Chandel Lab is interested in the mechanisms by which mitochondria regulate differentiation in the skin. The homeostatic maintenance of the skin epidermis is regulated by the controlled differentiation of stem cell populations within the basal layer of the epidermis as well as in the hair follicle. The signaling pathways which regulate epidermal differentiation remain understood. Reactive oxygen species (ROS) have been demonstrated to act as signaling intermediates required for the propagation of diverse cellular signaling pathways. Recently, ROS have been implicated in regulation of stem cell maintenance and differentiation. The lab has shown that generation of ROS at the mitochondria is a key determinant of keratinocyte differentiation. Genetic disruption of mitochondrial ROS production by using TFAMfl/fl mice crossed to mice containing Cre recombinase under the keratin 14 promoter results in mice with impaired epidermal barrier function and which lack hair. Jaehyuk Choi, MD, PhD, Northwestern University, Department of Dermatology [email protected] / http://labs.feinberg.northwestern.edu/choi/
We employ cutting-edge genomics approaches to identify the genetic basis of inherited and acquired immunological disorders and skin cancer. As an example, we have recently identified the genes and mutations underlying cutaneous T cell lymphoma, an incurable non-Hodgkin lymphoma of skin-homing T cells. The genes are components of the DNA damage, chromatin modifying, NF-kB, and the T cell receptor signaling pathways. We are currently employing a comprehensive approach using human tissues and animal models to investigate the functions of these genes. We are confident these studies will allow us to elucidate the pathophysiology of this cancer and lead to the identification of novel therapeutic targets. Lisa Godsel, PhD, Northwestern University, Department of Pathology [email protected]
The Godsel laboratory is interested in the regulation of the intercellular adhesive junction, the desmosome. Desmosomes are required for maintaining tissue integrity, particularly those tissues under large amounts of stress, such as the skin and heart. The importance for desmosomal proteins in maintaining this adhesive strength is highlighted by diseases that result from mutations in these molecules. Plakophilin 2 (PKP2) and desmoplakin are located in the cytoplasmic plaque of the desmosome and are necessary structural components for this cell-cell junction. We are interested in the protein-protein interactions and trafficking of these molecules during junction formation in epithelial cells and cardiac myocytes. We hypothesize that desmosome proteins act as signaling scaffolds that modulate the organization of the cytoskeletal architechture, which can have an impact on cell-cell adhesive junctions, cell migration and extracellular matrix attachment during tissue development and homeostasis. Robert Goldman, PhD, Northwestern University, Department of Cell & Molecular Biology [email protected] / www.goldmanlab.northwestern.edu Dr. Goldman’s long-standing research centers on determining the structure and function of cytoskeletal intermediate filaments (IF). In humans, IF represent a large cytoskeletal protein family encoded by ~65 genes expressed in a developmentally regulated and cell-type specific fashion. IF are known to function in cell shape determination, and in establishing and maintaining the mechanical integrity of cells. The Goldman lab has recently discovered that IF’s are not static, but rather are highly dynamic in vivo, and that their assembly is regulated by a steady state exchange between soluble subunits and polymers in living cells. As a result, they have been developing targeted mimetic peptides, which alter the steady state in vivo resulting in the disruption of IF structure and function. They are providing important new insights into the function of IF in a wide variety of cell-types, including epithelial cells, fibroblasts and neurons.
Northwestern University, Feinberg School of Medicine Page 5 of 11
Cara Gottardi, PhD, Northwestern University, Department of Medicine, Division of Pulmonary [email protected]
The ability of individual cells to adhere and coalesce into distinct tissues is a major feature of multicellular organisms. Research in my laboratory centers on a protein complex that projects from the cell surface and forms a structural “Velcro” that holds cells to one another. This complex is comprised of a transmembrane “cadherin” component that mediates Ca++-dependent homophilic recognition, and a number of associated “catenins” that link cadherins to the underlying cytoskeleton. A major focus in our lab is to understand how these catenins direct static versus fluid adhesive states at the plasma membrane, as well as gene expression and differentiation in the nucleus. These basic questions are shedding new light on how dysregulation of the cadherin/catenin adhesion system drives pathologies such as asthma, fibrosis and cancer. Kathleen J. Green, PhD, Northwestern University, Department of Pathology [email protected] / www.kgreen.northwestern.edu Dr. Green's research program is directed toward elucidating the structure and function of epithelial adhesion molecules and adhesive structures in epidermal morphogenesis and differentiation, as well as in pathological processes such as cancer, autoimmune and inherited disease. A particular focus is on the assembly and regulation of an intercellular junction called the desmosome, which is the most prominent adhesive structure in complex epithelial tissues such as the epidermis. Green’s work was instrumental in the discovery of a new gene family, now called the plakin family and helped facilitate the identification of human genetic diseases affecting the skin and heart, resulting from mutations in desmoplakin. Current studies utilize a combination of cell biological (including live cell imaging), biochemical, in vivo human organotypic and mouse models to define the mechanism of junction assembly and regulation, as well as adhesion-dependent and –independent functions in epidermal differentiation and morphogenesis. The role of desmosome proteins as targets in autoimmune bullous and infectious disease as well as inherited keratodermas and cardiomyopathies is being explored in collaboration with researchers in the US, Germany, U.K. and Japan. The engagement of desmosomal cadherins in bi-directional signaling with receptor tyrosine kinases and ADAM family member proteases in oral cancer progression is also being investigated. These studies promise to establish the contribution of desmosomes to the processes of wound healing, cancer and other cutaneous disorders. Alan Hauser, MD, PhD, Northwestern University, Department of Microbiology-Immunology [email protected] / http://bugs.mimnet.northwestern.edu/labs/Hauser/labsite/index.htm Our laboratory investigates the pathogenesis of the multidrug resistant gram-negative bacteria Pseudomonas aeruginosa, Acinetobacter baumannii, and Klebsiella pneumonia. We focus on virulence factors such as the type III secretion, an apparatus that injects toxins directly into host cells. Other interests are the use of genomic approaches for the identification of novel virulence determinants and the development of novel translational approaches to treat bacterial infections. Our studies utilize a broad range of techniques, including molecular and cellular assays as well as animal models and epidemiologic studies on human populations. Thomas Hope, PhD, Northwestern University, Department of Cell & Molecular Biology [email protected] The Hope laboratory focuses on utilizing the methods of cell biology to study HIV and I was one of the pioneers of taking this approach. We have developed a series of novel tools and approaches to facilitate our work. Our core approach has been deconvolution microscopy. Much of our effort has focused on live cell observations, which reveal novel insights into the dynamics of biological functions. We have found that HIV moves on microtubules using live cell microscopy. Recently, we have begun to look at where and how HIV can penetrate the epithelial barriers with a specific focus on the initial interactions of virus and penile epithelia. This is particularly important in order to understand the potential mechanisms of protection from HIV acquisition conferred by male circumcision. Our studies have elucidated mechanisms for how HIV can penetrate epithelial barriers at surfaces exposed to virus during sexual transmission as well as characterizing each of the epithelial surfaces of the penis. In the course of these studies, we have also determined that there is no difference in the keratin associated with the epithelium of the inner and outer foreskin as is widely believed and have developed algorithms that allow the accurate measurements of different layers of the epithelium in tissue sections. The studies proposed here will build upon preliminary data generated in the lab to determine how circumcision leads to changes in the penile epithelial structure and barrier function and therefore decreases female-to-male acquisition of HIV. Hopefully, this study will resolve this issue for the future so the field can move forward to identify the real reasons that circumcision appears to provide protection for HIV acquisition in heterosexual men.
Northwestern University, Feinberg School of Medicine Page 6 of 11
Steven Kosak, PhD, Northwestern University, Department of Cell & Molecular Biology http://www.feinberg.northwestern.edu/faculty-profiles/az/profile.html?xid=17996 Our lab is studying the relationship between form and function of the human genome. Nuclear organization and nuclear function are inextricably linked. For example, gene expression is related to nuclear localization, with silenced genes frequently positioned at heterochromatin and the nuclear periphery, and active genes enriched in the nuclear interior. Moreover, we have determined a relationship between gene expression and genomic organization during cellular differentiation by contrasting the linear arrangement of co-regulated genes and the organization of all chromosomes in stem cells and derived cell types. We suggest that the inter-linked functions of the nucleus results in its self-organization, defined as the emergence of a global structure from combined local activities. The commitment and differentiation of human embryonic and adult stem cells provide an ideal model to examine the functional role of nuclear organization, since their gene expression profiles are related to changes in genome structure according to cell type. Thus, we aim to broadly characterize and test the mechanistic role nuclear organization of gene expression plays in cellular function, differentiation, and disease. One of our ongoing projects aims to test the hypothesis that nuclear gene localization is functionally related to the cellular context of their function. To do so, we have teamed up with the SDRC to study the relationship between the nuclear organization of genes that encode hemidesmosome (HD) components and their polarized localization during epidermal differentiation. We find that HD genes are positioned towards the basal side of the nucleus in basal progenitor cells, where these genes are highly expressed, but not in differentiated suprabasal cells where they are transcriptionally repressed. We are exploring underlying mechanisms that may account for our findings of gene polarity during epidermal differentiation and how this phenomenon may impact human skin disorders. Todd A. Kuiken, MD, PhD Northwestern University, Department of Physical Medicine and Rehabilitation, McCormick School of Engineering [email protected] The Kuliken laboratory is working developing bionic technologies to improve the function of artificial limbs for people with very proximal amputations. The main research focus of the lab is developing a technique using nerve transfers to improve of myoelectric prosthesis control called ‘targeted reinnervation’. By transferring the residual arm nerves in an upper limb amputee to spare regions of muscle it is possible to make new signals for the control of robotic arms. This allows simultaneous control of multiple joints in a natural way. The procedure has been very successful in patients with increases in speed of 50- 500%. Similarly, hand sensation nerves can be directed to reinnervate spare skin in or near the residual limb so that when this skin is touched, the amputee feels like their missing hand is being touched including light touch, graded pressure hot/cold, sharp/dull and vibration. This is an exciting pathway to producing true sensory feedback to amputees from their prosthesis. Of specific relevance to dermatology is the opportunity to study direct skeletal attachment of prostheses with the skin interface being the key. Laimonis A. Laimins, PhD, Northwestern University, Department of Cell & Molecular Biology [email protected] The efforts of the Laimins laboratory are focused on the pathogenesis of high risk human papillomaviruses and their relationship to cervical cancer. Efforts can be divided into three main areas: 1) the pathogenesis of papillomaviruses in differentiating epithelia 2). The regulation of viral gene expression and 3). The role of the viral oncoproteins, E6 and E7 in oncogeneisis. 1). The papillomaviruses life cycle is closely linked to epithelial differentiation and progeny virus are replicated in terminally differentiated epithelial cells. We have used organotypic tissue culture systems to faithfully reproduce the differentiation program of epithelial cells in the laboratory and to generate papillomavirus virions. Recently we developed methods to genetically analyze HPV functions during the viral life cycle. Current efforts are directed at analyzing the function of viral early protein in the life cycle. Over fifty different mutant viral genomes have been examined to date. 2). The viral oncoproteins, E6 and E7 with cellular proteins. In particular, E6 binds the p53 protein and facilitates its degradation by a ubiquitin-mediated pathway. E7 binds the retinoblastoma gene product and alters its cell cycle regulatory properties. Additional studies examine the activation of telomerase by E6 as well as signal transduction pathways by both E6 and E7. 3). The regulation of viral gene expression occurs at both the initiation of transcription and through post-transcriptional mechanisms. Ongoing studies are examining the transcription factors that regulate early gene expression in undifferentiated cells and late gene expression in differentiated cells. This laboratory will provide the Fellow with opportunities for basic studies of the pathogenesis of human papillomavirus infections of the genital tract using a broad spectrum of techniques including sophisticated cell culture methods and techniques for generating mutant HPVs.
Northwestern University, Feinberg School of Medicine Page 7 of 11
Robert Lavker, PhD, Northwestern University, Department of Dermatology [email protected] Dr. Lavker’s current research interests center on 2 areas: the biology of epithelial stem cells and the roles of microRNAs in epithelial homeostasis. With respect to the biology of epithelial stem cells, in collaboration with Tung-Tien Sun (NYU Medical School), the lab has identified and characterized epithelial stem cells of the epidermis, corneal epithelium and hair follicle. These studies have been of major importance for their implications regarding corneal regeneration, hair follicle growth, wound repair, and carcinogenesis. Most recently we have focused on elucidating the roles that “factor inhibiting hypoxia-inducible factor-1” (FIH-1) plays in regulating epidermal homeostasis. FIH-1 functions on three levels in cultured human keratinocytes:: (i) it blocks Notch-dependent epidermal differentiation; (ii) it enhances proliferation either through Notch and/or EGFR signaling; and (iii) it positively regulates migration by interacting with leucine rich repeat kinase 1 (LRRK1) to maintain EGFR signaling. LRRK1, which is expressed in epithelial stem cell-rich tissues (e.g., hair follicle bulge, limbal epithelium), is a novel substrate for FIH-1 that positively regulates proliferation and migration via EGFR signaling. The laboratory is continuing to focus on how FIH-1/LRRK1 interact to regulate proliferation/quiescence and migration of epidermal stem and transient amplifying cells. The second research focus of the lab is the characterization of microRNAs (miRNAs) to understand how these miRNAs regulate epithelial stem cell behavior and epithelial differentiation. We reported that miRNAs-184, -205 and -31 are enriched in the corneal epithelium and demonstrated how these miRNAs regulated cell migration, differentiation and glycogen metabolism via specific gene targets. Recently, we have begun to define the miRNA expression patterns in the stem cell-enriched limbal epithelium, and have identified miRs-103/107 as an important regulatory family. miRs-103/107 target the ribosomal kinase p90RSK2, thereby arresting cells in G0/G1 and contributing to a slow-cycling phenotype. Furthermore, miRs-103/107 increase the proliferative capacity of keratinocytes by targeting Wnt3a, which enhances Sox 9 and YAP 1 levels and thus promotes a stem cell phenotype. This miRNA family also regulates keratinocyte cell-cell communication by targeting: (i) the scaffolding protein NEDD9, preserving E-cadherin-mediated cell adhesion; and (ii) the tyrosine phosphatase PTPRM, which negatively regulates connexin 43-based gap junctions. Such regulation of cell communication and adhesion molecules maintains the integrity of the stem cell niche ultimately preserving self-renewal, a hallmark of epithelial stem cells. Finally, the laboratory is investigating the relationship between micropinocytosis and autography as a means of maintaining epithelial stem cell homeostasis. Richard M. Longnecker, PhD, Northwestern University, Department of Microbiology-Immunology [email protected] Research in the Longnecker laboratory focuses on herpes simplex virus (HSV) and Epstein-Barr virus (EBV). These viruses typically cause self-limiting disease within the human population but both can be associated with serious complications. EBV is associated with variety of hematopoietic cancers such as African Burkitt lymphoma, Hodgkin Lymphoma and adult T-cell leukemia. EBV-associated lymphoproliferative disease occurs in individuals with congenital or acquired cellular immune deficiencies. The two notable epithelial diseases associated with EBV infection are nasopharyngeal cancer and oral hairy leukoplakia. Similar to EBV, HSV latent infections are very common in humans. HSV typically does not cause severe disease but is associated with localized mucocutaneous lesions, but in some cases can cause meningitis and encephalitis. The Longnecker laboratory focuses on several aspects of EBV and HSV replication and pathogenesis. First, the molecular basis EBV transformation and how it relates to cancer is being investigated. The laboratory is currently screening selective inhibitors that may be beneficial in EBV-associated cancers such as Hodgkin lymphoma, Burkitt lymphoma and proliferative disorders that occur in HIV/AIDS and transplant patients. Second, the laboratory is investigating herpesvirus latency in the human host and pathogenesis associated with infections in humans. In this regard, the laboratory is developing animal models for EBV and HSV infections. Finally, the laboratory is investigating the function of herpesvirus encoded proteins and the cellular receptors that are important for infection both using in vivo culture models as well as animal models. Ultimately, studies by the Longnecker laboratory may provide insight for the development of novel therapeutics for the treatment of herpesvirus infections in humans and better understanding of the herpesvirus life cycle in the human host.
Northwestern University, Feinberg School of Medicine Page 8 of 11
Stephen Miller, PhD, Northwestern University, Department of Microbiology-Immunology [email protected] / http://millerlab.northwestern.edu/index.html Dr. Miller’s laboratory investigates the cellular and molecular mechanisms of multiple aspects of the immunopathogenesis and specific immunoregulation of T cell-mediated autoimmune responses employing two mouse models of multiple sclerosis (MS) - Theiler's virus-induced demyelinating disease (a virus-induced model of MS) and Relapsing Experimental Autoimmune Encephalomyelitis (R-EAE) (an autoimmune model of MS). Dr. Miller is eager to train an investigator to apply his work to autoimmune skin disorders and GVHD. Cellular and Molecular Mechanisms of T Cell Tolerance: In conjunction with the study of the effects of antigen-specific tolerance on the experimental T cell diseases described below, the laboratory utilizes transgenic and molecular approaches to study the cellular and molecular mechanisms of T cell tolerance induced by peptide-pulsed, chemically-fixed antigen presenting cells. This includes study of the differential effects of tolerance induction on specific immune functions mediated by the Th1 and Th2 subsets of CD4+ T cells, study of the effects of tolerance on expression of T cell lymphokine-specific mRNA and protein levels, and determination of the role of CTLA-4 and the mechanisms of tolerance in experimental animals (clonal deletion, clonal anergy, and/or induction of specific immunoregulatory T cells) employing both conventional and T cell receptor transgenic mice. Immunopathology of Theiler's Murine Encephalomyelitis Virus (TMEV)-Induced Demyelinating Disease: MS is a T cell-mediated autoimmune demyelinating disease which is thought to be initiated by a virus infection. TMEV, a natural mouse pathogen, is a picornavirus which induces a chronic, CD4+ T cell-mediated demyelinating disease with a clinical course and histopathology similar to that of chronic-progressive MS. Demyelination in TMEV-infected mice is initiated by a mononuclear inflammatory response mediated by virus-specific CD4+ T cells targeting virus which chronically persists in the CNS of susceptible mouse strains. Beginning 3-4 weeks after onset of clinical disease, autoimmune T cell responses to multiple myelin epitopes arise in an ordered progression and play a major pathologic role in the progression of chronic disease. Recent kinetic and functional studies have shown that T cell responses to the myelin epitopes arise due to de novo priming of self-reactive T cells to sequestered autoantigens released secondary to virus-specific T cell-mediated demyelination (i.e., epitope spreading) and are not a consequence of cross-reactivity between TMEV and self-epitopes (i.e., molecular mimicry). Epitope spreading represents an important alternate mechanism to explain the etiology of virus-induced organ-specific autoimmune diseases. We have also recently developed a molecular mimicry model of virus-induced CNS demyelination wherein mice infected with recombinant Theiler’s viruses encoding encephalitogenic myelin epitopes leads to a rapid onset paralytic disease which can be prevented by the prior induction of tolerance to the expressed myelin peptide. Current studies are directed toward: identification of the relevant immunodominant determinants on the viral capsid proteins responsible for induction of DTH and antibody responses in susceptible and resistant hosts; characterization of immunopathologic T cells isolated from the periphery and CNS of affected mice as to antigen-specificity, cytokine profile, and T cell receptor usage; isolation and molecular characterization of virus-specific Th1 and Th2 clones with the potential to produce and/or inhibit disease in vivo; immunoregulation of the demyelinating disease using antigen-nonspecific (monoclonal antibody therapies directed against costimulatory molecules) and antigen-specific (induction of virus-specific and myelin epitope-specific tolerance) mechanisms; and further characterization of the molecular mimicry model by determining the ability of TMEV expressing ‘mimics’ of myelin antigens to induce T cell-mediated demyelinating disease. Immunopathology of Murine Relapsing-Remitting EAE (R-EAE): Following immunization with myelin antigens or the adoptive transfer of myelin-specific Th1 lines/clones, SJL/J mice develop a paralytic demyelinating disease characterized by a relapsing-remitting clinical course. The laboratory is using this model to determine the mechanisms of pathogenesis and intrinsic regulation of a Th1-mediated autoimmune disease and to study the efficacy various immunoregulatory strategies as potential therapies for human autoimmune diseases. Recent studies have revealed that progression of this relapsing-remitting disease involves epitope spreading, i.e. the induction of T cell responses to endogenous encephalitogenic epitopes exposed to the immune system subsequent to acute CNS damage mediated by T cells specific for the inducing epitope. Current studies are directed toward: identification of the relative contribution of immune responses to various CNS antigens [myelin basic protein (MBP), proteolipid protein (PLP), myelin oligodendrocyte glycoprotein (MOG), myelin-associated glycoprotein (MAG), etc.] in R-EAE induction and relapses; study of the intrinsic regulation of T cell-mediated autoimmune processes by signals delivered via the B7/CD28/CTLA-4 family of T cell costimulatory molecules and by the Fas/Fas-L system; cellular and molecular characterization of the fine specificity, T cell receptor usage, and cytokine synthesis patterns of CNS-infiltrating T cells at varying times during the relapsing-remitting disease process; study of the molecular mechanisms of antigen processing and presentation of self-myelin epitopes by CNS-resident antigen presenting cells (i.e., astrocytes, microglia, and cerebrovascular endothelial cells); determination of the cellular and molecular mechanisms of specific T cell tolerance using chemically-fixed antigen presenting cells and antagonists of B7/CD28-mediated costimulation; and determination of the immunoregulatory effects of other relevant monoclonal antibodies which can potentially interfere with the induction or expression of neuroantigen-specific Th1 responses.
Northwestern University, Feinberg School of Medicine Page 9 of 11
Chad Mirkin, PhD, Northwestern University, Department of Chemistry [email protected] Chad Mirkin first discovered and reported methods for synthesizing polyvalent DNA-functionalized-gold nanoparticles, now termed spherical nucleic acids or SNAs, in 1996. After roughly a decade of development, Mirkin began to explore the potential of these structures, including those comprised of siRNA, in intracellular environments as tools in biomedicine. In collaboration with Amy Paller, Mirkin has tested the ability of SNAs to suppress gene expression in cultured primary keratinocytes and a variety of cutaneously-derived cell lines. SNAs are taken up by cells as single-entities (no transfection agents or other physical means of transfection) in ~100% of cells. Studies in mouse skin and human skin equivalents have shown rapid penetration through the stratum corneum and entire epidermis within hours, leading to gene suppression. No toxicity has been seen in cells at effected concentrations and in animal models. Ongoing studies are addressing cancer models (melanoma; Ras-induced epidermal hyperplasia), diabetic wound healing, and dominant negative gene defects. The postdoctoral fellow would work jointly with the Mirkin and Paller laboratories to continue this important work at the interface of nanoscience and technology, chemistry, biology, medicine, and the life sciences (see paragraph from the Paller laboratory). Dr. Chad Mirkin is Director of the International Institute for Nanotechnology, and he is the George B. Rathmann Prof. of Chemistry, Chemical and Biological Engineering, Biomedical Engineering, Materials Science & Engineering, and Medicine at Northwestern University. A chemist and a world-renowned nanoscience expert, Mirkin is known for his development of nanoparticle-based biodetection and therapeutics schemes, the invention and development of Dip-Pen Nanolithography and related cantilever-free nanopatterning methodologies, On-Wire Lithography (OWL), and Co-Axial Lithography (COAL), and contributions to supramolecular chemistry and nanoparticle synthesis. He has authored over 700 manuscripts and 1,000 patents and applications (over 300 issued), and he has founded multiple companies, including Nanosphere (acquired by Luminex in 2016), AuraSense, and Exicure. Mirkin has received more than 120 national and international awards, including the Sackler Prize in Convergence Research from the National Academy of Sciences (NAS), the RUSNANOPRIZE, the Wilhelm Exner Medal, and the Dan David Prize. He is a Fellow of the NAS, the National Academy of Engineering, the National Academy of Medicine, the American Academy of Arts and Sciences, the National Academy of Inventors, the American Institute for Medical and Biological Engineering, and the Materials Research Society. Mirkin has served on the Editorial Advisory Boards of over 20 scholarly journals, he is the Founding Editor of Small, and he is an Associate Editor of Journal of the American Chemical Society. He served of the President’s Council of Advisors on Science and Technology (PCAST, Obama Administration) for eight years. Brian J. Mitchell, PhD, Northwestern University, Department of Cell and Molecular Biology [email protected] / http://labs.feinberg.northwestern.edu/mitchell/ Cilia Polarity. The ability of ciliated epithelia to generate directed fluid flow is an important aspect of diverse developmental and physiological processes including proper respiratory function. To achieve directed flow, ciliated cells must generate 100-200 cilia that are polarized along a common axis both within and between cells. My lab is currently working towards understanding the molecular mechanisms for how cell polarity is coordinated as well as how individual cilia interpret the cells polarity. Centriole Duplication. Centrioles are microtubule based structures with nine fold symmetry that are involved in both centrosome organization and aster formation during cell division. During the normal cell cycle centrioles duplicate once, generating a mother / daughter pair, and in most post-mitotic vertebrate cells the mother centriole then goes on to form the basal body of a sensory cilium. Abnormalities in the duplication of centrioles (and centrosomes) are prevalent in many cancers suggesting a link between centriole duplication and cancer progression. My laboratory is addressing this fundamental question in cell biology from a novel direction with the use of Xenopus motile ciliated cells. Ciliated cells are unique among vertebrate cells in that they naturally generate hundreds of centrioles therefore providing a great system for studying the regulation of centriole duplication. Understanding how nature has overcome the typically tight regulation of centriole duplication will lend insight into the molecular mechanisms of cancer progression. Intercalation. Multiciliated cells in the skin of Xenopus embryos initially differentiate in a distinct sub-layer of the epithelium and must undergo a short directed migration prior to intercalating into the outer epithelium. We are exploiting this reiterated developmental process to study the molecular mechanisms by which cells migrate in a directed manner and how migrating cells penetrate through epithelial barriers. We have found that this process requires a delicate regulation of cytoskeletal dynamics. We are currently exploring numerous cytoskeletal regulators to understand how cells achieve directed movement and how these cells manipulate the junctional complexes of surrounding cells to facilitate their incorporation into the skin.
Northwestern University, Feinberg School of Medicine Page 10 of 11
William A. Muller, MD, PhD, Northwestern University, Department of Pathology [email protected] The Muller lab studies the inflammatory response at the cellular and molecular level. They are focused on the process of diapedesis, the "point of no return" in inflammation where leukocytes squeeze between tightly apposed endothelial cells to enter the site of inflammation. They have identified and cloned several molecules that are critical to the process of diapedesis (PECAM (CD31), CD99, and VE-cadherin) and are studying how they regulate the inflammatory response using in vitro and in vivo models. One such in vivo approach is a murine dermatitis model, in which therapeutic drugs, antibodies, etc., can be tested and a variety of knockout strains can be used to dissect disease mechanisms. The Muller lab has recently described the Lateral Border Recycling Compartment, a novel para-junctional organelle that contains PECAM, CD99, and other molecules involved in transmigration and is critical for diapedesis to occur. They are currently investigating how this compartment regulates diapedesis in the hope of finding novel targets for anti-inflammatory therapy. We are currently using spinning disc confocal intravital microscopy in a variety of mouse models. This allows us to study the mechanisms of inflammation and response to our treatments in live animals and in real time with unprecedented temporal and spatial resolution. Amy Paller, MD, Northwestern University, Department of Dermatology [email protected] Dr. Paller's laboratory is focused on two major areas with potential translational relevance: A new way to reverse the wound healing defect of diabetes: Work from the Paller laboratory has shown that expression of ganglioside GM3 is significantly upregulated in human diabetic foot, as well as the skin of diabetic mouse models. The laboratory has leveraged this novel information to show that wound healing occurs normally in diet-induced obese diabetic GM3 synthase (GM3S) knockout mice and in diet-induced obese diabetic mice with only regional suppression of GM3S expression by topically applied spherical nucleic acids (SNAs), gene regulating nanoconstructs (see below). Building on these studies, the laboratory is now: i) extending studies with SNAs to other diabetic mouse models; ii) investigating the capacity of GM3S knockdown or siRNA gene therapy to improve cutaneous sensory innervation and vascularization in diabetic models; iii) investigating the molecular mechanism of acceleration of migration in keratinocytes; and iv) understanding how GM3 content modulation affects interactions between growth factors and other lipid raft-based molecules at the membrane level in keratinocytes. Topically-delivered spherical nucleic acid nanoconjugates to suppress gene expression in skin disease: In collaborative studies with the Mirkin laboratory, the Paller group is evaluating spherical nucleic acids (SNAs), oligonucleotide in liposomal structures or conjugated to gold nanoparticles in a dense spherical array as a means to suppress gene expression in skin after topical delivery. These siRNA- and DNA-nanoconjugates easily enter cultured cells through scavenger receptor-dependent endocytosis and can suppress gene expression in cultured keratinocytes at pM to nM concentrations. SNAs are able to traverse mouse and human abdominoplasty skin, as well as human skin explants and 3D cultures. These SNAs and others that are hollow/ micellar/self-assembling (and other variants) have been develop to target upregulated genes in genetic skin disorders, epidermal hyperplasia/SCC, psoriasis, atopic dermatitis, scar formation, and diabetic wound healing (see above). SNA technology is already in clinical studies. The fellow would be involved in generating new nanoconstructs and testing them in vitro and in vivo, as well as leveraging their use for discovery. John Rogers, PhD, Northwestern University, Department of Materials Science and Engineering [email protected] / http://rogersgroup.northwestern.edu/ Dr. Rogers is a member of the National Academy of Sciences, the National Academy of Engineering and the American Academy of Arts and Sciences. He is the Louis Simpson and Kimberly Querrey Professor of Materials Science and Engineering, Biomedical Engineering, and Neurological Surgery, with appointments by courtesy in Electrical Engineering and Computer Science, Mechanical Engineering and Chemistry. He serves as Director of the Center for Bio-Integrated Electronics. Rogers is internationally renowned for designing and developing classes of electronic devices that can bend, stretch, and twist, be integrated with the human body, and offer diverse diagnostic and therapeutic functions with clinical relevance. His research spans disciplines and exploits novel approaches to problems with the potential to change the fields of industrial, consumer, and biomedical electronics. Rogers’ research includes fundamental and applied aspects of nano and molecular scale fabrication as well as materials and patterning techniques for unusual electronic and photonic devices, with an emphasis on bio-integrated and bio-inspired systems. His research has been recognized with many awards He has published more than 550 papers, and is an inventor on over 100 patents and patent applications, more than 70 of which are licensed or in active use by large companies and startups that he has co-founded, and has received numerous honors and awards for his work, including the Lemelson-MIT Prize, a MacArthur Fellowship, a Smithsonian Award for American Ingenuity in the Physical Sciences, and election into the National Academy of Inventors.
Northwestern University, Feinberg School of Medicine Page 11 of 11
Robert Schleimer, PhD, Northwestern University, Department of Medicine, Division of Allergy [email protected] Dr. Schleimer has a longstanding interest in the mechanisms of action of glucocorticoids in allergic diseases. Past studies have ranged from translational investigations in human subjects to molecular biological assessment of glucocorticoid action. Mechanisms of the pathogenesis of allergic diseases including asthma, rhinosinusitis, atopic dermatitis and others have also been an area of investigation. Recent studies have focused on the role of epithelial cells as integrators of responses in the airways, including inflammation, innate immunity and adaptive immunity. Jonathan Silverberg, MD/PhD, MPH, Northwestern Univesity , Department of Dermatology [email protected] Dr. Silverberg’s research interests include studying the classical, molecular and genetic epidemiology of skin disease. Dr. Silverberg completed a PhD involving basic science studies of neuroimmunology and an MPH in biostatistics and epidemiology. His goal is to fuse the disparate fields of immunology and molecular biology with large-scale population-based epidemiology research. Recent studies have focused on the epidemiology, comorbidities and burden of atopic dermatitis and other inflammatory skin disorders. Potential fellows would train with faculty of the Institute for Public Health and Medicine at Northwestern, including Dr. Silverberg, in epidemiological research in a wide range of possible areas related to dermatology, dermato-epidemiology, patient-reported outcomes and health services research. The fellow will have an opportunity to obtain a master's degree (choices include in Clinical Investigation, Epidemiology and Biostatistics, Health Services and Outcomes Research, Informatics, or Public Health) during the fellowship period. Sergey Troyanovsky, PhD, Northwestern University, Department of Dermatology [email protected]
Dr. Troyanovsky’s research focuses on cadherin, intercellular, adhesion, and signaling. Classic cadherins are critical proteins mediating cell-cell adhesion and various signaling pathways responsible for cellular proliferation, differentiation, and morphogenesis. Abnormalities in this system are causal factors in many pathologies, including cancer. The molecular mechanisms of cadherin-based adhesion, however, are largely unknown. How do cadherins establish the adhesion contact? How do they interact with the cytoskeleton? What are the signaling pathways they control? The laboratory’s work is centered on these questions. We are currently working on the following specific projects: (i) cadherin -g-secretase interactions: roles in cell-cell adhesion, notch signaling and amyloid processing; (ii) mechanisms of cadherin inactivation during tumor progression; (iii) live cell imaging of cadherin endocytosis; (iv) cadherin interactions with the actin cytoskeleton; and (v) the dynamics of adherens junctions during frog skin development John Varga, MD, Northwestern University, Department of Medicine, Division of Rheumatology [email protected]
Dr. Varga is internationally renowned for his research on scleroderma. His laboratory currently focuses on the role of the TGF-ß in fibrosis using animal models, as well as on Smad signal transduction pathways and Smad interactions with other kinase cascades. The group is currently evaluating small molecule inhibitors of these pathways in vitro and in vivo, including imatinib as a novel anti-fibrotic agent for cutaneous sclerosis and keloidal processes. Dr. Varga is interested in the role of epidermal cells in inducing fibrosis, particularly in scleroderma and morphea. Douglas Vaughan, MD, Northwestern University, Department of Medicine, Division of Cardiology [email protected] Dr. Vaughan directs a multidisciplinary research group focused on investigating the role of the plasminogen activator system in cardiovascular disease. Active experimental programs are underway at the molecular and cellular level in animals and in humans. Transgenic and knockout mice are used in a variety of studies designed to explore the tissue-specific expression of PAI-1 in vivo and the role of the fibrinolytic system in vascular disease and tissue remodeling. Interestingly, his PAI-1 transgenic mouse showed a hair defect and Dr. Vaughan is actively collaborating with dermatology in further investigations of the interface between PAI-1 and the follicle and leveraging the discovery towards human alopecia. In addition to the formal mentors, we have four scientists (listed below) who, at the time of re-submission of this T-32, have external funding, but do not have NIH funding; we anticipate that they will have independent NIH funding during the initial 1-2 years of this T-32. Thus we are designating these scientists as “junior mentors” for post-doctoral fellows with appropriate supervision from one of the above senior mentors.
Oregon Health & Science University
OREGON HEALTH & SCIENCE UNIVERSITY Training in the Basis of Skin/Mucosa Pathobiology
Positions for two (2) pre-doctoral and three (3) post-doctoral trainees are open each year in an NIH-funded program for training highly qualified candidates for academic careers in basic and translational research in skin diseases, including cancer, psoriasis and atopic dermatitis. The OHSU Department of Dermatology has a strong history of clinical and scientific research and a 40-year record in training dermatology residents including physician scientists and postdoctoral scientists on the path to independence. Candidates who desire an academic career in investigative dermatology or basic skin/mucosa research with a strong clinical translational component will be selected. Criteria will include potential for independence, letters of recommendation, publication record and evidence of potential for impact in dermatology.
To apply please e-mail cover letter, statement of research (current and future interests and aims), CV and three letters of reference to Molly Kulesz-Martin, Ph.D., at [email protected].
Applications are accepted continuously.
Note: To be eligible for a pre-doctoral slot, candidates must be enrolled in a Ph.D. program at OHSU. To be eligible for a postdoctoral slot, candidates must first identify mentor(s) in our program and join their lab(s).
Trainees supported by this training grant must be U.S. citizens or permanent residents. Applicants from diverse backgrounds that may be underrepresented in academics and science are especially encouraged to apply. Postdoctoral stipends are paid at standard NIH levels, pre-doctoral stipends at OHSU graduate research assistant levels. For more information contact:
Skin/Mucosa Research Training Program Molly Kulesz-Martin, Ph.D., Director Dept. of Dermatology, L468R Oregon Health & Science University 3181 SW Sam Jackson Park Road Portland, Ore. 97239-3098 Voice: 503 418-4273 Fax: 503 418-4266 E-mail: [email protected]
http://www.ohsu.edu/xd/education/schools/school-of-medicine/departments/clinical-departments/dermatology-research/research-training-program/index.cfm
Shriners Hospitals for Children
SHRINERS HOSPITALS FOR CHILDREN (SHC) Research Fellowship Award Program (RFAP)
DESCRIPTION OF RESEARCH CONDUCTED BY THE LAB: Our lab focuses on wound healing, scar formation, and tissue engineering. Our goals are to understand how the process of wound healing goes awry in susceptible individuals, resulting in development of keloids or hypertrophic scars, and to develop novel, effective strategies for improved healing and suppression of scarring. In addition, we are involved in development of next-generation skin substitutes, with increased homology with native human skin, for improved treatment of traumatic skin loss injuries and cutaneous disease. NATURE OF THE AVAILABLE TRAINING POSITION: We have an opportunity for a talented postdoctoral fellow interested in obtaining fellowship funding to study wound healing at the Shriners Hospitals for Children – Cincinnati, in the laboratory of Dorothy Supp, PhD. This is a competitive process involving the Shriners Hospitals for Children (SHC) Research Fellowship Award Program (RFAP), and funding is not guaranteed. The successful candidate will prepare and submit a fellowship application, with Dr. Supp’s guidance, for a two-year research project involving an area of interest to the laboratory. Dr. Supp will serve as the applicant’s sponsor and mentor. To be eligible, the applicant must be either a citizen or permanent resident of the United States, or should have appropriate visa status to work as a scientist in the U.S. Additionally, the candidate must have earned the MD, MD-PhD, or PhD degree within the past five years, or expect to receive the doctoral degree by the award date. A background check will be required. Awards provide salary, fringe benefits, and an allowance for supplies, animals, travel, and other expenses. APPLICATION DEADLINE: The deadline for submission of the fellowship application is September 15, 2017, for a start date of January 1, 2018. Applicants will be notified of award status by mid-November, 2017. Please contact Dr. Supp as soon as possible if you are interested in this opportunity to ensure sufficient time for development of a successful fellowship application. CONTACT INFORMATION: Dorothy Supp, PhD Shriners Hospital for Children Cincinnati, Ohio [email protected] or [email protected] (513) 872-6346 Shriners Hospitals for Children, Cincinnati is a pediatric hospital specializing in burns and other complex wounds, plastic and reconstructive surgery, and cleft lip and palate. Research labs are located within the hospital, facilitating interactions between researchers and clinicians. SHC-Cincinnati is affiliated with the University of Cincinnati Medical Center, and is located across the street from Cincinnati Children’s Hospital Medical Center. To learn more, visit http://www.shrinershospitalsforchildren.org/Locations/cincinnati
The Wang Lab, Stanford University School of Medicine
STANFORD UNIVERSITY SCHOOL OF MEDICINE The Wang Lab
The Wang Lab in the Department of Dermatology (http://wanglab.derm.stanford.edu/), located within the Stanford School of Medicine, is currently seeking qualified postdoctoral fellows. The lab takes an interdisciplinary approach to studying fundamental mechanisms controlling gene expression in mammalian cells, and how epigenetic mechanisms such as DNA methylation, chromatin modifications, and RNA influence chromatin dynamics to affect gene regulation. The lab is specifically interested in: How various dynamic epigenetic changes in chromatin structure impact gene expression during stem cell
pluripotency/self-renewal, cellular differentiation, and reprogramming Epigenetic mechanisms of the pruritus (itch) circuitry
How three-dimensional chromosomal structure and dysregulation contribute to development of diseases such as aging
and cancer. The postdoctoral position will commonly involve close interactions both within the lab and with collaborating groups at Stanford University and at other institutions. Postdoctoral training includes participation in seminars and retreats of the Stanford Program in Epithelial Biology, the Stanford Program in Cancer Biology, and the Stanford Institute for Stem Cell Biology and Regenerative Medicine. General Information about postdoctoral fellowships at Stanford may be found at the Stanford Postdoctoral Scholars site: postdocs.stanford.edu. The position will be available until filled. Postdoctoral applicants should email a cover describing your past and future projects, career goals, what you hope to get out of the Wang Lab, and what you hope to bring to the Wang Lab. Please enclose your CV and the names, emails, and phone numbers of three (3) references to: Kevin C. Wang, M.D., Ph.D [email protected].
Stanford University School of Medicine
STANFORD UNIVERSITY SCHOOL OF MEDICINE Training Opportunity in Epithelial Biology
The Stanford Postgraduate Training Grant in Epithelial Biology at Stanford Medical Center, under the direction of Paul Khavari, provides the basis for a collaborative interdisciplinary effort involving multiple departments that aims to focus developments in basic science towards the ultimate goal of positively impacting human skin disease. We train highly qualified basic research scientists and physicians as post-doctoral fellows for future research careers in skin sciences and related fields and focus on producing individuals capable of pursuing their research interests as independent investigators in a full-time academic position. Virtually all postdoctoral applicants to our training program apply directly to a specific P.I. in the program based upon that investigator’s field of interest and specialization, and publication record. The decision to follow-up an application with a personal interview is dependent upon the earlier work of the applicant, publication record, and discussions both with the applicant and references provided. Interested individuals may apply directly to the Training Grant faculty: Paul Khavari, Dermatology [email protected] https://med.stanford.edu/profiles/epibio/paul-khavari/ Howard Chang, Dermatology [email protected] https://med.stanford.edu/profiles/epibio/howard-chang/ Andrew Fire, Pathology [email protected] https://med.stanford.edu/profiles/andrew-fire Minx Fuller, Developmental Biology [email protected] https://med.stanford.edu/profiles/margaret-fuller Peter Marinkovich, Dermatology [email protected] https://med.stanford.edu/profiles/epibio/matt-marinkovich/ Garry Nolan, Microbiology & Immunology [email protected] https://med.stanford.edu/profiles/epibio/garry-nolan/ Roel Nusse, Developmental Biology [email protected] https://med.stanford.edu/profiles/epibio/roeland-nusse/ Anthony Oro, Dermatology [email protected] https://med.stanford.edu/profiles/epibio/anthony-oro/ Michael Snyder, Genetics [email protected] https://med.stanford.edu/profiles/michael-snyder Jean Tang, Dermatology [email protected] https://med.stanford.edu/profiles/epibio/jean-tang/ Joanna Wysocka, Chemical.Systems Biology [email protected] https://med.stanford.edu/profiles/joanna-wysocka Training Opportunity in Epithelial Biology http://epibio.stanford.edu
The Sarin Laboratory, Stanford University School of Medicine
STANFORD UNIVERSITY SCHOOL OF MEDICINE The Sarin Laboratory
Research Summary The Sarin laboratory in Stanford Department of Dermatology is seeking a postdoctoral research fellow to join our translational skin cancer genomics research group. Using next generation sequencing technologies, we investigate the genetic alterations involved in skin cancer development, response to therapy, and prognosis. We also employ genomic technologies to understand inherited susceptibility to skin cancer. We are interested in individuals with diverse experiences in basic, quantitative and/or clinical research who are interested in developing multidisciplinary skills, work independently, and are passionate about their studies. Responsibilities The successful applicant will be responsible for independent research focused on the genomics of skin cancer and skin cancer risk. Research fellows will participate in clinical trials, translational genomics research, and bioinformatics analysis. The primary responsibility of this position will be scientific research, additional duties include: reading scientific literature, giving talks, attending seminars and conferences, writing manuscripts and mentoring students. Desired Qualifications • PhD or MS in cancer genetics or bioinformatics related field • A minimum of one accepted first-author publication in a high-or mid-tier peer-reviewed journal. • Highly motivated with excellent interpersonal skills. • Excellent communication and technical writing skills. Programming skills a plus! • Preference given to candidates with an independent source of funding. Contact Interested applicants should send a CV and cover letter why you are interested in our work and how you would be a good fit to Rachel Morgan [email protected]
SUNY, Stony Brook University
STONY BROOK UNIVERSITY SCHOOL OF MEDICINE Dr. Jiang Chen’s Laboratory
The laboratory of Dr. Jiang Chen investigates skin and hair follicle morphogenesis and skin cancers with an emphasis on the primary cilia, intracellular trafficking, small GTPase, and signaling. Projects are basic science in nature but are also highly relevant to dermatological disorders. Mouse models and mammalian cells are primary model systems of the laboratory. Diverse molecular and cell biology techniques are used. A postdoctoral position is available for a dedicated PhD or MD/PhD, who has relevant experience in skin or epithelial biology. The ideal candidate is a team player, eager to break new grounds, and has a clear academic career path. Position is available immediately until filled. Long Island offers superb opportunity to achieve excellent work-life balance, and is ideal for raising a family. Contact: Jiang Chen, MD Departments of Pathology and Dermatology Stony Brook University School of Medicine Basic Science Tower, Level 9, Room 151 Stony Brook, NY 11794 Office: (631) 444-3199 Lab: (631) 444-6484 E-mail: [email protected]
Dr. Karen Taraszka-Hastings Laboratory, University of Arizona, College of Medicine
UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE Dr. Karen Taraszka Hastings Laboratory
The University of Arizona, College of Medicine, Phoenix Department of Basic Medical Sciences invites applicants to apply for a challenging and rewarding opportunity to contribute as a Postdoctoral Research Associate in the laboratory of Dr. Karen Taraszka Hastings. Exciting opportunity to take on a newly funded, up to four year, project investigating antigen presentation and T-cell responses in cutaneous autoimmunity and melanoma in the laboratory of Dr. Karen Taraszka Hastings at the University of Arizona College of Medicine – Phoenix. Our laboratory studies the role of gamma-interferon-inducible lysosomal thiol reductase (GILT) in antigen presentation, control of T cell activation and tolerance to cutaneous antigens, and in melanoma outcome, using mouse models, cell culture systems, and patient specimens. Opportunities for professional development include presentation of research findings at national meetings, mentorship in grant and manuscript writing, teaching, and public policy, which will enhance career progression. Dr. Hastings’ laboratory is located in the state-of-the art Arizona Biomedical Collaborative-1 building on the downtown Phoenix Biomedical Campus. The atmosphere is highly collaborative, and the laboratory interacts with local researchers at the Mayo Clinic Arizona and the University of Arizona in Tucson, as well as scientists at the University of California San Francisco and Yale University. For further information, please visit http://phoenixmed.arizona.edu/directory/hastings-karen and http://hastings.lab.arizona.edu or E-mail [email protected]. Available for in-person interviews at the Society for Investigative Dermatology annual meeting in Portland, OR in April 2017. The Successful Candidate will: Design and perform experiments, interpret data, and analyze results independently under the direction of the principal
investigator. Prepare manuscripts for publication in peer-reviewed journals. Present research findings at internal, local and national scientific meetings. Participate in grant writing, including generation of preliminary data, grant submission, and preparation of progress
reports. Assist in training and supervision of technical staff and/or students. Qualifications for the Position: PhD or equivalent degree in Immunology, Cancer Biology, or a related field Expertise with multicolor flow cytometry, adoptive T cell transfer, bone marrow chimeras, APC and T cell isolation from
lymphoid organs and skin, and/or mouse models of autoimmunity and cancer, redox biology and/or autophagy. For full job description and to apply please visit http://uacareers.com/postings/15336 or http://uacareers.com Posting Number P20305. Outstanding UA benefits include health, dental, and life insurance; vacation, sick leave and holidays; UA/ASU/NAU tuition reduction for employee and qualified family members; access to campus cultural and recreational activities and more.
University of Arizona, College of Medicine
UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE
Earn a Graduate Degree in Clinical Translational Sciences! The University of Arizona offers a Ph.D. and M.S. in this vital new field.
Open to applicants with a terminal health-sciences degree (M.D., D.P.H., etc.) or a bachelor’s or master’s degree.
Carry out significant research to illuminate clinical findings.
Customize your coursework with courses in medicine, microbiology, pharmacology, public health, and other disciplines.
Gain professional skills including grant writing, presentation, and research ethics.
For more information about the CTS program: https://cts.uahs.arizona.edu/
E-mail: [email protected]
Phone: Mike Renning, (520) 626-9561
APPLICATION DEADLINES:
For Spring admission: Nov 15 (U.S. or International applicants)
For Fall admission: May 1 (U.S. applicants) or April 15 (International)
University of California, Irvine
UNIVERSITY OF CALIFORNIA, IRVINE The University of California, Irvine Department of Dermatology is currently seeking applicants for a volunteer clinical research specialist position to begin July 2017. This opportunity is a one-year, full-time fellowship under the direction of Natasha Mesinkovska, M.D., Ph.D., Director of the Dermatology Clinical Research Center. Dr. Mesinkovska is a board-certified dermatologist and dermatopathologist. The fellow will gain experience in the operation of industry-sponsored and investigator-initiated clinical trial protocols (IRB submission, patient recruitment, enrolling research subjects, preparing for study patient visits, collecting laboratory samples, maintenance of regulatory and IRB records, data management and maintenance of registry databases). Fellows will have opportunities to pursue scholarly activities such as publishing case reports, review articles and research findings when appropriate. Fellows will also have the opportunity to participate in departmental grand rounds and conferences. Support will be provided for efforts to obtain extramural funding. The fellow will have the opportunity to shadow physicians in the dermatology clinics to provide exposure to dermatologic conditions and treatments. This fellowship position is intended to provide a foundation for the individuals to advance their academic careers in the field of dermatology. Completion of this fellowship will not guarantee acceptance to a dermatology residency program, but the experience will increase this probability. Applicant must have an M.D. or completed medical school (MSIII or greater). This position does not require eligibility for a medical license in the state of California. The position is for a one (1) 1 year commitment. We are seeking highly motivated individuals with strong organizational, writing, and clinical skills and with a genuine interest in pursuing clinical research in dermatology. Proficiency in English is required. Interested candidates should email their Curriculum Vitae, letter of intent, USMLE scores (if applicable), medical school transcripts (unofficial is fine), and three (3) letters of recommendation to: Jerry L. McCullough, Ph.D. Dermatology Clinical Research Center University of California, Irvine Department of Dermatology Email: [email protected]
University of Michigan
UNIVERSITY OF MICHIGAN Postdoctoral Fellowship Opportunities in Cutaneous Biology
NIH T32-funded postdoctoral fellowships are available at the University of Michigan Medical School, Department of Dermatology in Ann Arbor, Michigan. Training opportunities exist in cutaneous oncology, hair follicle stem cell biology, skin aging, and the immunology and genetics of psoriasis and other inflammatory skin diseases. Successful candidates will possess MD, PhD, or MD/PhD degrees with relevant life sciences training, and will be interested in a career in Dermatology / cutaneous biology research. Core Dermatology Faculty:
A. Dlugosz [email protected]
J.T. Elder [email protected]
G.J. Fisher [email protected]
J.E. Gudjonsson [email protected]
A. Johnston [email protected]
S. Wong [email protected]
More information about the ongoing research of our core faculty is available online at: experts.umich.edu
Due to restrictions associated with the funding mechanism, only U.S. citizens or permanent residents will be eligible for
these opportunities.
Applications preferred by May 1, 2017 but will be accepted throughout the year if positions remain available.
The University of Michigan is an Equal Opportunity/Affirmative Action Employer.
Please send CV and references to: James T. Elder, MD, PhD Department of Dermatology University of Michigan Medical School Email: [email protected] Or send to the faculty member of interest to you.
University of Michigan
UNIVERSITY OF MICHIGAN Research Opportunities in Molecular Genetic Dermatology
Research Opportunities are available for MD, PhD, or MD-PhD-trained individuals in the molecular genetics and immunology of psoriasis and psoriatic arthritis. Additional opportunities are available in keratinocyte growth regulation via autocrine EGF receptor ligands. Medical students interest in taking at least one year off from their medical training are also welcome to apply. Research in psoriasis will be focused on the integration of genetic variation and biological responses in psoriasis and psoriatic arthritis. Project will involve disease-related alterations in signal transduction and/or chromatin structure and gene expression. Research on keratinocyte growth control will focus on the role of the intracellular domains of EGF receptor ligands in the regulation of keratinocyte cell cycle, migration, differentiation, and survival. The University of Michigan is an Equal Opportunity Employer. Please send Curriculum Vitae to: James T. Elder, MD, PhD Department of Dermatology University of Michigan 7421 Medical Sciences 1 1300 E. Catherine Ann Arbor, MI 48109-5675 Email: [email protected]
Web: [email protected]
http://www.derm.med.umich.edu/training/
Page 1 of 7 University of Pennsylvania, Perelman School of Medicine
UNIVERSITY OF PENNSYLVANIA Perelman School of Medicine
Postdoctoral fellowships, and short-term (2–3 month) or long-term (one year) pre-doctoral research opportunities are available in the Department of Dermatology at the University of Pennsylvania, Perelman School of Medicine. These positions are supported by our Dermatology NIH T32 training grant and by the grants of individual investigators. Applications are accepted on a rolling basis. Please see our departmental website for online application forms for the training grant (https://dermatology.upenn.edu/t32/) and detailed research descriptions (https://www.pennmedicine.org/departments-and-centers/dermatology/about-us/physicians-and-faculty-members). BRIAN CAPELL, MD, PHD / [email protected] Research description: Epigenetics and chromatin regulatory mechanisms, histone modifications, enhancers, and transcriptional regulation in skin cancer, aging, and inflammatory diseases. Selected recent citations: Capell BC, Berger SL. “The role of epigenetics in disease and treatment”. Harrison’s Principles of Internal Medicine. 20th Ed: 2017. Capell BC, Drake A, Shah PP, Dorsey J, Simola DF, Dou Z, Zhu J, Sammons M, Donahue G, Rai TS, Natale CA, Ridky TW, Adams PD,
Berger SL. “MLL1 is essential for the senescence-associated secretory phenotype.” Genes & Development. 30(3): 2016. Ghosh K, Capell BC. “The senescence-associated secretory phenotype: critical effector in skin cancer and aging.” Journal of
Investigative Dermatology. 136(11): 2016. Dou Z, Xu C, Donahue G, Ivanov A, Pan J, Zhu J, Capell BC, Catanzaro JM, Ricketts MD, Shimi T, Adam SA, Mamorstein R, Zong WX,
Goldman RD, Johansen T, Adams PD, Berger SL. "Autophagy mediates degradation of nuclear lamina." Nature. 527(7576): 2015. Capell BC, Berger SL. “Genome-wide epigenetics.” Journal of Investigative Dermatology. 133(6): 2013. Capell BC, Tlougan BE, Orlow SJ. “From the rarest to the most common: insights from progeroid syndromes into skin cancer and
aging.” Journal of Investigative Dermatology. 129(10): 2009. Capell BC, Olive M, Erdos MR, Cao K, Faddah DA, Whipperman M, San H, Qu X, Ganesh SK, Chen X, Avallone H, Kolodgie F, Virmani R,
Nabel EG, Collins FS. “A farnesyltransferase inhibitor prevents the onset and late progression of cardiovascular disease in a progeria mouse model”. Proceedings of the National Academy of Sciences. 105(41): 2008.
Capell BC & Collins FS. “Human laminopathies: nuclei gone genetically awry”. Nature Reviews Genetics. 7(12): 2006. Capell BC, Erdos MR, Madigan JP, Fiordalisi JJ, Varga R, Conneely KN, Gordon LB, Der CJ, Cox AD, Collins FS. “Inhibiting the
farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome”. Proceedings of the National Academy of Sciences. 102(36): 2005.
GEORGE COTSARELIS, MD / [email protected] Research description: Hair follicle stem cells and biology, alopecia, wound healing, skin regeneration. Selected recent citations: Plikus MV, Guerrero-Juarez CF, Ito M, Li YR, Dedhia PH, Zheng Y, Shao M, Gay DL, Ramos R, His TC, Oh JW, Wang X, Ramirez A,
Konopelski SE, Elzein A, Wang A, Supapannachart RJ, Lee HL, Lim CH, Nace A, Guo A, Treffeisen E, Andl T, Ramirez RN, Murad R, Offermanns S, Metzger D, Chambon P, Widgerow AD, Tuan TL, Mortazavi A, Gupta RK, Hamilton BA, Millar SE, Seale P, Pear WS, Lazar MA, Cotsarelis G. (2017). Regeneration of fat cells from myofibroblasts during wound healing. Science 355, 748-752
Gay, D., Kwon, O., Zhang, Z., Spata, M., Plikus, M.V., Holler, P.D., Ito, M., Yang, Z., Treffeisen E., Kim, C.D., Nace, A., Zhang, X., Baratano, S., Wang, F., Ornitz, D.M., Millar, S.E., Cotsarelis, G. Fgf9 from dermal T cells induces hair follicle neogenesis after wounding. Nat. Med. 2013 19(7): 916-923.
Garza LA, Liu Y, Yang Z, Alagesan B, Lawson JA, Norberg SM, Loy DE, Zhao T,Blatt HB, Stanton DC, Carrasco L, Ahluwalia G, Fischer SM, Fitzgerald GA, Cotsarelis G. (2012). Prostaglandin d2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Sci Transl Med. 4, 126ra34.
Garza LA, Yang CC, Zhao T, Blatt HB, Lee M, He H, Stanton DC, Carrasco L, Spiegel JH, Tobias JW, Cotsarelis G. (2011). Bald scalp in men with androgenetic alopecia retains hair follicle stem cells but lacks CD200-rich and CD34-positive hair follicle progenitor cells. J Clin Invest. 121, 613-22.
Ito M, Yang Z, Andl T, Cui C, Kim N, Millar S, Cotsarelis G. Wnt-dependent de novo hair follicle regeneration in adult mouse skin after wounding. Nature. 2007 447: 316-19.
Ito M, Liu Y, Yang Z, Nguyen J, Liang F, Morris RJ, Cotsarelis G. Stem cells in the hair follicle bulge contribute to wound repair but not to homeostasis of the epidermis. Nat Med. 2005 11:1351-4
Morris RJ, Liu Y, Marles L, Yang Z, Trempus C, Li S, Lin JS, Sawicki JA, Cotsarelis G. Capturing and profiling adult hair follicle stem cells. Nat Biotechnol. 2004 22:411-7
Page 2 of 7 University of Pennsylvania, Perelman School of Medicine
JOEL M. GELFAND, MD, MSCE / [email protected] Research description: Clinical trials; psoriasis; epidemiology Selected recent citations: Yeung H, Takeshita T, Mehta NN, Kimmel Se, Ogdie A, Margolis DJ, Shin DB, Attor R, Troxel AB, Gelfand JM: Psoriasis severity and the
prevalence of major medical co-morbidities: a population based study. JAMA Dermatology 149: 1173-9, 2013. Ogdie A, Haynes K, Troxel AB, Love TJ, Hennessy S, Choi H, and Gelfand JM: Risk of mortality in patients with psoriatic arthritis,
rheumatoid arthritis, and psoriasis: a longitudinal cohort study. Ann Rheum Disease 73(1): 149-53, January 2014. Wan J, Wang S, Haynes K, Denburg MR, Shin DB, and Gelfand JM: The risk of moderate to advanced kidney disease in patients with
psoriasis: a population-based cohort study. British Medical Journal 15: 347:593, October 2013. Mehta NN, Li R, Krishnamoorthy P, Yu Y, Farver W, Rodriguez A, Raper A, Wilcox M, Baer A, DerOhannesian S, Wolfe M, Reilly MP, Rader
DJ, Van Voorhees A, Gelfand JM: Abnormal Lipoprotein particles and cholestrol efflux capacity in patients with psoriasis. Atherosclerosis (224), 218-21, 2012.
Mehta N, Yu YD, Saboury B, Foroughi N, Krishnamoorthy P, Raper A, Baer A, Antigua J, Van Voorhees AS, Torigian DA, Alavi A, and Gelfand JM: Systemic and Vascular Inflammation in Patients with Moderate to Severe Psoriasis as measured by [18F]-Fluorodeoxyglucose Positron Emission Tomography/Computed Tomography (FDG-PET/CT): A Pilot Study. Archives of Dermatology 147(9): 1031-1039, September 2011.
Langan SM, Seminara, NM, Shin, DB, Troxel A, Kimmel SE, Mehta NN, Margolis DJ, and Gelfand JM: Prevalence of metabolic syndrome in patients with psoriasis: A population-based study in the United Kingdom. Journal of Investigative Dermatology Advance Online Publication, November 2011.
Gelfand JM, Wan J, Callis Duffin, K, Krueger GG, Kalb RE, Weisman JD, Sperber BR, Stierstorfer MB, Brod BA, Schleicher SM, Bebo BF, Troxel AB, Shin DB, Steinemann JM, Goldfarb J, Yeung H, and Van Voorhees AS: Comparative Effectiveness of Commonly Used Systemic Treatments or Phototherapy for Moderate to Severe Plaque Psoriasis in the Clinical Practice Setting. Archives of Dermatology 148(4): 487-94, April 2012
Gelfand, JM, Neimann, AL, Shin, DB, Wang, X, Margolis, DJ, and Troxel, AB. The risk of myocardial infarction in patients with psoriasis. Journal of the American Medical Association. 2006;296:1735-1741.
ELIZABETH GRICE, PHD / [email protected] Research description: Skin microbiome; host-microbe interactions; microbe-microbe interactions; biofilms; chronic wounds; microbiota-derived secondary metabolites; bioinformatic tool development. Selected recent citations: Loesche M, Gardner SE, Kalan L, Horwinski J, Zheng Q, Hodkinson BP, Tyldsley AS, Franciscus CL, Hillis SL, Mehta S, Margolis DJ, Grice
EA (2017) Temporal stability in chronic wound microbiota is associated with poor healing. The Journal of Investigative Dermatology 137(1):237-44. PMCID: PMC5279919.
Kalan L, Loesche M, Hodkinson BP, Heilmann K, Ruthel G, Gardner SE, Grice EA (2016). Redefining the chronic wound microbiome: Fungal communities are prevalent, dynamic, and associated with delayed healing. mBio 7(5):e01058-16. PMCID: PMC5013295.
Meisel JS, Hannigan GD, Tyldsley AS, SanMiguel AJ, Hodkinson BP, Zheng Q, Grice EA (2016). Skin microbiome surveys are strongly influenced by experimental design. Journal of Investigative Dermatology 136(5):947-56. PMCID: PMC4842136.
Bradley CW, Morris DO, Rankin SC, Cain CL, Misic AM, Houser T, Mauldin EA, Grice EA (2016). Longitudinal evaluation of the skin microbiome and association with microenvironment and treatment in canine atopic dermatitis. Journal of Investigative Dermatology. 136(6):1182-90. PMCID: PMC4877200.
Hannigan GD, Meisel JS, Tyldsley AS, Zheng Q, Hodkinson BP, SanMiguel AJ, Minot S, Bushman FD, Grice EA (2015). The human skin double-stranded DNA virome: Topographical diversity, genetic enrichment, and dynamic associations with the host microbiome. Mbio 6(5):e01578-15 PMCID: PMC4620475.
Rafail S, Kourtzelis I, Foukas PG, Markiewski MM, DeAngelis RA, Guariento M, Ricklin D, Grice EA, Lambris JD (2015). Complement deficiency promotes cutaneous wound healing in mice. Journal of Immunology 194(3): 1285-91. PMCID: PMC4297721.
Chehoud C, Rafail S, Tyldsley AS, Seykora JT, Lambris JD, Grice EA (2013). Complement modulates the cutaneous microbiome and inflammatory milieu. Proceedings of the National Academy of Sciences of the United States of America 110(37):15061-6. PMCID: PMC3773768
Page 3 of 7 University of Pennsylvania, Perelman School of Medicine
THOMAS LEUNG, MD, PHD / [email protected] Research description: Understanding the molecular and cellular mechanisms underlying mammalian tissue regeneration, development of novel therapeutics for regenerative medicine, clinical translation, inflammation, wound healing Selected recent citations:
Gorrell E.S., Leung T.H., Khuu P., and Lane A.T. (2014) Purified Type I Collagen Wound Matrix Improves Chronic Wound Healing in Patients with Recessive Dystrophic Epidermolysis Bullosa. Pediatr Dermatol. PMID: 25557742
Sebastiano V., Zhen H.H., Derafshi B.H., Bashkirova E., Melo S., Wang P., Leung T.L., Siprashvili Z., Tichy A., Li J., Ameen M., Hawkins J., Lee S., Li L., Schwertschkow A., Bauer G., Lisowski L., Kay M.A., Kim S.K., Lane A.T., Wernig M., and Oro A.E. (2014) Human COL7A1-corrected induced pluripotent stem cells for the treatment of recessive dystrophic epidermolysis bullosa. Science Translational Medicine. 26;6(264):264ra163, 2014. PMID: 25429056.
Leung T.H., Zhang L., Wang J., Ning S., Knox S., and Kim S.K. (2013) Hypochlorite ameliorates NF-κB-mediated skin diseases. The Journal of Clinical Investigation. 123(12):5361-70, 2013. PMID: 24231355.
Covert M.W.*, Leung T.H.*, Gaston J.E. and Baltimore D. (2005) Achieving Stability of LPS-Induced NF-κB Activation. Science. 309(5742): 1854-7, 2005. PMID: 16166516. *These authors contributed equally to this work.
Leung T.H., Hoffmann A., and Baltimore D. (2004) One nucleotide change in a kappa B site can determine cofactor specificity for NF-κB dimers. Cell. 118(4): 453-64, 2004. PMID: 15315758.
DAVID J. MARGOLIS, MD, PHD / [email protected] Research description: Clinical trials, epidemiology, pharmacoepidemiology of chronic wounds (venous leg ulcers, diabetic foot ulcers and pressure ulcers), acne, and atopic dermatitis, genetic epidemiology of atopic dermatitis; comparative effectiveness of wound therapies; spatial correlation of lower extremity amputation; Selected recent citations: Margolis DJ, Gupta J, Apter AJ, Ganguly T, Hoffstad O, Papadopoulos M, Rebbeck TR, Mitra N. Filaggrin-2 variation is associated with
more persistent atopic dermatitis in African American subjects. J Allergy Clin Immunol. 2014 Mar;133(3):784-9. doi: 10.1016/j.jaci.2013.09.015. Epub 2013 Nov 1. PubMed PMID: 24184149; PubMed Central PMCID: PMC3943564.
Barbieri JS, Hoffstad O, Margolis DJ. Duration of oral tetracycline-class antibiotic therapy and use of topical retinoids for the treatment of acne among general practitioners (GP): A retrospective cohort study. J Amer Acad Dermatol, 75(6): 1142-1150, 2016.
Chang J, Mitra N, Hoffstad O, Margolis DJ. Filaggrin loss of function and thymic stromal lymphopoietin variation as predictors of treatment use in atopic dermatitis. JAMA Dermatology, in press 2016.
Lim HW, Collins SAB, Resneck JS, Bolognia JL, Hodge JA, Rohrer TA, Van Beek MJ, Margolis DJ, Sober AJ, Weinstock MA, Nerenz DR, Begolka WS, Moyano JV. The burden of skin disease in the United States, J Amer Acad Dermatol, 2017 on line
Langan SN, Abuabara K, Henrickson SE, Hoffstad O, Margolis DJ. Increased risk of cutaneous and systemic infections in atopic dermatitis-A cohort study. Journal of Investigative Dermatology, 2017 in press.
Chang J, Bilker WB, Hoffstad O, Margolis DJ. Cross sectional and longitudinal comparisons of patient-reported disease control, disease severity, and symptom frequency in children with atopic dermatitis, British Journal of Dermatology in press 2017.
SARAH E. MILLAR, PHD / [email protected] Research description: Signaling mechanisms regulating development, stem cells and regeneration of the skin and its appendages including hair follicles, mammary glands and teeth; genetic analyses of histone deacetylase functions in skin development, homeostasis, stem cells and cancer. Selected recent citations: Xu M, Horrell J, Snitow M, Cui J, Gochnauer H, Syrett C, Kallish S, Seykora JT, Liu F, Gaillard D, Katz JP, Kaestner KH, Levin B, Mansfield
C, Douglas JE, Cowart BJ, Tordoff T, Liu F, Zhu X, Barlow L, Rubin A, McGrath JA, Morrisey EE, Chu EY, Millar SE. (2017). WNT10A mutation causes ectodermal dysplasia by impairing progenitor cell proliferation and KLF4-mediated differentiation. Nature Communications, in press.
Choi YS, Zhang Y, Xu M, Yang Y, Ito M, Peng T, Cui Z, Nagy A, Hadjantonakis AK, Lang RA, Cotsarelis G, Andl T, Morrisey EE, Millar SE. (2013). Distinct functions for Wnt/β-catenin in hair follicle stem cell proliferation and survival and interfollicular epidermal homeostasis. Cell Stem Cell. 13, 720-33.
Teta M, Choi YS, Okegbe T, Wong G, Tam OH, Chong MM, Seykora JT, Nagy A, Littman DR, Andl T, Millar SE. (2012). Inducible deletion of epidermal Dicer and Drosha reveals multiple functions for miRNAs in
postnatal skin. Development 139, 1405-16. Plikus MV, Baker RE, Chen CC, Fare C, de la Cruz D, Andl T, Maini PK, Millar SE, Widelitz R, Chuong CM. (2011). Self-organizing and stochastic behaviors during the regeneration of hair stem cells. Science. 332,
586-9.
Page 4 of 7 University of Pennsylvania, Perelman School of Medicine
LeBoeuf M., Terrell A., Trivedi S., Sinha S., Epstein J. A., Olson E. N., Morrisey E. E., Millar S. E. (2010). Hdac1 and Hdac2 act redundantly to control p63 and p53 functions in epidermal progenitor cells. Developmental Cell 19, 807-18.
Liu, F., Dangaria, S., Andl, T., Zhang, Y., Wright, A. C., Damek-Poprawa, M., Piccolo, S., Nagy, A., Taketo, M. M., Diekwisch, T. G. H., Akintoye, S. O., Millar, S. E. (2010) Beta-catenin initiates tooth neogenesis in adult rodent incisor. J Dent Res. 89, 909-14.
Zhang Y, Tomann P, Andl T, Gallant NM, Huelsken J, Jerchow B, Birchmeier W, Paus R, Piccolo S, Mikkola ML, Morrisey EE, Overbeek P, Scheidereit C, Millar SE*, Schmidt-Ullrich R*. (2009). Reciprocal requirements for Eda/Edar/NF-κB and Wnt/ -catenin signaling pathways in hair follicle induction. Developmental Cell 17, 49-61. *Joint last and corresponding authors.
Zhang Y., Andl T., Yang S. H., Teta M., Liu F., Seykora J. T., Tobias J. W., Piccolo S., Schmidt-Ullrich R., Nagy A., Taketo M. M., Dlugosz A. A., Millar S. E. (2008). Activation of beta-catenin signaling programs embryonic epidermis to hair follicle fate. Development 135, 2161-72.
Liu F, Thirumangalathu S, Gallant NM, Yang SH, Stoick-Cooper CL, Reddy ST, Andl T, Taketo MM, Dlugosz AA, Moon RT, Barlow LA, Millar SE. Wnt-beta-catenin signaling initiates taste papilla development. Nat Genet. 2007 Jan;39(1):106-12.
Andl T, Murchison EP, Liu F, Zhang Y, Yunta-Gonzalez M, Tobias JW, Andl CD, Seykora JT, Hannon GJ, Millar SE. The miRNA-processing enzyme dicer is essential for the morphogenesis and maintenance of hair follicles. Curr Biol. 2006 May 23;16(10):1041-9.
Andl, T., Reddy S. T., Gaddapara, T. & Millar, S. E. (2002). WNT signals are required for the initiation of hair follicle development. Developmental Cell, 2, 643-653
MICHAEL MING, MD, MSCE / [email protected] Research description: Melanoma and dysplastic nevi, epidemiology, dermatopathology. Selected recent citations: Brauer JA, Shin DB, Levy RM, Shapiro M, Ming ME: Characteristics of dermatologists who read dermatopathology slides. J Cutan
Pathol. 34: 687-692, 2007. Brauer JA, Wriston CC, Troxel AB, Elenitsas R, Shin DB, Guerry D, Ming ME: Characteristics associated with early and late melanoma
metastases. Cancer 116: 415-23, 2010. Clark LN, Shin DB, Troxel AB, Khan S, Sober AJ, Ming ME: Association between the anatomic distribution of melanoma and sex. J Amer
Acad Dermatol. 56: 768-773, 2007. AIMEE S. PAYNE, MD, PHD / [email protected] Research description: Defining the B cell repertoire in pemphigus at the molecular genetic level; targeted immunotherapy for pemphigus. Selected recent citations: Ellebrecht CT, Payne AS. (2017) Setting the target for pemphigus vulgaris therapy. JCI Insight, 2(5):e92021. Ellebrecht CT, Bhoj VG, Nace A, Choi EJ, Mao X, Cho MJ, Di Zenzo G, Lanzavecchia A, Seykora JT, Cotsarelis G, Milone MC, Payne AS
(2016) Reengineering chimeric antigen receptor T cells for targeted therapy of autoimmune disease. Science, 353:179-184 Cho MJ, Ellebrecht CT, Hammers CM, Mukherjee EM, Sapparapu G, Boudreaux CE, McDonald SM, Crowe JE, Jr., Payne AS (2016)
Determinants of VH1-46 cross-reactivity to pemphigus vulgaris autoantigen desmoglein 3 and rotavirus antigen VP6. J. Immunol., 197(4):1065-73.
Cho MJ, Lo ASY, Mao X, Nagler AR, Ellebrecht CT, Mukherjee EM, Hammers CM, Choi EJ, Sharma PM, Uduman M, Li H, Rux AH, Farber SA, Rubin CB, Kleinstein SH, Sachais BS, Posner MR, Cavacini LA, Payne AS. (2014) Shared VH1-46 gene usage by pemphigus vulgaris autoantibodies indicates common humoral immune responses among patients. Nature Commun., 5:4167.
Ellebrecht CT, Choi EJ, Allman DM, Tsai DE, Wegener WA, Goldenberg DM, Payne AS. (2014) Subcutaneous veltuzumab, a humanized anti-CD20 antibody, for treatment of refractory pemphigus vulgaris. JAMA Dermatol., 150(12):1331-1335.
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TODD W. RIDKY, MD, PHD / [email protected] Research description: 3-D Human Cancer Models, Cancer Invasion and Metastasis, Stem Cells, Tumor-Stroma Interaction, Targeted Therapeutics. Selected recent citations: Duperret EK, Natale CA, Monteleon C, Dahal A, Ridky TW. The integrin αv-TGFβ signaling axis is necessary for epidermal proliferation
during cutaneous wound healing. Cell Cycle. 2016 Aug 2;15(15):2077-86. Natale CA, Duperret EK, Zhang J, Sadeghi R, Dahal A, O'Brien KT, Cookson R, Winkler JD, Ridky TW. Sex steroids regulate skin pigmentation through nonclassical membrane-bound receptors. Elife. 2016 Apr 26;5.
pii: e15104. Duperret EK, Dahal A, Ridky TW. Focal-adhesion-independent integrin-αv regulation of FAK and c-Myc is necessary for 3D skin
formation and tumor invasion. J Cell Sci. 2015 Nov 1;128(21):3997-4013. McNeal AS, Liu K, Nakhate V, Natale CA, Duperret EK, Capell BC, Dentchev T,Berger SL, Herlyn M, Seykora JT, Ridky TW. CDKN2B Loss
Promotes Progression from Benign Melanocytic Nevus to Melanoma. Cancer Discov. 2015 Oct;5(10):1072-85. Monteleon CL, McNeal A, Duperret EK, Oh SJ, Schapira E, Ridky TW. IQGAP1 and IQGAP3 Serve Individually Essential Roles in Normal
Epidermal Homeostasis and Tumor Progression. J Invest Dermatol. 2015 Sep;135(9):2258-65. Ridky TW, Cotsarelis G. Vismodegib resistance in basal cell carcinoma: not a smooth fit. Cancer Cell. 2015 Mar 9;27(3):315-6. Duperret EK, Ridky TW. Kindler syndrome in mice and men. Cancer Biol Ther. 2014 Sep;15(9):1113-6. Duperret EK, Oh SJ, McNeal A, Prouty SM, Ridky TW. Activating FGFR3 mutations cause mild hyperplasia in human skin, but are
insufficient to drive benign or malignant skin tumors. Cell Cycle. 2014;13(10):1551-9. Duperret EK, Ridky TW. Focal adhesion complex proteins in epidermis and squamous cell carcinoma. Cell Cycle. 2013 Oct
15;12(20):3272-85. Ridky T.W., Khavari PA. (2010) The hair follicle bulge stem cell niche resists transformation by the hedgehog pathway. Cell Stem Cell.
Apr 2;6(4):292-4. Rieger KE, Ridky TW, Sundram UN. (2010) Skin nodules in a patient with acute myeloid leukemia and neurological deterioration--quiz
case. Disseminated fusariosis. Arch Dermatol. 2010 Sep;146(9):1037-42. Ridky T.W., Chow, J.M., Wong, DJ, and Khavari, P.A. (2010) Invasive 3-Dimensional Organotypic Neoplasia from Multiple Normal
Human Epithelia. Nat Med. (2010) Dec;16(12):1450-5. Epub 2010 Nov 21.
PANTELIS ROMPOLAS, PHD / [email protected] Research description: Biology of skin stem cells and regeneration by live imaging. Mechanisms of cell fate and the role of the niche microenvironment in keratinocyte self-renewal or differentiation. Epithelial cell plasticity in homeostasis and pathophysiology. Selected recent citations: Rompolas P., Deschene E.R., Zito G.,Gonzalez D., Saotome I., Haberman A. & Greco V. (2012). Live imaging of stem cell and progeny behavior in
physiological hair-follicle regeneration. Nature. 7408, 496-9. PMID: 22763436 Rompolas P., Mesa K. and Greco V. (2013). Spatial organization within a niche as a determinant of stem cell fate. Nature 7472, 513-8.
PMID: 24097351 Rompolas P.*, Greco V. Stem cell dynamics in the hair follicle niche. (2014) Issue: “Development of Ectodermal Organs”. Seminars in
Cell and Developmental Biology. 25-26:34-42. *Corresponding author PMID: 24361866 Deschene E.R., Myung P., Rompolas P., Zito G., Sun T.Y., Taketo M.M., Saotome I.& Greco V. (2014). β-catenin activation regulates tissue
growth via a non-cell autonomous mechanism within the hair stem cell niche. Science. 343, 1353-6. PMID: 24653033 Mesa K.R., Rompolas P., Zito G., Myung P., Sun T.Y., Brown S., Gonzalez D.G., Blagoev K.B., Haberman A.M. & Greco V. (2015). Niche-
induced cell death and epithelial phagocytosis regulate hair follicle stem cell pool. Nature. PMID: 25849774
Page 6 of 7 University of Pennsylvania, Perelman School of Medicine
ALAIN H. ROOK, MD / [email protected] Research description: The immunopathogenesis and treatment of cutaneous T-cell lymphoma; Effects of Toll like receptor agonists. Selected recent citations: Wysocka M, Newton S, Benoit BM, Introcaso C, Hancock AS, Chehimi J, Richardson SK, Gelfand JM, Montaner LJ, Rook AH. Synthetic
imidazoquinolines potently and broadly activate the cellular immune response of patients with cutaneous T-cell lymphoma: synergy with interferon-gamma enhances production of interleukin-12. Clin Lymphoma Myeloma. 2007 ;7(8):524-34.
JS Yoon, M Wysocka, AB Troxel, SB Newton, SD Hess, SK Richardson, JH Lin, BM Benoit, M Kasprzycka, MA Wasik, AH Rook. Interleukin-21 enhances antitumor responses without stimulating proliferation of malignant T-cells of patients with leukemic cutaneous T-cell lymphoma. J Invest Dermatol. 2008; 128(2):473-80.
Walsh PT, Benoit BM, Wysocka M, Dalton NM, Turka LA, Rook AH. A role for regulatory T cells in cutaneous T-Cell lymphoma; induction of a CD4 + CD25 + Foxp3+ T-cell phenotype associated with HTLV-1 infection. J Invest Dermatol. 2006 Mar; 126(3):690-2.
Kim EJ, Hess S, Richardson SK, Newton S, Showe LC, Benoit BM, Ubriani R, Vittorio CC, Junkins-Hopkins JM, Wysocka M, Rook AH. Immunopathogenesis and therapy of cutaneous T cell lymphoma. J Clin Invest. 2005 Apr; 115(4):798-812.
JOHN SEYKORA, MD, PHD / [email protected] Research description: Murine models of skin cancer, mutations driving the early stages of UV-induced carcinogenesis, Notch signaling, Nuclear Pore Complex in cancer, anti-oncogenic mechanisms of Srcasm, topical treatment of skin cancer, regulation of UV-induced DNA damage. Selected recent citations: Ratushny, V., Gober, M., Hick, R., Ridky, T., and Seykora, J. From keratinocyte to cancer: the pathogenesis and modeling of cutaneous
squamous cell carcinoma. J Clin Invest. 122(2):464–472. 2012. PMCID: PMC3266779 Gober MD, Bashir HM, Seykora JT. Reconstructing skin cancers using animal models. Cancer Metastasis Rev. 32: 123-128 2013 PMCID:
PMC3625682 Zhao, L., Li, W., Marshall, C., Griffin, T., Hanson, M., Hick, R., Dentchev, T., Williams, E., Werth, A., Miller, C., Bashir, H. Pear, W. and
Seykora, J.T. Srcasm inhibits Fyn-induced cutaneous carcinogenesis with modulation of Notch 1 and p53. Cancer Research 69: 9439-9447. 2009.
Meulner, M., Ayli, E., Elenitsas, R., and Seykora, J. Decreased Srcasm expression in hyperproliferative cutaneous lesions. J. Cutan. Path. 36: 291-5. 2009
Ayli EE, Li W, Brown TT, Witkiewicz A, Elenitsas R, Seykora JT. Activation of Src-family tyrosine kinases in epidermal hyperproliferative disorders. J. Cutan. Path. 35: 273-7. 2008
Li, W., Marshall, C., Mei, L., Gelfand, J., Seykora, J. T. Srcasm corrects Fyn-induced epidermal hyperplasia by kinase downregulation. Journal of Biological Chemistry. 282: 1161-69. 2007 Pulitzer, M., Li, W., Hanson, M., Singh, F., Elenitsas, R., VanVoorhees, A., Gelfand, J., and Seykora, J. Srcasm overexpression in psoriasis-
insights into pathogenesis. J. Cutan. Path. 34: 160-65. 2007 Li W, Marshall C, Mei L, Dzubow L, Schmults C, Dans M, Seykora J.T. Srcasm modulates EGF and Src-kinase signaling in keratinocytes.
J Biol Chem. 2005 280:6036-46
Page 7 of 7 University of Pennsylvania, Perelman School of Medicine
VICTORIA P. WERTH, MD / [email protected] Research description: Pro-inflammatory effects of ultraviolet light on skin; the immunopathogenesis and treatment of autoimmune skin diseases and photoaging; clinical trials in autoimmune connective tissue and blistering disease. Selected recent citations:
Liu ML, Williams KJ, Werth VP. Microvesicles in autoimmune diseases. Adv Clin Chem 77, 125-175, 2016. Chen Y, Li G, Liu Y, Werth VP, Williams KJ, Liu ML. Translocation of Endogenous Danger Signal HMGB1 from Nucleus to
Membrane Microvesicles in Macrophages. Journal of Cellular Physiology 231:2319-26, 2016. Tiao J, Feng R, Werth VP. The Reliability of the Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) Among
Dermatologists, Rheumatologists, and Neurologists. Br J Dermatol 176:423-430. Werth VP, Fiorentino D, Sullivan BA, Boedigheimer MJ, Chiu K, Wang C, Arnold GE, Damore MA, Bigler J, Welcher AA, Russell CB,
Martin DA, Chung JB. Pharmacodynamics, Safety, and Clinical Efficacy of AMG 811, a Human Anti-Interferon-γ Antibody, in Subjects with Discoid Lupus Erythematosus. Arthritis Rheumatol. 2017 Jan 24. doi: 10.1002/art.40052.
Robinson ES, Feng R, Okawa J, Werth VP. Improvement in the cutaneous disease activity of patients with dermatomyositis is associated with a better quality of life. Br J Dermatol 172:169-74, 2015
Foering J, Chang A, Piette E, Okawa J, Werth V.P. Characterization of clinical photosensitivity in cutaneous lupus erythematosus. J Am Acad Dermatol 69:205-218, 2013.
Braunstein I, Klein R, Okawa J, and Werth VP. The IFN-inducible gene signature is elevated in SCLE and DLE and correlates with CLASI score. Br J Dermatol 166:971-5, 2012.
Kim JS, Bashir MM, Werth, VP. Gottron’s papules exhibit dermal accumulation of CD44 variant 7 (CD44v7) and its binding partner osteopontin: a unique molecular signature. J Invest Dermatol 132:1825-32, 2012.
Klein R, Moghadam-Kia S, LoMonico J, Okawa J, Coley CH, Taylor L, Troxel AB, Werth VP. Development of the CLASI as a tool to measure disease severity and responsiveness to therapy in cutaneous lupus erythematosus. Arch Dermatol 142:203-8, 2011.
Bashir MM, Sharma M, Werth V.P. UVB and pro-inflammatory cytokines synergistically activate TNF-production in keratinocytes through enhanced gene transcription. J Invest Dermatol 129: 994-1001, 2009.
University of Pennsylvania, Perelman School of Medicine
UNIVERSITY OF PENNSYLVANIA Perelman School of Medicine
Junko Takeshita, MD, PhD, MSCE Assistant Professor of Dermatology and Epidemiology University of Pennsylvania Perelman School of Medicine Philadelphia, PA 19104 Description of research: Dr. Takeshita’s research is focused on identifying and understanding health and healthcare disparities in chronic inflammatory skin diseases (primarily psoriasis and atopic dermatitis) with an aim to reduce disparities in dermatology. Her current work was inspired by her prior study of psoriasis treatment in the Medicare population that newly identified racial disparities in the utilization of biologics for psoriasis. Dr. Takeshita uses a mixed methods approach with both classic epidemiologic/quantitative and qualitative methods to better understand existing disparities in psoriasis treatment as well as identify and understand other disparities in dermatology. She also has interests in translational research with an ongoing study evaluating the cutaneous microbiome of psoriasis and its response to phototherapy. Nature of the available training position:
One (1) year pre-doctoral and two year post-doctoral positions are available pending funding Deadline to apply:
Pre-doc deadline, Jan 1, 2018 Post-doc deadline, Nov 1, 2018
Relevant contact information:
Junko Takeshita, MD, PhD, MSCE Email: [email protected] Office phone: 215-349-5551 Website: https://www.med.upenn.edu/apps/faculty/index.php/g275/p8473751
