Fisiopatologia Del Cancer [Modo de Compatibilidad]

7/27/2019 Fisiopatologia Del Cancer [Modo de Compatibilidad]

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Physiopathology of cancer

Dr. Julio Hilario Vargas

Department of Physiology

School of Medicine

National University of Trujillo

Brain Cancer Cell

Source: http://www.alternative-cancer.net/Cell_photos.htm


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Is a class of disease in which a group of cells display

uncontrolled growth through division beyond normal

limits, invasion that intrudes upon and destroys

adjacent tissues, and sometimes metastasis, in which

cancer cells spread to other locations in the body vialymph or blood. These three malignant properties of

cancers differentiate them from benign tumors, which

are self-limited, and do not invade or metastasize.

CANCER


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By the type of cell that the tumor resembles and is thereforepresumed to be the origin of the tumor. These types include:

Carcinoma: Cancer derived from epithelial cells. This group

includes many of the most common cancers, including those of

the breast, prostate, lung and colon.

Sarcoma: Cancer derived from connective tissue, ormesenchymal cells.

Lymphoma and leukemia: Cancer derived from hematopoietic

(blood-forming) cells

Germ cell tumor: Cancer derived from pluripotent cells. In adults

these are most often found in the testicle and ovary, but are more

common in babies and young children

Blastoma: Cancer derived from immature "precursor" or

embryonic tissue. These are also commonest in children

Cancers classification


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Tipos comunes de cncer

- American Cancer Society: Cancer Facts and Figures for Hispanics/Latinos 2006-2008. Atlanta, Ga: American Cancer

Society, 2006. Disponible tambin en Internet.

- Lipworth L, Tarone RE, McLaughlin JK: The epidemiology of renal cell carcinoma. Journal of Urology 176(6 pt 1):2353-

2358, 2006


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Genomic Instability

An increased tendency of the GENOME to acquire MUTATIONS when

various processes involved in maintaining and replicating the genomeare dysfunctional


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Phenotypic Changes in the Progression of Neoplasia


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Phenotypic Changes in the Progression of Neoplasia


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Zitvogel L et al., Nat. Rev. Immunol., 2006, 6:715.

Cancer Immunoediting: The New

Surveillance Hypothesis


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Dunn GP et al., Nat. Immunol., 2002, 3:991.

Surveillance

At equilibrium immune selection develops leading to tumor escape

Cancer Immunoediting: Three Es


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The three Es of cancer immunoediting: host protective versus tumor

sculpting actions of immunity

Dunn GP, Old LJ, Schreiber RD. The immunobiology of cancer immunosurveillance and immunoediting. Immunity. 2004 Aug;21(2):137-48.


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Cancers are primarily an environmentaldisease with 90-95% of cases due

environmental factors such as lifestyle, and

5-10% directly due to heredity.

Common environmental factors leading tocancer include: tobacco (25-30%), diet and

obesity (30-35%), infections (15-20%),

radiation, lack of physical activity, and

environmental pollutants.

Some viruses and bacteria are included too.


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HTLV: Human T-cell leukemia-lymphoma virus; HHV-8: Human herpesvirus-8; KSHV: Kaposis

sarcoma herpesvirus

Oncogenic Human Viruses


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Is a normal gene that can become an oncogene due tomutations or increased expression. The resultant protein

may be termed an oncoprotein.

Proto-oncogenes code for proteins that help to regulate cell

growth and differentiation. Proto-oncogenes are often

involved in signal transduction and execution of mitogenic

signals, usually through their protein products. Upon

activation, a proto-oncogene (or its product) becomes a

tumor-inducing agent, an oncogene. Examples of proto-

oncogenes include RAS, WNT, MYC, ERK, and TRK

Proto-oncogene


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Biochim Biophys Acta 1602(2), M. Frame, Src in Cancer, 114-130, 2002

Src-induced signaling from membrane/adhesions that controls cell behaviour


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Is a gene that has the potential to cause cancer


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Representative Oncogenes Activated in Human Tumors


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Representative Tumor Suppressor Genes Inactivated in

Human Tumors or the Human Germline


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Rescuing the function of mutant p53

Alex N. Bullock & Alan R. Fersht. Nature Reviews Cancer1, 68-76 (October 2001)


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Retinoblastoma : the tumor suppressor gene paradigm


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DNA damage, repair mechanisms, and consequences

2001 Nature Publishing Group Hoeijmakers, J. H. J. Genome maintenance mechanisms for

preventing cancer. Nature 411, 366374 (2001)


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DNA repair mechanisms


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Loca l symp toms:Are restricted to the site of the primary cancer. They

can include lumps or swelling (tumor), hemorrhage (bleeding from the

skin, mouth or anus), ulceration and pain. Although local pain commonly

occurs in advanced cancer, the initial swelling is often painless.

Metastat ic symptom s:are due to the spread of cancer to other locations

in the body. They can include enlarged lymph nodes (which can be felt or

sometimes seen under the skin), hepatomegaly (enlarged liver) orsplenomegaly (enlarged spleen) which can be felt in the abdomen, pain

or fracture of affected bones, and neurological symptoms.

Systemic symptoms:occur due to distant effects of the cancer that are

not related to direct or metastatic spread. Some of these effects can

include weight loss (poor appetite and cachexia), fatigue, excessivesweating (especially night sweats), anemia (low blood count) and other

specific conditions termed paraneoplastic phenomena. These may be

mediated by immunological or hormonal signals from the cancer cells

Signs and symptoms

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Fisiopatologia Del Cancer [Modo de Compatibilidad]