Preventing inflammation in fat tissue of obese people may hold the key to preventing or even reversing type 2 diabetes, new research has found.

Institute researchers, with colleagues from the RIKEN Institute, Japan, found they could ‘reverse’ type 2 diabetes in laboratory models by dampening the inflammatory response in fat tissue.

Controlling inflammationDr Ajith Vasanthakumar, Dr Axel Kallies and

colleagues discovered that specialised immune cells, called regulatory T cells (Tregs), played a key role in controlling inflammation in fat tissue and maintaining insulin sensitivity.

More than 850,000 Australians are estimated to have type 2 diabetes and its prevalence is rising. The disease is strongly linked with ‘lifestyle’ factors, such as being overweight or having high blood pressure. Long-term complications of type 2 diabetes include kidney, eye and heart disease, and there is no cure.

People with type 2 diabetes have reduced sensitivity to insulin, which is thought to be a result of long-term, low-level inflammation of fat tissue in

people who are obese. Dr Vasanthakumar said Tregs acted as the

guardians of the immune system, preventing the immune response from getting out-of-hand and attacking the body’s own tissues. “When Treg numbers are reduced, inflammatory diseases such as type 2 diabetes and rheumatoid arthritis can occur,” he said.

Preserving immune cellsRecent studies have shown fat tissue has its

own unique type of Tregs, which disappear during obesity. “The fat tissue of obese people has lower numbers of Tregs than the fat tissue of people in a healthy weight range,” Dr Vasanthakumar said. “With fewer Tregs, levels of inflammation-causing cells increase, and this rise in inflammation can lead to insulin resistance and high blood glucose levels, a classic hallmark of type 2 diabetes.”

The research team discovered a key hormone called IL-33 (interleukin-33) was able to selectively boost Treg populations in fat tissue, effectively halting the development of type 2 diabetes, and even reversing the disease in preclinical models.

“Treating fat tissues with IL-33 restored normal Treg cell levels, which reduced inflammation and decreased blood glucose levels,” Dr Vasanthakumar said.

“Treatments that mimic IL-33 could have the potential to reduce obesity-related inflammation and type 2 diabetes.”

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Dr Axel Kallies (L), Dr Ajith Vasanthakumar and colleagues have found a signalling molecule could prevent inflammation in fat tissue, reversing symptoms of type 2 diabetes.

From the directorProfessor Doug Hilton on our centenary and honouring Professor Don Metcalf.

Recognising research excellencePhD student Julia Marchingo wins cancer research award.

Revealing silent cell death secretsSecret to hiding cell death from the immune system discovered.

Unexpected trigger of skin inflammationUnusual suspect behind inflammatory skin diseases such as psoriasis.

Chemist wins innovation medalCancer drug discovery earns medicinal chemist inaugural innovation medal.

Staff profilesPostdoctoral researcher Dr Emma Carrington PhD student Dr Michael Christie

Vale Professor Donald Metcalf ACTribute to the ‘father of haematology’, Professor Don Metcalf.

Protein key to lymphomaNew research shows blocking a ‘survival’ protein halts blood cancer development.

New cancer research fundingCancer Council Victoria grant to aid search for cancer-causing genes.

Honouring an Australian iconMetcalf Scholarship Fund established to support young scientists.

Enabling bowel cancer discoveriesShepherd Foundation supports study into preventive treatments for bowel cancer.

Coming eventsHelp us celebrate 100 years of discoveries for humanity through public talks, events, discovery tours and science film festivals.

“Treatments that mimic IL-33 could… reduce obesity-related

inflammation and type 2 diabetes.”

Could immune cells be key to reversing type 2 diabetes?

I L L U M I N A T EIssue Number 23 | March 2015

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WEHIresearch WEHIalumni @WEHI_research WEHImovies Walter and Eliza Hall Institute

Cancer research excellence award for PhD studentMs Julia Marchingo, a PhD student at the

Walter and Eliza Hall Institute and The University of Melbourne, has won a 2014 Picchi Award for Excellence in Cancer Research.

The Picchi Award recognises researchers’ originality, innovation and contribution to cancer research. Ms Marchingo will receive a $10,000 scholarship to present her research findings at international scientific meetings in 2015.

Modelling immune responseMs Marchingo was part of an institute-led team

that combined laboratory data with mathematical modelling to understand how complex external signals affect the magnitude of the immune response. Ms Marchingo was the first author on the resulting publication, which was published in the journal Science.

“Our research showed that the more times T

cells divide, the more powerfully they can fight their target,” Ms Marchingo said.

The recent success of treatments that harness the immune system to kill cancer cells provides great potential for Ms Marchingo’s research discoveries to help develop new, and improve existing, cancer treatments.

Recognising cancer researchThe Picchi Award is sponsored by the Picchi

Brothers Foundation, and recognises, develops and supports the top PhD students in the Victorian Comprehensive Cancer Centre (VCCC) partners. The Walter and Eliza Hall Institute is the research powerhouse of the VCCC, which is a collaborative network of Victorian hospitals and research centres improving the prevention, diagnosis and treatment of cancer.

Help us celebrate our centenary

From mid-March, supporters passing our Parkville campus may notice a new addition to our building – a 15-metre tall LED screen will be illuminated on our building’s eastern wall. We also look forward to many supporters participating in our centenary public talks series, bringing research experts together with the community to discuss the latest research and future treatments in health and medical research.

I know that many of the readers of Illuminate have direct connections with the institute, either as supporters or alumni. For those from whom we have not heard recently, our centenary is a great reason to re-connect either in person or online.

Vale Don MetcalfThe year 2014 finished on a sad note for the

institute community, with the passing of Professor Donald Metcalf on 15 December. Don was an inspiration to all that met him in his 60 years at the institute, and the fruits of his research have benefitted millions of lives worldwide.

Thank you to the more than 80 donors to the Metcalf Scholarship Fund, a permanent fund through which we will continue to train outstanding young scientists, a fitting tribute to a man who was a mentor to many, including me.

The Metcalf Scholarship Fund remains open for donations, and I encourage our supporters to consider a contribution in honour of one of Australia’s greatest scientists.

Very best wishes,Doug

Donations to the Metcalf Scholarship Fund can be made online or by contacting Susanne Williamson on 03 9345 2962.

Welcome to our centenary year. With 100 years of discoveries for humanity to celebrate in 2015, we have a busy program of events planned for our supporters and we look forward to your participation throughout the year. This is, of course, on top of what promises to be another exciting year of discoveries and achievements from our researchers.

Inaugural centenary fellowsI am delighted to announce we have appointed

our first centenary fellows. The centenary fellowships program aims to secure support for 100 promising young researchers to establish their careers at the institute.

Fittingly, our founding donor, the Walter and Eliza Hall Trust, was our inaugural centenary fellowship supporter. We are also pleased that CSL Ltd, an industry partner since 1916, as well as the L.E.W. Carty Charitable Fund, the Felton Bequest and the Dyson Bequest have also supported centenary fellowships.

At a time when many young researchers are feeling the challenges of an increasingly competitive funding environment, I am excited that we are doing everything possible to enable our brightest research minds to prosper.

Ms Kristy Meiselbach (L) and Ms Nancy Fintic

Ms Julia Marchingo

From the director

Internship program recruits talented budding scientists

Two promising young scientists joined the institute in early 2015 as part of a new partnership with the CareerTrackers Indigenous Internship Program.

CareerTrackers is a national non-profit organisation that creates multi-year internship opportunities for high-performing Aboriginal and Torres Strait Islander university students.

Meet our CareerTrackersMs Kristy Meiselbach, a biomedicine student at

RMIT University in Melbourne, joined Dr Tracy Putoczki’s lab in the Inflammation division, working to understand why some people are more susceptible to inflammatory bowel disease than others.

Ms Meiselbach said the program had been one of the most enriching programs she had participated in. “My time at the institute has allowed personal and intellectual growth, insight into a possible career path and a realistic scientific experience,” she said.

Ms Nancy Fintic, a medical laboratory science student at James Cook University in Townsville, has been working in Dr Alyssa Barry’s and Professor Ivo Mueller’s labs in the Infection and Immunity division to study the spread of malaria in Papua New Guinea.

Dr Barry said the results would be used to gain a better understanding of how malaria parasites regulate their genes. “Nancy has displayed the aptitude and work ethic necessary to succeed in a scientific career,” she said. “We are lucky to have her!”

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Around the institute

Unusual suspect behind inflammatory skin diseaseInflammatory skin diseases such as psoriasis may be the result of abnormal activation of cell death processes previously believed to suppress inflammation.

Mr James Rickard, Associate Professor John Silke and institute colleagues made the surprise discovery, which could help in the development of new ways of treating inflammatory diseases.

Inflammation and diseaseCells in the body frequently die in a

programmed cell death process called apoptosis. The cells die without harming neighbouring cells or alerting the immune system.

Mr Rickard said another form of cell death known as necroptosis also instructed cells to die by a ‘programmed’ series of events, with a key difference.

“Necroptosis is a recently discovered form of cell death that occurs when something has gone wrong with the ‘normal’ apoptosis process,” Mr Rickard said. “It signals that something sinister

might be happening, alerting and recruiting key immune cells to the ‘scene of the crime’,” he said.

Unexpected culpritAlthough previous research had linked

necroptosis with inflammatory diseases such as psoriasis and Crohn’s disease, Mr Rickard said the association was more complicated.

“We were surprised to discover that apoptosis was the culprit in the development of inflammatory skin disease, similar to psoriasis,” he said. “However more extensive, system-wide inflammation such as in the liver and spleen was driven by necroptosis, which is more reminiscent of Crohn’s disease. This was quite unexpected, because apoptosis is not normally associated with inflammation.”

The researchers said that better understanding mechanisms of cell death would help to develop better strategies for treating inflammatory diseases in the future.

Institute researchers have revealed how dying cells are hidden from immune ‘police’ that patrol the body.

The research answers a decades-old mystery about the death of cells, and how cells decide whether to alert the immune system to potential danger, or to ‘silence’ cell death so it goes unnoticed by the immune system.

Avoiding alarmSilent cell death, or apoptosis, allows the body

to get rid of unwanted cells that may be damaged, old, or surplus to the body’s requirements, without causing collateral damage or triggering an immune response. In contrast, the death of cells at sites of infection or trauma can alert the immune system to be on the lookout for danger.

Dr Michael White, Professor Benjamin Kile and colleagues revealed proteins called caspases were integral in preventing an immune response to apoptotic cell death.

Dr White said caspases hastened cell death by breaking down key components within the dying

cell, but the team found they also played another role.

“We revealed that when cells undergo apoptosis without involving caspases, the cells release signaling molecules called interferons that trigger an immune response,” he said.

“By dissecting the step-by-step process that occurs within dying cells, we showed one of the key roles of caspases is suppressing interferon release. This confirmed that caspases are crucial for hiding apoptotic cell death from the immune system.”

Problems of over-reactingProfessor Kile said the discovery provided new

insights into the links between cell death, the immune system and disease.

“Our good health depends on our immune system distinguishing between the cells that are supposed to die to make space for new cells, and the unexpected death of cells that signals danger,” he said. “The over-reaction of immune cells to apoptosis may even be a factor contributing to inflammatory diseases such as rheumatoid arthritis.”

The research would also provide important insights into how the body may tolerate potential new drugs, Professor Kile said.

“New caspase-inhibiting medications are currently in clinical trials, for example being tested for their potential to keep cells alive for organ transplants,” he said. “However our work suggests that any use of these medications should look much more closely at the effects they could have on immune cells.”

Dr Michael White and colleagues have discovered how ‘silent’ cell death avoids activating the immune system.

Mr James Rickard

“Caspases are crucial for hiding apoptotic cell death from the immune system.”

Secrets of silent cell death revealed

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Dr Emma Carrington Postdoctoral fellowDescribe your job… I work on white blood cells called dendritic cells and factors that control their lifespan in the body.

How long have you worked here? Seven years.

If you weren’t doing your job, what would you be doing? When I was younger, I wanted to be a journalist.

Best aspect of your job? Getting to contribute to a pool of knowledge that will, in some way, impact people’s lives, through either a better understanding of disease or improved treatment options for patients.

Worst aspect of your job? When experiments don’t work out the way you thought they would (this can sometimes be one of the best aspects, too!).

What’s one thing most people would be surprised to know about you? I am one quarter Austrian.

What’s the smartest thing you’ve been told? Always do what makes you happy.

Best things about living in Melbourne? The cafes: you can always find a good coffee and all-day breakfast on the weekends. Also, the AFL

– go Saints!

Your favourite overseas destination? Thailand. It’s a great place for relaxing on the beach.

Who do you most admire? The late Professor Don Metcalf: an absolutely stellar scientist whose discovery of colony stimulating factors has improved the lives of millions of people worldwide.

What do you want to be remembered for? Performing good quality research.

Dr Michael Christie PhD studentDescribe your job… I’m researching how a signalling pathway impacts the development of bowel cancer. I am also a molecular pathologist at the Royal Melbourne Hospital.

How long have you worked here? Three years.

If you weren’t doing your job, what would you be doing? Playing the guitar to a very small audience.

Best aspect of your job? The moment of discovery: seeing something for the very first time.

Worst aspect of your job? Paperwork.

What is the smartest thing you’ve been told? Trust your instincts.

What’s one thing most people would be surprised to know about you? I used to play lead guitar in a heavy metal band. It seems like a long time ago.

Best thing about living in Melbourne? The food: Melbourne has the best in the world.

What is your favourite overseas destination? Nepal. The Himalayas are breathtaking in real life.

What is the most unusual thing you’ve been asked to do as part of your job at the institute? Construct a (very scientific) model of the human intestine using a cactus plant and some stickers.

Who do you most admire? Charles Darwin.

What do you want to be remembered for? Helping as many people as I could.

Associate Professor Guillaume Lessene has won the inaugural Dr John Dixon Hughes Medical Research Innovation Medal.

Associate Professor Guillaume Lessene was awarded the inaugural Dr John Dixon Hughes Medical Research Innovation Medal in December 2014 for his discovery and development of potential anti-cancer drugs.

The medal, from the National Foundation for Medical Research and Innovation, included a cash prize of $50,000 to support Associate Professor Lessene’s research into new and improved cancer therapies.

Aiding cell deathAssociate Professor Lessene’s work has

contributed to the discovery of a new class of drugs, BH3-mimetics, that ‘trick’ cancer cells into dying. BH3-mimetics have transformed the field of cancer therapy, and are already showing great promise for treating some blood cancers, such as chronic lymphocytic leukaemia.

Associate Professor Lessene said his group set out to develop novel inhibitors of pro-survival proteins involved in programmed cell death (apoptosis), which are major factors in cancer development and chemotherapy resistance.

“Cancer cells avoid death by producing high levels of one or more ‘pro-survival’ proteins, called the BCL-2 family of proteins,” he said.

“Harnessing the power of small molecule inhibitors

to interrogate biological pathways controlling cell death will not only lead to a better understanding of cell death and its role in cancer, but also deliver new chemical leads in areas of unmet need in cancer treatment.”

Collaborative cultureAssociate Professor Lessene said he was

honoured to receive the award. “This medal represents the importance of collaboration within the institute, and externally, to develop potential new drugs for clinical use,” he said. “I would like to recognise my team and my collaborators, who also share in this award.”

Institute director Professor Doug Hilton said Associate Professor Lessene was one of the institute’s shining stars. “The type of molecules that regulate apoptosis are not conventional drug targets, and many in the pharmacological industry considered them undruggable,” he said.

“Undeterred, Guillaume and his team have discovered pharmaceutical agents with exquisite specificity for the apoptotic machinery. His outstanding contribution to biomedicine has garnered a strong international reputation and signals his emergence as a leader in medical research and innovation.”

Inaugural innovation medal awarded for cancer drug discovery

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Staff profiles

Professor Donald Metcalf – Don to most with whom he worked – was a colossus of science.

Working at the Walter and Eliza Hall Institute and supported by Cancer Council Victoria from 1954 to 2014, Don stood astride the world of haematology (the study of blood cells) for 60 years.

The achievements of Don, the scientist, are legion. Don introduced cancer research to the Walter and Eliza Hall Institute at a time when its director, the Nobel Prize winner Sir Frank Macfarlane Burnet, viewed cancer as an

“inevitable disease”, with “anyone who wants to do cancer research, either a fool or a rogue”. Don politely ignored him.

Discovering CSFs Studying leukaemia in 1964, Don and Ray

Bradley, from The University of Melbourne, discovered it was possible to grow bone marrow cells in plates of partly set agar jelly. Don’s genius lay not in this breakthrough, but in the realisation that it could be used to understand the cellular basis of blood cell production and to discover the hormones, which he named colony-stimulating factors (CSFs), that regulate blood cell production in the body.

Don worked single-mindedly on this theme for the next 50 years. He characterised blood stem cells and their daughter cells, which are committed to producing the multiple types of white blood cells that fight infection and prevent bleeding. In doing so he made the blood cell system the ‘poster child’ of medical research and shone a light into the darkness for those who followed him.

Championing collaboration Don also understood his limitations. He knew

he needed collaborators who would take him out his comfort zone, so he assembled a team of

researchers who worked with him for 40 years. Decades ahead of its time, his model of collaborative, multidisciplinary science shaped the culture of the Walter and Eliza Hall Institute and is now seen by scientists as almost mandatory if big problems are to be tackled successfully.

After two decades, Don and his team succeeded in isolating four of the blood CSFs, paving the way for their mass-production and clinical testing. Don found that injecting the hormones into animals resulted in a rapid increase in the number of blood cells responsible for battling infection and surmised that they might be used to help cancer patients overcome one of the major side effects of chemotherapy: a loss of white cells and susceptibility to life-threatening infection.

Don’s hunch about clinical use was proven correct. Over the past 20 years, more than 20 million cancer patients (including Spanish tenor Jose Carreras) have been treated with CSFs and, as a result, have been given the best possible chance of beating their cancer. CSFs are now standard treatment and every year the number of people alive because of Don’s work grows.

An institute icon Don was also loyal. He was loyal to the Walter

and Eliza Hall Institute, working there almost continuously for 60 years despite lucrative offers from all over the world. Don enjoyed the ‘tyranny of distance’, which he believed made it easier for Australian scientists to pursue highly original research, away from the latest trends and fads.

Don was human – he was no uncaring science machine. He loved banter over afternoon tea, often laughing until tears streamed down his face at some silly anecdote or remark. He loved an annual week on the Sunshine Coast with his wife, which included body surfing, into his late 70s, on waves of any size. He enjoyed a meal and a glass

of wine with friends. And more than anything he loved his family – his wife of more than 60 years, Josephine (Jo), his four daughters and his six grandchildren meant everything to him. He knew, and often publicly acknowledged, that without them he would have achieved little of note.

Don enjoyed relative good health until August last year. Feeling under the weather, he went on leave hoping some time away from the laboratory would rejuvenate him. He returned feeling worse and was quickly diagnosed with metastatic pancreatic cancer.

Knowing the likelihood of cure was not high, his priorities were to undertake some treatment to give him a few extra weeks or months so as to avoid letting down his collaborators and, most importantly, to spend as much time as possible with his beloved Jo and his daughters - but how to do both of these things? The solution for the scientist and family man until the end – have his microscope moved into his home. Don performed his last experiment in October and died surrounded by his family on 15 December 2014. He would have wanted it no other way.

Professor Doug Hilton, Professor Warren Alexander and Professor Nick Nicola

Vale Professor Donald Metcalf ac26 February 1929 – 15 December 2014

Once more unto the breach, dear friends, once more,Or close the wall up with our English dead!In peace there’s nothing so becomes a manAs modest stillness and humility,But when the blast of war blows in our ears,Then imitate the action of the tiger:Stiffen the sinews, summon up the blood.

King Henry, excerpt from Henry V by William Shakespeare.

One of Don’s favourite passages, inspiring the title of his autobiography Summon up the Blood.

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New funding to search for cancer-causing genesInstitute scientists have received $1 million from Cancer Council Victoria to support a ‘visionary’ project identifying key cancer-causing genes in leukaemia, lymphoma and breast cancer development.

Professor Andreas Strasser, Dr Marco Herold, Professor Jane Visvader and Professor Geoff Lindeman received one of four Cancer Council Victoria Metcalf Venture Grants to discover the processes that drive tumour development and to help identify potential new anti-cancer targets.

Halting cancer developmentLead researcher Professor Strasser said the

research team aimed to uncover key genes responsible for preventing cancer development.

“Our bodies have ‘tumour suppressive’ genes

that prevent cells from starting on a pathway that can lead to cancer,” Professor Strasser said.

“Cancers develop when tumour suppressor genes are silenced or stop functioning, allowing cells to accumulate defects that lead to cancer.”

Professor Strasser said the research team would use new gene modification technology to search for novel tumour suppressor genes and pathways that are critical for cancer development in blood and breast cancers.

“Discovering key tumour suppressive processes and the genes that control them will give us new targets for anti-cancer treatments,” he said.

Institute researchers Dr Marnie Blewitt and Dr Chris Burns also received funding as co-investigators on a joint project with scientists from the Peter MacCallum Cancer Centre, which aims to develop treatments targeting leukaemia stem cells.

Targeting a cell survival protein called MCL-1 could help to treat some lymphomas, including those cancers with genetic defects that make them resistant to existing therapies.

Dr Stephanie Grabow, Dr Alex Delbridge, Dr Liz Valente and Professor Andreas Strasser found that removing MCL-1 caused the death and elimination of lymphoma cells that had become resistant to conventional cancer treatments.

Disrupting cancer growthT-cell and B-cell lymphomas are types of white

blood cell cancers known as non-Hodgkin lymphomas. Non-Hodgkin lymphomas are the most common blood cancers in Australia, with about 3500 people diagnosed each year.

MCL-1 is a key regulator of programmed cell death (apoptosis), a process that – when disrupted – can cause cancer to develop and enable cancer cells to survive abnormally well when exposed to anti-cancer treatments.

Dr Grabow said the team discovered that MCL-1 ‘helped’ these cancer cells to survive by subverting the normal process of apoptosis.

“Half of all cancers become resistant to chemotherapy and radiotherapy by acquiring mutations in the tumour-suppressing p53 protein,” she said. “When we removed MCL-1 in models of

T-cell lymphoma that had ‘lost’ p53, cancers could not develop, demonstrating that MCL-1 is critical for the development of T-cell lymphomas.”

Dr Grabow said there were several pro-survival proteins that promoted the sustained survival of cancer cells. “The challenge is to identify which one is the most important in keeping each type of cancer cell alive,” she said.

Valuable targetProfessor Strasser said the finding reinforced

the need to develop drug-like compounds that specifically targeted MCL-1, which they have shown is critical for cancer cell survival in B-cell lymphoma and acute myeloid leukaemia.

“Targeting MCL-1 could allow us to develop new therapies for cancers that have stopped responding to other anti-cancer drugs.”

Our immune system relies on a key ‘energy producing’ protein in immune cells to develop immunity to vaccines and disease, an international research team has found.

The protein, called HuR, is critical for controlling metabolism in B cells, which make antibodies that are essential in fighting infections and in developing long-term immunity after vaccination.

Dr Kirsten Fairfax, now at the Walter and Eliza Hall Institute, worked with colleagues at the Babraham Institute, Cambridge, UK, on the discovery.

Maturing immunityDr Fairfax said the team showed removing

HuR prevented B cells from developing properly. “Immune cells called B cells mature in response to vaccines or exposure to new disease and are essential for immunity,” she said. “HuR ‘manages’ a set of genes that determine how much energy B cells produce, known as the metabolic rate.

“We showed that without HuR to instruct them, these critical metabolic genes can no longer instruct the B cell to make the energy it needs to function, and B cells are unable to mature into antibody-producing cells that provide immunity to disease.”

Dr Fairfax said maturation of B cells required a substantial amount of energy and occurred within the ‘B-cell factory’ called the germinal centre.

“If the immune cell’s metabolism is compromised, maturation in the germinal centre stalls, preventing us from developing immunity in response to vaccines or exposure to disease,” she said.

Dr Kirsten Fairfax

Dr Alex Delbridge, Dr Stephanie Grabow, Dr Liz Valente and Professor Andreas Strasser (L-R) found MCL-1 is an essential survival protein in T-cell lymphomas.

“Targeting MCL-1 could allow us to develop new therapies for

cancers that have stopped responding to other anti-cancer drugs.”

Immune cell energy vital for fighting disease

Blocking ‘survival’ protein halts lymphoma development

Professor Andreas Strasser

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In December 2014 we were deeply saddened by the passing of the institute’s revered and celebrated cancer researcher Professor Donald Metcalf.

In memory of Don and in recognition of his significant contributions to science, more than 80 donations have been pledged to support the Metcalf Scholarship fund. The fund will support promising young researchers studying at the institute, providing conference, travel and bench costs.

Professor Metcalf worked in his lab at the Walter and Eliza Hall Institute for an impressive six decades and made an outstanding contribution not just to medical science, but also to the careers of many young researchers.

Enduring legacyInstitute director Professor Doug Hilton and his

wife Adrienne made the founding donation of $10,000 to the Metcalf Scholarship fund. “There is no better way to honour Don’s memory than by

encouraging the next generation of scientists,” Professor Hilton said.

Mr Chris Thomas, board president, and his wife Cheryl pledged to match the first $100,000 of public donations to the Metcalf Scholarship fund with a gift from the Thomas Family Fund, a sub-fund of Australian Communities Foundation.

“Scientists such as Professor Metcalf work tirelessly in the background, providing an immeasurable service to us all,” Mr Thomas said.

“I hope that many others take this opportunity to pay tribute to an outstanding researcher and

inspirational Australian who has helped tens of millions of cancer patients worldwide.”

Longtime institute partner CSL Limited pledged $100,000 and The University of Melbourne pledged a further $30,000. The Metcalf Scholarship fund now has a base of $300,000. The first Metcalf Scholarships will be awarded in May 2015 at the institute’s annual general meeting.

Remembering DonProfessor Hilton said the scientific community

would remember and pay tribute to Professor Metcalf’s legacy for many decades to come. “Don was an inspiration to us all at the institute and we miss him,” he said.

“I am overwhelmed by the community’s generosity in remembering Professor Metcalf, and I know Don would be excited about the opportunities that young researchers will receive through this fund, just as he was supported as a young researcher.”

Shepherd Foundation support to prevent bowel cancer An ambitious research project that could lead to a preventive treatment for bowel cancer will commence soon thanks to the support of the Shepherd Foundation.

The Shepherd Foundation, established in 1970, provides research grants for preventive health projects.

The study, led by institute researcher Professor Tony Burgess, will examine a drug combination that could kill precancerous cells before they develop into tumours. Professor Burgess said he hoped the research would lead to the initiation of new clinical trials in people with bowel cancer.

Halting cancer developmentMore than 80 per cent of bowel cancers arise

from precancerous lumps called polyps. Most polyps are caused by a single genetic change that makes them grow in an uncontrolled way. Eventually these polyps turn cancerous.

Professor Burgess said previous laboratory studies had shown a combined drug treatment could intercept the growth signals that allowed

the polyps to survive.“Working with collaborators from the Alfred

Hospital, we previously showed that while treatment with a single drug had a weak effect, the combination of two anti-cancer drugs could effectively kill the cancerous cells,” Professor Burgess said.

“Potential treatments such as this could one day prevent up to 95 per cent of bowel cancers. We are very grateful for the support of the Shepherd Foundation, which will help us to understand the impact of this combination therapy and determine the appropriate doses for the first human trials.”

Philanthropy funds shortfallProfessor Burgess was among the 76 per cent

of applicants who missed out on funding from the National Health and Medical Research Council in 2014. However the research project will proceed thanks to the generous support of the Shepherd Foundation, Twin Towns Services Community Foundation and the Shirley Cuff Cancer Research Foundation.

If you would also like to support this study, contact Ms Susanne Williamson, head of Fundraising, on 9345 2962 or williamson.s@wehi.edu.au.

Honouring an Australian iconProfessor Don Metcalf (L) and Dr Catherine Carmichael. Professor Metcalf was a keen mentor of early-career researchers.

Professor Tony Burgess

“There is no better way to honour Don’s memory than

by encouraging the next generation of scientists”

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Join us as institute director Professor Doug Hilton reflects on our achievements.Thursday 21 May 2015, 4:30-5:30pm

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We are incredibly proud to be the first Australian medical research institute to celebrate 100 years.In that time, we have developed antivenoms for snakebites, revolutionised immunology with Nobel Prize-winning research, and improved the lives of more than 20 million cancer patients who have been treated with CSFs.

Throughout 2015, we have an exciting program of events to commemorate and celebrate 100 years of discoveries for humanity. Join us as we reflect on the past century of medical research and look ahead to the years to come.

Centenary public talks

What does the future hold for medical research?

Join our researchers for presentations on the latest research followed by an extended Q&A session.

10 June: Infectious diseases 28 October: Cancers

Registration essential: www.wehi.edu.au/publictalks

June

10October

28

Centenary scientific seminar

Professor Pamela Bjorkman, Caltech, US

Biochemist Professor Pamela Bjorkman will present a special scientific seminar as part of our Centenary seminar series.

Wednesday 24 June 2015, 1-2pm

Registration essential: www.wehi.edu.au/centenary

June

24Keep up to date with the institute’s centenary events by visiting

www.wehi.edu.au/centenaryor liking us on Facebook www.facebook.com/WEHIresearch

Centenary scientific symposium

The Centenary scientific symposium will celebrate 100 years of discoveries for humanity.

Featuring 20 distinguished speakers from Australia and around the world, this free symposium on the institute’s latest research will include presentations from Nobel laureates Professor Elizabeth Blackburn (University of California San Francisco, US) and Professor Tom Steitz (Yale University, US).

Wednesday 29 July – Friday 31 July 2015

Registration essential: www.wehi.edu.au/centenary

July

29-31

Public discovery tour

What happens inside a medical research institute?Discover our science on a free public tour. You will meet some of our researchers, visit a working laboratory and hear how their work is improving health outcomes across the world.

Wednesday 22 April 2015, 1:45-3pm and Wednesday 22 July, 10:45am-12pm

Registrations: www.wehi.edu.au/events

April

22July

22

Celebrating our centenary

In August, the institute will take over Melbourne’s Federation Square with exhibitions, forums and performances to delight and inform audiences of all ages. Coinciding with National Science Week, the Science in the Square Festival will include:

Comedy debate 15 August 2015This lively debate will entertain with well-known comedians and personalities and feature live performances from original science rock band Ologism. Ticketed event.

Science Fiction Film Festival 20-22 August 2015Hollywood loves a good science fiction film, but where are the facts among the fiction? Watch feature films including Gattaca, Outbreak and Contagion before hearing from a panel of experts as they attempt to separate the possible from the just plain ridiculous. Ticketed event. M15+

Art of Science exhibition 4-17 August 2015This free public exhibition will share scientific discoveries from an artistic perspective, showcasing finalists of the institute’s annual

‘Art of Science’ competition. Free event.

Talking Science: When will there be a cure for cancer? 19 August 2015Hear from Melbourne’s cancer experts and discuss whether there will ever be a cure for cancer at this free public forum with an extended Q&A session. Free event.

August

4-22Science in the Square Festival

S U P P O R T O U R R E S E A R C H w w w . w e h i . e d u . a uP a g e 8

Com

ing events

Support our discoveries… donate today

The Walter and Eliza Hall Institute’s researchers are working to understand, prevent and treat diseases including blood, breast, ovarian, bowel and lung cancers, type 1 diabetes, rheumatoid arthritis, coeliac disease and malaria.We are doing this because:• One in eight Australian women will be diagnosed with

breast cancer by the age of 85.• Malaria kills up to 700,000 people each year.• More than 120,000 Australians have type 1 diabetes. • As many as 1 in 60 Australians have coeliac disease. More than 100 clinical trials based on discoveries made at the institute are underway, including a new class of anti-cancer drugs and vaccines for type 1 diabetes, coeliac disease and malaria.

The Walter and Eliza Hall Institute relies on donations from the community to continue its vital research. Donations of $2 or more are tax deductible in Australia.

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