A Look Inside the Geoffrey Beene Cancer Research Center
The Geoffrey Beene Cancer Research Center at Memorial Sloan-Kettering Cancer Center was established in 2006. The total value in combined funding to date from Geoffrey Beene is $138,000,000.
G. Thompson Hutton, the Trustee of the Geoffrey Beene Foundation and President of Geoffrey Beene, LLC, has orchestrated the activities to build and support this ambitious research initiative. “The hallmark of the Geoffrey Beene Cancer Research Center at Memorial Sloan-Kettering Cancer Center is its focus on revolutionary new research approaches across a variety of cancers, strategies that will lead to prevention through improved diagnostics and enhanced quality of life treatments toward the ultimate goal of making cancer a more manageable and perhaps one day, a curable disease.”
Since its creation, the Geoffrey Beene Cancer Research Center has served as the focal point for an array of projects, aimed at translating works at the cellular level into revolutionary new research approaches to preventing, diagnosing, and treating the disease. It brings together researchers and physicians from two complementary areas: the Cancer Biology and Genetics Program, based in the Sloan-Kettering Institute (SKI), which studies the genetic and biochemical events that trigger the transformation of normal cells into cancerous ones, and the Memorial Hospital-based Human Oncology and Pathogenesis Program, which pursues new insights into the molecular mechanisms of cancer from the perspective of clinical oncology.
“The Geoffrey Beene Cancer Research Center has helped galvanize our efforts to gain new insights into cancer and to apply that knowledge to the development of more effective strategies for patient care,” said Harold Varmus, former President of Memorial Sloan-Kettering Cancer Center, and now Director of the National Cancer Institute. “We are especially grateful to Tom Hutton and his colleagues at Geoffrey Beene, LLC for recognizing the significance of the work being done here.”
The funds from Geoffrey Beene support advanced new research initiatives spanning the entire range of translational research, funding core research labs, research projects, the establishment of senior and junior faculty chairs, graduate fellowships, the annual Geoffrey Beene Symposium, and the annual Geoffrey Beene Research Retreat.
The Center provides support for the Geoffrey Beene Translational Oncology Core, directed by Dr. Charles Sawyers. The core performs genomic analyses of clinical material by applying state of the art genome-scale molecular profiling technologies. Geoffrey Beene salutes Dr. Sawyers for the extraordinary accomplishment of winning the prestigious 2009 Lasker-DeBakey Clinical Medical Research Award. His award is based on the development of molecularly-targeted treatments for chronic myeloid leukemia, converting a fatal cancer into a manageable chronic condition.
The Center also provides support for the Microchemistry and Proteomics Core Facility and Genomics Core Facility, both of which are aimed at significantly augmenting Memorial Sloan-Kettering’s capacity for translational cancer research in genomics.
Since 2006, 86 grants have been awarded and 12 proposals for shared resources have been funded. Each grant funds initial-stage research and is renewed for a second year. Each year the Geoffrey Beene Cancer Research Center’s Executive Committee reviews submissions of innovative research proposals. This highly competitive review process awards grants to the most compelling and profound ideas proposed by researchers from the Memorial Sloan-Kettering Cancer Center community. After completion of the funded project, grant recipients have gone on to develop their novel ideas and apply for further grants from external sources. Since 2007, for every dollar of direct support from the Geoffrey Beene Cancer Research Center, grant awardees received an additional $1.64 in follow-up funding from external sources based on the early-stage ideas supported by the Geoffrey Beene Cancer Research Center.
Oversight of The Geoffrey Beene Cancer Research Center is provided by an Executive Committee. Scott Lowe, PhD, Chair of Cancer Biology and Genetics Program (CBG) was appointed to the Geoffrey Beene Chair in 2011. In 2013 David Solit, MD, Associate Member in the Human Oncology and Pathogenesis Program (HOPP) was appointed to a Geoffrey Beene Senior Chair. Ping Chi, MD, PhD, Assistant Member in the HOPP, Kitai Kim, PhD, Assistant Member in CBG, and Joseph Sun, PhD, Assistant Member in Immunology, are currently appointed as Geoffrey Beene Junior Faculty Chairs. Andrea Ventura, MD, PhD, Assistant Member in the CBG, and Johanna Joyce, PhD and Ross Levine, MD, Assistant Members in HOPP have previously held the Geoffrey Beene Junior Faculty Chairs. Since the establishment of the Geoffrey Beene Cancer Research Center, twenty-one Geoffrey Beene Graduate Fellowships have been awarded. We are proud to announce that in 2014 three Geoffrey Beene Graduate Fellowships were awarded to PhD students Hannah Johnsen, Michael Langberg and Ryan Smith.
Geoffrey Beene research has resulted in many successes including the latest breakthroughs.
President, Memorial Sloan-Kettering Cancer Center Craig B. Thompson, MD
Regarding the American diet, Dr. Thompson explains “… one of the fundamental things about the Geoffrey Beene Foundation is to shine a light on that issue. So the question is what are those unhealthy foods? For a long time we thought that the foods were the fats that we eat. It turns out for cancer not to be the big culprit. It turns out to be the sugars, the simple sugars that we eat that are the most dangerous and that came from basic research that was funded here by the Geoffrey Beene Foundation at Memorial Sloan- Kettering.”
Marilyn Resh, PhD – Tackling lethal pancreatic cancer
Pancreatic cancer is an extremely lethal cancer for which no effective therapies are currently available. The laboratory of Marilyn Resh is focused on a molecular pathway which is controlled by the Sonic hedgehog (Shh) protein and contributes to pancreatic cancer development. Shh is produced by embryos as they develop. After birth, Shh expression is turned off, and most normal adult tissues do not make Shh. However, in pancreatic cancer, Shh is aberrantly turned back “on”. This abnormal expression of Shh helps to promote the growth of pancreatic cancer. In order to function normally, Shh must be modified by attachment of a fatty acid, palmitate. This process is known as palmitoylation, and is mediated by a protein termed Hhat (Hedgehog palmitoyl acyltransferase). Dr. Resh and her colleagues hypothesized that it would be possible to block the action of Shh by inhibiting the ability of Hhat to attach palmitate to Shh.
Using funds from the Geoffrey Beene Cancer Research Center, Dr. Resh set up a strategy to test her hypothesis and in doing so develop potential new strategies to treat pancreatic cancer. In order to identify Hhat inhibitors, she developed a method to measure Shh palmitoylation and used it to screen a “library” of 85,000 chemical compounds. This screen identified 95 compounds that directly inhibit Hhat, and they chose the 4 best compounds for further study. Additional testing of one of the compounds, #43, revealed that it enters cells, where it directly inhibits palmitoylation of Shh. Consistent with Dr. Resh’s hypothesis, compound 43 also inhibits the growth of human pancreatic cancer cells. These features support the concept that compound 43 can be developed into an effective drug for therapeutic treatment of pancreatic cancer in patients.
Stimulated by the success of her Geoffrey Beene funded project, Dr. Resh is continuing to develop agents that target Shh into novel therapies. In collaboration with the Tri-Institutional Therapeutics Discovery Institute and Takeda Pharmaceuticals, we are developing drugs that work as Hhat inhibitors. To date, no other studies have used Hhat as a target in pancreatic cancer (or any other cancer), thereby making our approach innovative and unique. The Hhat inhibitors will be tested for their ability to block tumor growth in models of pancreatic, breast and lung cancer in the laboratory, and ultimately in the clinic.
- The abnormal expression of Shh(Sonic hedgehog) drives the growth of pancreatic cancer
- Dr. Resh planned to modify the abnormal expression of Shh by attaching a fatty acid, palmitate.
- After much experimentation Dr. Resh identified compound 43 as a compound capable of blocking Hhh action and pancreatic cancer cell growth
- Further development of compound 43 may lead to new treatments for pancreas cancer
Andrea Ventura, MD, PhD – New tools for studying complex cancer lesions
In addition to funding specific research projects designed to produce new insights into the origins and treatment of cancer, the Geoffrey Beene Cancer Research Center supports the career development of promising young investigators. Specifically, through its Geoffrey Beene Junior Chairs program, it provides unrestricted funds that enable early career scientists to test new ideas prior to obtaining funding from traditional research grants that often favor established investigators.
Andrea Ventura exemplifies the potential of this program. Enabled by the freedom created by the Geoffrey Beene junior chair program, he recently developed a new strategy to create models harboring a particular type of cancer-associated change, termed translocation, that have been difficult to study in the laboratory. These events involve the inappropriate fusion of two chromosome regions not normally associated together leading to the production of a new molecule that promotes cancer development. Even more remarkably, Dr. Ventura showed that the models are predictive of a patient responses to chemotherapies used against patients that have the same genetic change. The method will be broadly useful in understanding how these chromosomal events cause cancer and the resulting models will be extraordinarily useful for identifying strategies to treat patients with these types of events.
- Developed a new strategy to create models with a specific type of cancer-associated change (translocation)
- The models produced using this method will be useful in understanding how chromosomal events cause cancer
- These models will also facilitate the development of new therapies designed to treat patients whose tumors harbor these type of “translocation” events.
Michael Berger, PhD – “Having an IMPACT on treatment decisions”
The concept of precision cancer medicine is based on the premise that each patient’s cancer is unique and should be treated based on the molecular changes occurring in their tumor. A growing number of cancer drugs specifically target cancers with particularly genetic events and thus are being administered according to the presence or absence of key tumor genetic alterations that predict the likelihood of the therapy’s success. Accordingly, high-throughput mutation profiling of the DNA from every cancer for the mutational status of every known cancer gene is central for the success of precision cancer medicine.
With the support of the Geoffrey Beene Cancer Research Center, a test called MSK-IMPACT, which is capable of detecting all possible mutations involving 341 genes with the greatest clinical and/or biological significance for cancer, was developed. Through extensive experimentation, Dr. Berger and colleagues optimized the performance of the test for “challenging” types of clinical specimens. Following initial success in pilot studies, Dr. Berger has since deployed production-scale MSK-IMPACT testing retrospectively for translational research and prospectively for clinical diagnosis of patients.
In the last 2 years, Dr. Berger and his colleagues have published more than 20 research articles describing studies with MSK-IMPACT to identify clinically relevant mutations. Most significantly, the MSK-IMPACT platform has been successfully implemented in the clinical molecular diagnostics laboratory of Memorial Sloan Kettering Cancer Center to directly inform treatment decisions. Based largely on the success of the work funded by the Geoffrey Beene grant, Dr. Berger assumed oversight of the development of validation of MSK-IMPACT as a clinical test. Dr. Berger obtained full approval from the New York State Department of Health allowing him to report results back to patients and their doctors. This promises to improve treatment decisions for numerous patients and to pre-identify patients eligible for current and future clinical trials.
- MSK-IMPACT was developed to detect all possible mutations involving 341 genes
- MSK-IMPACT enables informed treatment decisions and can pre-identify patients for eligible for clinical trials to test new drugs or drug combinations
- Over 20 research articles have been published where MSK-IMPACT has been used
- MSK-IMPACT has been implemented into the molecular diagnostics lab to directly inform treatment decisions
Omar Abdel-Wahab, MD, PhD- Dramatic Clinical Efficacy of RAF Inhibitors in Hairy Cell Leukemia and the Systemic Histiocytoses
While the Geoffrey Beene Cancer Center supports research into the genetic basis of cancer and on studies to understand cancer behavior, it also directly supports innovative clinical trials to test new ideas for treating cancer patients. As an example, in 2012 and 2013, the Center provided critical support to fund 2 different clinical studies of the drug vemurafenib: one for the disease Hairy Cell Leukemia and another for a group of disease called the “Systemic Histiocytoses.” Recently it was discovered that these 2 sets of diseases, which are each forms of blood cancer, are caused by mutations in a gene called BRAF. BRAF mutations promote uncontrolled cell division and were previously know to contribute to melanoma skin cancers. Additionally, drugs that target BRAF are one of the few therapies which extend lifespan of melanoma patients. Based on this, Dr. Abdel-Wahab and a group of investigators here at MSKCC started 2 clinical trials of the BRAF inhibitor vemurafenib as mentioned above. Thus far, the team has treated 21 patients with Hairy Cell Leukemia on this study and 20 with Histiocytoses. The results of the clinical trials have been remarkable and revealed unprecedented efficacy of these drugs. Importantly, these studies enrolled patients with no other treatment options at the time making this an especially important for our patients. In fact, we are now initiating conversations with the FDA to seek FDA-approval for vemurafenib in both of these conditions based on the results of these studies.
The Figure shows images from first 2 patients histiocytosis patients treated on the study and are representative of all patients treated thus far. Patient A had extensive disease involving the brain, bones, and abdomen and has had a complete radiographic response and marked clinical benefit. Previously entirely wheelchair bound and unable to perform any activities needed for daily life, she is now able to move with minimal assistance and is once again independent. See a video on YouTube where she describes her experience at MSKCC here: http://youtu.be/zmJLvazVi58?t=3m20s.
It is important to note that both of these disorders are poorly understood by the medical community. Thus, in parallel to offering clinical therapy we have performed a number of laboratory-based studies to understand the biological basis for these diseases in more detail. We expect the clinical trials to be completed and published in 2015.
- BRAF mutations contribute to a range of cancers, including melanoma and two types of blood cancers, called Hairy Cell Leukemia and Systemic Histiocytoses.
- A group of investigators here at MSKCC started clinical trials using the BRAF inhibitor vemurafenib to treat patients with BRAF mutant blood cancers.
- The results of the clinical trials have been positive and revealed an unprecedented efficacy of these drugs
Ross L. Levine, MD- Understanding the origins of myeloid malignancies
Ross Levine is another junior faculty member who was recruited to MSKCC through support from the Geoffrey Beene Cancer Research Center. Acute myeloid leukemia represents an aggressive blood cancer for which new therapies are urgently needed. It is known that AML shows substantial differences in the genetic makeup and clinical behavior between patients. Work from MSK investigators and elsewhere has identified a poorly understood class of mutations that contributes to some forms of AML. These so-called “epigenetic” regulators do not directly impact the proliferation and survival of cancer cells but indirectly regulate other genes that do. Three of these genes are called TET2, ASXL1, and DNMT3A, and their inactivation occurs in a large fraction of AML patients.
With support from the Geoffrey Beene Cancer Research Center the Levine group demonstrated these mutations influence the aggressiveness of AML. They then used these data to identify clinical implications of genetic alterations in AML, and to develop a clinically useful predictor that can predict overall outcome in AML and improve the ability of oncologists to decide on the best treatment strategy. As one example, their efforts identified certain subsets of AML patients that benefit from dose-intensified chemotherapy, which allows oncologists to reserve more toxic regimens from the patients for which this toxic strategy would be ineffective. Like the IMPACT assay, this work has led to the widespread use of mutational profiling of AML patients and to the development of state-of-the-art genomic profiling assays for patients at MSKCC and nationally/internationally.
- The Levine Lab performed comprehensive mutational profiling of the largest US cohort of AML patients.
- The Levine Lab identified specific genetic alterations that predicted the likelihood of cure or relapse after chemotherapy.
- The Levine Lab developed a novel, prognostic algorithm to show how genetic profiling can be used to predict outcome in AML, which is now in clinical practice.
Yu Chen, MD, PhD – “The Newest Precision Medicine Tool: Prostate Cancer Organoids”
Research led by investigators at Memorial Sloan Kettering Cancer Center has shown for the first time that organoids derived from human prostate cancer tumors can be grown in the laboratory, giving researchers an exciting new tool to test cancer drugs and personalize cancer treatment.
The researchers, whose results were published in Cell, successfully grew six prostate cancer organoids from biopsies of patients with metastatic prostate cancer and a seventh organoid from a patient’s circulating tumor cells. Organoids are three-dimensional structures composed of cells that are grouped together and spatially organized like an organ. The histology, or tissue structure, of the prostate cancer organoids is highly similar to the metastasis sample from which they came. Sequencing of the metastasis samples and the matched organoids showed that each organoid is genetically identical to the patient’s cancer from which it originated.
“Identifying the molecular biomarkers that indicate whether a drug will work or why a drug stops working is paramount for the precision treatment of cancer,” said Yu Chen, MD, PhD, Assistant Attending Physician in the Genitourinary Oncology Service and Human Oncology and Pathogenesis Program at MSK. “But we are limited in our capacity to test drugs — especially in the prostate cancer setting, where only a handful of prostate cancer cell lines are available to researchers.”
With the addition of the seven prostate cancer organoids described in the Cell paper, Dr. Chen’s team has effectively doubled the number of existing prostate cancer cell lines.
“We now have a new resource at our disposal that captures the molecular diversity of prostate cancer. This will be an invaluable tool we can use to test drug sensitivity,” he added.
The use of organoids in studying cancer is relatively new, but the field is exploding quickly according to Dr. Chen. In 2009, Hans Clevers, MD, PhD, of the Hubrecht Institute in the Netherlands demonstrated that intestinal stem cells could form organoids. Dr. Clevers is the lead author on a companion piece also published in Cell today that describes how to create healthy prostate organoids. Dr. Chen’s paper is the first to demonstrate that organoids can be grown from prostate cancer samples.
The prostate cancer organoids can be used to test multiple drugs simultaneously, and Dr. Chen’s team is already retrospectively comparing the drugs given to each patient against the organoids for clues about why the patient did or didn’t respond to therapy. In the future, it’s possible that drugs could be tested on a patient’s organoid before being given to the patient to truly personalize treatment.
After skin cancer, prostate cancer is the most common cancer in American men — about 233,000 new cases will be diagnosed in 2014. It is also the second leading cause of cancer death in men; 1 in 36 men will die of the disease.
Despite its prevalence, prostate cancer has been difficult to replicate in the lab. Many mutations that play a role in its growth are not represented in the cell lines currently available. Cell lines can also differ from their original source, and because they are composed of single cells, they do not offer the robust information that an organoid — which more closely resembles a living organ — can provide.
Researchers from Weill Cornell Medical College and the Hubrecht Institute of the Royal Netherlands Academy of Arts and Sciences contributed to the research.
Johanna Joyce, PhD- Cathepsin S and breast cancer
Most cancer deaths occur when the disease spreads, or metastasizes, from the original tumor site to a distant location. In breast cancer patients, metastasis to the brain can occur months or years after seemingly successful treatment of the primary tumor. Johanna Joyce, an inaugural Geoffrey Beene Jr. Chair recipient and researchers at MSK have found that a protein called cathepsin S may play a key role in the spread of breast cancer to the brain. A complex interplay between breast cancer cells and certain surrounding cells called macrophages induces both cell types to secrete increased levels of cathepsin S, an enzyme that promotes the cancer cells’ ability to metastasize. Dr. Joyce’s lab recently showed that cathepsin S could be an important target for new drugs. The Joyce lab was interested in how these noncancerous cells at metastatic sites react when they encounter the tumor cells. To investigate these questions, the research team studied mice implanted with human breast cancer cell lines that are known to spread to the brain, bone, and lung. They looked at how both the tumor and its surrounding microenvironment change during cancer speading. The cancer cells and surrounding cells were subjected to genetic analysis to see which genes were more active than normal. In mice with brain metastases, the cathepsin S gene was significantly overexpressed. Interestingly, the tumor cells produced more cathepsin S at the beginning of metastasis and then tapered production, in parallel with a progressive increase in macrophage cathepsin S levels within the brain.
The researchers showed that cathepsin S enables the cancer cells to penetrate through the blood-brain barrier, a densely packed vascular structure that protects the brain from most large molecules in the blood. The researchers found that cathepsin S cleaves a protein called (JAM)-B, which normally helps hold cells in the blood-brain barrier together. The higher levels of cathepsin S presumably negate (JAM)-B’s effect and allow the cancer cells to penetrate the barrier.
To validate the role of cathepsin S in promoting brain metastases, the researchers inhibited it with experimental drugs. This significantly reduced the development of brain metastasis in the animals. The Joyce lab would like to move forward with clinical trials for cathepsin S inhibitors on cancer cells in the near future.
- Breast cancer patients are susceptible to metastasis to the brain after months or years of successful treatment of their primary tumor
- Cathepsin S may play a key role in the spread of breast cancer to the brain
- The research of the Joyce lab showed the cathepsin S enables the cancer cells to penetrate through the blood-brain barrier, allowing the cancer cells to penetrate the brain
- Experimental drugs were used to inhibit cathepsin S and this significantly reduced the development of brain metastasis in animals
Scott W. Lowe, Ph.D. – New therapeutic targets for drug development
Besides providing direct support for cancer researchers, the Geoffrey Beene Cancer Research Center provides funds to support the development and implementation of new technologies or services that can enable cutting edge research across MSKCC. One such technology involves RNA interference (RNAi), which is a natural process occurring in all cells in which a small RNA molecule leads to silencing of the particular genes. For biologists, this process can be harnessed to shut off any gene of interest in order to study what that gene does. One form of RNAi uses “short hairpin RNAs” (shRNAs) to inhibit gene function, and their use can be applied in high throughput screens to identify genes involved in virtually any cellular process. When applied to cancer, it is possible to use this technology to identify genes that are required for the proliferation or survival of cancer cells but not normal cells. Such genes, and the proteins they encode, are a potential “Achilles Heel” of particular cancers and may be targets for future cancer drugs. In 2012, the Geoffrey Beene Cancer Research Center supported the development of an “RNAi Core” to bring the newest tools and methods to all MSK investigators.
The laboratory of Scott Lowe, who chairs the Geoffrey Beene Center for Cancer Research, recently used technology from the RNAi core to search for molecules needed for the survival of liver cancer cells. This tumor type – called hepatocellular carcinoma – is increasing in incidence worldwide but is not responsive to any existing therapy. Using shRNAs, The Lowe laboratory identified a molecule called the cyclin-dependent kinase 9 (CDK9) as a protein that was essential for proliferation of hepatocellular carcinoma cells with a particular alteration in a gene called MYC. Interestingly, MYC is well known to contribute to a range of cancers but has not been amenable to drug development. Working as part of a broad MSK collaboration involving Charles Sawyers, Jason Lewis, and Scott Armstrong, they showed that RNAi molecules or small molecules that inhibited CDK9 can have anti-cancer effects. While these molecules are not sufficiently potent or selective to be given to patients, the work suggests that further development of CDK9 inhibitors may lead to new treatments for liver cancer.
- RNA interference (RNAi) describes a process in which scientists can specifically inhibit the function of any gene
- RNAi can be used in the laboratory to identify new genes that participate in a particular cellular process and has thus become a powerful experimental tool
- The Lowe laboratory used RNAi to identify CDK9 as a molecule needed for some liver cancer cells to proliferate
- Drugs that are developed to specifically target CDK9 may be useful for treating liver cancer and possibly other tumor types
Quotes from some of our scientists:
Director of the NIH and Nobel laureate, Harold Varmus, MD
Dr. Harold Varmus former chair of The Geoffrey Beene Cancer Research Center at Memorial Sloan-Kettering Cancer Center said, “the Center is dedicated to making revolutionary discoveries about how cancer works at the cellular level and using them for new approaches to diagnosis, treatment, and prevention.” Dr. Varmus adds, “The Geoffrey Beene Cancer Research Center has helped galvanize our efforts to gain new insights into cancer and to apply that knowledge to the development of more effective strategies for patient care. We are especially grateful to Tom Hutton and his colleagues at Geoffrey Beene, LLC for recognizing the significance of the work being done here.”
Andrea Ventura, MD, PhD
“It’s not only the money, I mean the money is clearly important for our research because our experiments expensive. But any support of the public or foundations like the Geoffrey Beene Foundation for a junior investigator it’s such a boost of confidence. We are starting our career and we find somebody that believes in our idea and it takes off and that is good. We will keep give you our support. Not only in terms of money but also in terms of moral support. This is also extremely important.”
Geoffrey Beene Gives Back
All net profits from Geoffrey Beene, LLC together with the Geoffrey Beene Foundation fund philanthropic causes that support initial-stage, out-of-the-box revolutionary research for treatments and prevention across all cancers as well as awareness and research for Alzheimer's, heart disease, scholarships, programs for veterans, protection of women and children and protection of animals.
November 18, 2014
November 19, 2013
The Geoffrey Beene Cancer Research Center at Memorial Sloan-Kettering helps to fund authors Scott Lowe and Ross Levine’s childhood leukemia research. Rare, inherited mutation leaves children susceptible to acute lymphoblastic leukemia
April 21, 2013
April 1, 2012
Oversight of the Geoffrey Beene Cancer Research Center is provided by the following members of its Executive Committee:
Scott Lowe, PhD
Chair, Geoffrey Beene Cancer Research Center
Craig Thompson, MD
President, Memorial Sloan-Kettering Cancer Center
Alexandra Rudensky, PhD
Chair, Immunology Program
Joan Massagué, PhD
Director, Sloan Kettering Institute
Larry Norton, MD
Deputy Physician-in-Chief, Breast Cancer Programs
Charles Sawyers, MD
Chair, Human Oncology & Pathogenesis Program
David Scheinberg, MD, PhD
Chair, Molecular Pharmacology & Chemistry Program
Scott A. Armstrong, MD, PhD
Member, Human Oncology & Pathogenesis Program
José Baselga, MD, PhD
Physician-in-Chief, Memorial Hospital
Nikola P. Pavletich, PhD
Chair, Structural Biology Program
G. Thompson Hutton
Trustee of the Geoffrey Beene Foundation and
President of Geoffrey Beene, LLC.