New Discoveries and Honors

Read about the latest discoveries by Damon Runyon scientists and honors received by scientists in the Damon Runyon scientific community.

October 16, 2018

Patients with metastatic breast cancer—when the tumor has spread to other organs in the body—face a terminal prognosis and toxic treatments. There is an urgent need for new ways to treat drug metastatic and resistant stages of the disease. Sarat Chandarlapaty, MD, PhD (Damon Runyon Clinical Investigator ’12-’17), and colleagues, have developed a novel class of drugs that may help these patients by potentially stopping or even destroying breast cancer tumors. The drugs can attach to the estrogen receptors (ER) in cancer cells and then hijack the cell's protein-disposal machinery to degrade the receptor. The new compounds also block the hormone estrogen from binding to its receptor. As a result, breast cancer cells in the laboratory stopped growing and multiplying. 


"Over the years, the roles of the ER in mediating tumor growth in breast cancer has gained importance, but current therapies targeting ER lack potency or work for a short time only. This new class of drugs eliminates the receptor through degradation, perhaps preventing relapse," says Sarat. The researchers plan to next test these compounds in animal models of cancer, with the hope of eventually moving them to clinical trials in humans. The research was published in the American Chemical Society ACS Medicinal Chemistry Letters.


October 15, 2018

Two Damon Runyon alumni were elected to the National Academy of Medicine. Election to the Academy is considered one of the highest honors in the fields of health and medicine and recognizes individuals who have demonstrated outstanding professional achievement and commitment to service.


Azad Bonni, MD, PhD (Damon Runyon Fellow ’96-‘97) at the Washington University School of Medicine, St. Louis, was recognized for discovering fundamental signaling networks governing brain development and how deregulation of these circuits contributes to cognitive disorders.


Matthew L. Meyerson, MD, PhD (Damon Runyon Fellow ’95-‘98) of Harvard Medical School and the Dana- Farber Cancer Institute, Boston, was recognized for the discovery of epidermal growth factor receptor (EGFR) mutations in lung cancer. His research showed that these mutations predict responsiveness to EGFR inhibitors and helped establish the current paradigm of precision cancer therapy.


September 25, 2018

Triple negative breast cancer (TNBC) is the most aggressive and hard-to-treat form of breast cancer. Doctors have observed that TNBC patients with higher numbers of immune cells in their tumors seem to have better survival than those with fewer, but it's not well understood why. Damon Runyon Fellow Leeat Yankielowicz-Keren, PhD, and Dale F. Frey Breakthrough Scientist Sean C. Bendall, PhD, at Stanford University, are addressing this question by using a new imaging technique to precisely identify the type and location of immune and cancer cells in patient tumors. The researchers found that patients whose tumors showed immune cells crowded along defined borders, outside and within, were significantly more likely to survive their cancers with treatment. When a patient’s tumor was dispersed with immune cells throughout, the prognosis was far worse. The researchers are now hoping to use the technique to investigate responses to immunotherapy and to better understand how the immune composition of tumors changes over time. This research was published in Cell.


September 17, 2018

One of the greatest challenges doctors face is predicting, which patients will respond to a particular cancer therapy. Ash Alizadeh, MD, PhD (Damon Runyon Clinical Investigator '14 - '17) and David Kurtz, MD, PhD (Damon Runyon Physician Scientist '16 - '20), at Stanford University School of Medicine have developed a new blood test to guide doctors when treating diffuse large B cell lymphoma (DLBCL). The blood test measures the levels of circulating tumor DNA (ctDNA)— fragments of DNA released by cancer cells—in patients before and after therapy. They observed in clinical trials that those who lived 24 months or more without a recurrence of their disease had a rapid drop in the amount of ctDNA in their blood within one or two treatments. However, patients whose cancer did not respond even after a full six treatments had ctDNA levels decline more slowly within the initial treatment period.


Rather than waiting five or six months for treatment to run its course, doctors may be able to choose the best therapeutic option for a patient within days or weeks using the blood test. “By identifying those people who are responding extremely well, we could spare them unnecessary treatments. Conversely, we could intensify the therapy or seek other options for those who are not responding,” explains David. "We are thinking about how to use the tools to best benefit patients and are very excited to test this approach in other types of cancers," adds Ash.


This research was published in the Journal of Clinical Oncology.


August 27, 2018

Christine Mayr, MD, PhD, (Damon Runyon Innovator ’13-‘15), Omar Abdel-Wahab, MD (Damon Runyon Clinical Investigator ’13-’16), and colleagues at Memorial Sloan Kettering Cancer Center, New York, report new results that suggest malfunctions in messenger RNA (mRNA) processing may be driving chronic lymphocytic leukemia (CLL). mRNAs carry the information encoded in DNA, which is then translated into proteins. Changes at both the DNA and mRNA level can result in malfunctioning proteins. The researchers found that even without a corresponding DNA alteration, some patients had altered proteins that either lacked their normal tumor-suppressive effect, or in other cases, even promoted cancer. Tumor suppressor proteins are necessary to prevent the body’s cells from turning cancerous.The altered proteins were attributed to changes at the mRNA level. These findings may help explain the puzzling observation that CLL cells have relatively few known DNA mutations. The study also demonstrates the need to go beyond genomic DNA analyses in cancer diagnostics, as mRNA alterations are also widespread contributors to cancer pathogenesis through the inactivation of tumor suppressor genes. This work was published in Nature.


June 20, 2018

Matthew G. Vander Heiden MD, PhD (Fellowship Award Committee Member, Fellow ’06-’08, Innovator ’11-‘13) and colleagues at the Dana-Farber Cancer Institute and MIT’s Koch Institute, Boston, have found a new reason pancreatic cancer patients lose weight. They observed in mouse models that tumors interfered with the pancreas’ ability to secrete enzymes that digest food. Unable to obtain enough nutrients from food, the mice entered starvation mode in which their bodies broke down fat to survive. In an earlier study, the researchers observed tissue starts breaking down very early in pancreatic cancer patients, usually long before other signs of the disease appear. The scientists are studying this effect in humans, which may help doctors identify pancreatic cancers at an earlier stage. Difficult to detect and nearly impossible to treat, pancreatic cancer is the only major cancer with a five-year survival rate below 10 percent. This study was published in Nature.


June 19, 2018

John Mendelsohn, MD (Damon Runyon Grantee ’72-’74), President Emeritus of MD Anderson Cancer Center, Houston, shared the 2018 Tang Prize in Biopharmaceutical Science with former Damon Runyon Sponsors Tony Hunter, PhD, at the Salk Institute, La Jolla, and Brian J. Druker, MD, at the OHSU Knight Cancer Institute, Portland. Dr. Mendelsohn led the development of a novel targeted therapy: the anti-EGFR antibody cetuximab (Erbitux®). His efforts resulted in its approval by the FDA for the treatment of colon cancer and head/neck cancer. The trio is recognized for shaping the fields of precision medicine and targeted cancer drugs and will share the $1.33 million prize. 


May 25, 2018

Researchers have long been aware that several viruses have an innate ability to kill cancer cells. Dmitriy Zamarin, MD, PhD (Damon Runyon Fellow ’13-’16) and Jedd D. Wolchok, MD, PhD (Clinical Investigator ’03-08) both at Memorial Sloan Kettering Cancer Center, are combining that observation with currently approved cancer immunotherapies to deliver a "one-two punch" against cancer in clinical trials. The researchers have injected a non-pathogenic Newcastle Disease Virus (NDV) into a tumor, triggering a powerful, widespread immune response that kills cancer cells not only in the tumor, but also outside the virus-infected region. In combination with checkpoint inhibitors that unleash the immune system’s full cancer-fighting power, they have shown that the treatment can overcome and even prevent immunotherapy resistance in mice. Positive results in patients may help expand the use of immunotherapies to a broader range of cancers, including solid tumors. These findings were published in the Journal of Clinical Investigation.


 


May 23, 2018

Five Damon Runyon alumni are among the 19 individuals named Howard Hughes Medical Institute Investigators this week. These scientists were selected because they ask hard questions in uncharted territories of biology and have the potential to make breakthroughs that will benefit humanity. The appointment provides flexible funding of $8 million over a seven-year term for each scientist, enabling them to pursue provocative fundamental questions of critical importance to biomedical progress.

“We are delighted that our alumni are being recognized for their significant accomplishments and their promise to make future advances in healthcare. This is a testament to our strategy to foster the next generation of leaders while they are just venturing out into the research world with their bold, risky ideas,” said Lorraine Egan, President and CEO, Damon Runyon Cancer Research Foundation.

Meet our distinguished alumni:

Thomas Bernhardt, PhD (Damon Runyon Fellow ‘02-‘03) at Harvard Medical School, is focusing on how bacteria build their cell wall in order to grow and divide. Understanding the mechanisms of bacterial cell wall synthesis has critical implications for human disease and health—including new targets to combat drug-resistant infections. 

Howard Chang, MD, PhD (Damon Runyon Scholar ’06-’08) at Stanford University, is probing the mystery of a class of genes called long noncoding RNAs, which are pervasive in the human genome, but do not produce proteins like normal genes. Long noncoding RNAs are now known to be important in cancer and other human diseases, as well as development and aging.

Ralph DeBerardinis, MD, PhD (Damon Runyon Clinical Investigator ‘11-‘14) of the University of Texas Southwestern Medical Center, studies the metabolic pathways used by a cell to grow, develop, and expend energy. Understanding what goes wrong in these pathways when cancer and other diseases develop will lead to therapeutic agents that selectively target tumors, stopping their growth, while leaving metabolism in the rest of the body undisturbed.

Elizabeth Sattely, PhD (Damon Runyon Fellow ‘08-‘10) at Stanford University, is developing plants that can produce lifesaving drugs and building stronger plants along the way. Her lab engineered a common tobacco plant to produce a chemical that is used to create etoposide, a chemotherapy drug that treats various forms of cancer. This is potentially a less expensive and more efficient way of producing the vital drug.

Feng Zhang (Damon Runyon-Rachleff Innovator ‘12-‘14) of the Broad Institute of MIT and Harvard, is a leader in developing genome editing technologies, including CRISPR. His tools are being used globally to modify DNA for a wide range of applications, from improving crops to studying disease. The hope is genetic errors in patients’ cells will be corrected to treat disease someday.


May 3, 2018

Maria Mihaylova, PhD (Former Damon Runyon Fellow ‘13-’16) of the Whitehead Institute and MIT’s Koch Institute, Cambridge, has found benefits of intermittent fasting beyond weight loss. The researchers discovered that fasting for 24 hours dramatically improves stem cells’ ability to regenerate in the intestines of aged and young mice. When an injury or infection occurs, stem cells are key to repairing damage. This finding may help patients who suffer from GI infections or cancer patients undergoing chemotherapy. The researchers are now investigating compounds that will mimic the effect of fasting. These findings were published in the journal Cell Stem Cell. 


May 1, 2018

Two Damon Runyon alumni were elected to the National Academy of Sciences (the science “Hall of Fame”), one of the highest honors that can be earned by a U.S. scientist. Being elected into this prestigious group of scientists recognizes their distinguished and continuing achievements in biomedical research. This brings the total number of Damon Runyon scientists who are members of the National Academy of Sciences to 74.

Feng Zhang, PhD (Damon Runyon-Rachleff Innovator ‘12-‘14) of the Broad Institute of MIT and Harvard, Cambridge, is a pioneer in developing the CRISPR-Cas9 system to edit genomes in living cells, including human. CRISPR is turbo-charging research in labs around the world, being used to understand the molecular mechanisms of diseases such as cancer and hereditary diseases, diagnose infectious diseases, and explore gene-edited food. 


"I am thrilled to join this terrific community of thought-leaders, many of whom have mentored or inspired me. The support from the Damon Runyon Foundation was instrumental in our work, and having it recognized by this amazing group of scientists is such an honor.”

Roger J. Davis, PhD (Damon Runyon Fellow ’83-‘84) of the University of Massachusetts Medical School, Worchester, is investigating the underlying mechanisms of how inflammation contributes to diabetes, cancer, and stroke. His studies have led to the discovery of new genes, which play a role in these devastating diseases and the development of novel therapeutic strategies. 


“My recent election to the National Academy is an honor that would not have happened without that initial support from Damon Runyon. The postdoctoral fellowship was critical for completing my training and provided a foundation for my research career.”


April 26, 2018

Gavin Dunn, MD, PhD (Damon Runyon Clinical Investigator '17-'20), and colleagues at Washington University in St. Louis, are developing a way to detect brain tumor biomarkers through a simple blood test. Taking a biopsy of a brain tumor is a complicated and invasive surgical process. The new groundbreaking, proof-of-concept technique allows biomarkers from a brain tumor to pass through the tough blood-brain barrier into a patient's blood using noninvasive focused ultrasound and some tiny bubbles, potentially eliminating the need for a surgical biopsy. The blood test would reveal the amount of mRNA in the blood, which gives physicians specific information about the tumor that can help with diagnosis and treatment options. He plans to use the technique with immunotherapy, offering precision treatment that targets specific biomarkers in the brain. The study was published in the journal Scientific Reports. 


April 23, 2018

Benjamin L. Martin, PhD (Damon Runyon-Rachleff Innovator ’17-’18) and David Q. Matus, PhD (Damon Runyon-Rachleff Innovator ’17-’18, Damon Runyon Fellow '07-'10) of Stony Brook University, Stony Brook, and colleagues, have developed new cell imaging technology that allows scientists investigating cancer and other diseases insights into how cells operate in real-time. This is the first time high-resolution, three-dimensional footage of the process has been visualized in action. One video shows in stunning detail a breast cancer cell rolling, crawling, and invading out of a blood vessel in a zebrafish. These observations indicate that breast cancer cells mimic immune cells called leukocytes and may help researchers discover new targets to stop the spread of metastatic cancer cells. Published in Science, this technology has the potential to observe cells across different organisms and developmental stages and in conditions such as cell division, immune processes, and metastasis.


March 5, 2018

The most deadly process in cancer is metastasis, when tumor cells spread to distant organs. Key to preventing metastasis is understanding how these cells are able to move through the body. Carey K. Anders, MD (Damon Runyon Clinical Investigator ’12-’15) of the University of North Carolina Lineberger Comprehensive Cancer Center, Chapel Hill, is shedding light on this process using genetic “snapshots” of both the primary tumor and the tumor after it has spread. She and her colleagues found that the cancer typically did not spread outside the breast as a single cell, but most likely broke away as a collection of cells. The results suggest that metastatic cancers are most often made up of cells with different genetic drivers. These diverse mutations in the original cancer are also potentially responsible for the metastatic process, and the cancer may not need to acquire new traits to be able to spread. This study indicates that targeting the primary tumor with multiple drugs may be important in containing the cancer. The report was published in the Journal of Clinical Investigation. 


March 1, 2018

Two new studies confirm that pediatric and adult cancers have different mechanisms driving the disease. These are the first large-scale genomic comparisons, combing through the genomes of more than 1,700 tumors, from over 20 different kinds of childhood cancers. Daniela S. Gerhard, PhD (Damon Runyon Fellow ’83-’85) of NCI, Bethesda, and Angela J. Waanders, MD, MPH (Dale F. Frey Breakthrough Scientist ’15-’17, Damon Runyon-Sohn Pediatric Cancer Fellow ‘12-‘15) of Chilidren’s Hospital of Philadelphia, Philadelphia, contributed to these studies.


Adult cancers arise from multiple genetic mutations that combine to drive cancer progression and often these same drivers are shared across diverse cancer types. A different picture emerges from these research studies for young patients: pediatric cancers have fewer mutations than adult cancers and are frequently defined by a single driver gene. Interestingly, these driver mutations tend to be specific to individual pediatric cancer types, with minimal overlap across diseases. They also found that different genes are mutated in pediatric compared to adult cancers. One study found only 30% of significantly mutated genes overlap with adult pan-cancer analyses. The similarities and differences between adult and pediatric cancers unearthed by the recent studies shed light on potential new drug targets and a better understanding of how cancer arises in children. It is clear that different precision medicine approaches are urgently needed for young patients. These studies were recently published in the scientific journal Nature.


February 19, 2018

The big story in cancer research is the recent success of immunotherapy, which involves training and reengineering the immune system to kill cancers. The New York Times featured four women whose rare, aggressive ovarian cancers were unexpectedly cured with immunotherapy. This story resulted from research by Dmitriy Zamarin, MD, PhD (Damon Runyon Fellow '13-'16) of Memorial Sloan Kettering Cancer Center, New York, who studied these patients to understand why they responded to this treatment (nivolumab/Opdivo). In addition, two other Damon Runyon alumni were featured.  Jedd D. Wolchok, MD, PhD (Damon Runyon-Lilly Clinical Investigator '03-'08) of Memorial Sloan Kettering Cancer Center, New York, led the clinical trials for the first FDA-approved immunotherapy and continues research to understand why it works in some patients, but not others.  Eliezer M. Van Allen, MD (Damon Runyon Clinical Investigator '15-'18) of Dana-Farber Cancer Institute, Boston, identified a genetic mutation that may explain why these patients and those with other unique cancers have responded to this therapy, which may help identify others who might benefit from immunotherapy.


February 1, 2018

Helen M. Piwnica-Worms, PhD (Damon Runyon Fellow ’84-’85, Former Fellowship Award Committee Member) of MD Anderson Cancer Center, Houston, received the 2018 Laura Ziskin Prize in Translational Research from Stand Up to Cancer. She and her collaborator will apply their expertise in DNA damage repair mechanisms and imaging mass cytometry to investigate how the immune system recognizes breast cancer