New Discoveries and Honors

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

July 5, 2017

Catherine J.Wu, MD (Current Damon Runyon Physician-Scientist Mentor and Clinical Investigator '07-'12) of Dana-Farber Cancer Institute, Boston, has led one of the first studies that demonstrates the potential of personalized cancer vaccines. The study focused on six people with advanced melanoma, a type of skin cancer. The participants had surgery to remove their tumors, but about half of all such patients face a recurrence of cancer. The researchers formulated a personalized vaccine for each person that contained up to 20 protein fragments corresponding to the mutations in their individual tumors. Thirty-two months later, four of the patients were cancer free. Two patients had their tumors re-grow, but experienced complete remission when subsequently treated with a PD-1 inhibitor, a drug that blocks the ability of cancer cells to hide from the immune system. Two years after treatment, the patients’ blood still carried anti-melanoma immune cells, suggesting the vaccine’s benefits last. Currently, cancer patients begin treatment with traditional therapies about three to six weeks after an initial diagnosis. Her goal is to treat a patient with an individualized cancer vaccine in that same window. While this is a small-scale study, the promising results mean researchers can move ahead with larger clinical trials, which could potentially lead to new, more effective cancer treatments. The results were published in the scientific journal Nature.


May 3, 2017

C. Ryan Miller, MD, PhD (Damon Runyon Clinical Investigator ’09-’12) of the UNC Lineberger Comprehensive Cancer Center, Chapel Hill, and colleagues, reported two studies on the genetics underlying brain tumors. The first study showed that mutations in MAPK and PI3K affect how cancer starts in glial cells, brain cells that provide support and insulation for neurons. These mutations triggered tumor initiation and produced increasingly dense low-grade gliomas that quickly progressed to aggressive and often deadly glioblastoma (GBM). The other study, conducted in cell lines and mouse models, tested a combination of targeted drugs as a potential therapy against glioblastoma by inhibiting the MAPK and PI3K cellular pathways. While the treatments overcame resistance in cells grown in the laboratory, they did not reach high enough concentrations to be effective when tumors were in the brain. One of the fundamental challenges in treating brain cancer with drugs is overcoming the blood-brain barrier, a membrane that separates circulating blood from the fluid in the central nervous system. This barrier works to protect the brain from toxins; however, this security system is so effective at protecting the brain that it prevents many life-saving drugs from reaching the cancer. The studies were published in the journal Neuro-Oncology.


May 2, 2017

Election to the National Academy of Sciences is one of the highest honors that can be earned by a U.S. scientist.  In recognition of their distinguished and continuing achievements in biomedical research, members of the Damon Runyon community of scientists were inducted this month:  


Ardem Patapoutian, PhD (Damon Runyon Scholar ’03-‘05, Fellow ’96-‘99), Scripps Research Institute, La Jolla


Guillermina Lozano, PhD (Former Fellowship Award Committee Member), M.D. Anderson Cancer Center, Houston


April 13, 2017

Feng Zhang, PhD (Damon Runyon-Rachleff Innovator ’12-’14) and colleagues at the Broad Institute, Cambridge, have developed a new CRISPR-based genetic diagnostic tool that may make it faster, less expensive, and easier to diagnose acute and chronic diseases like Zika, Ebola, cancer, and other hereditary disorders. The new tool dubbed SHERLOCK (Specific High-sensitivity Enzymatic Reporter unLOCKing) can detect extremely low concentrations of Zika virus and cancer DNA in blood, urine, and saliva samples. Previous CRISPR systems target DNA, but this system targets and degrades RNA. While scientists have recognized the potential for such a diagnostic tool, this is the first time it is possible to use the system widely to detect small amounts of RNA that could indicate the onset of cancer or other disease. The study was published in the journal Science.


April 10, 2017

Jedd D. Wolchok, MD, PhD (Damon Runyon-Lilly Clinical Investigator ‘03-‘08) at Memorial Sloan Kettering Cancer Center, New York, and colleagues, reported that matching the size of a tumor to the body's immune response could help doctors tailor immunotherapy treatments for melanoma patients whose disease has spread. Immunotherapy activates tumor-fighting T cells to target cancer, but these immune cells can lose their effectiveness or become “exhausted.” The study identified three different ways by which PD-1 blocking immunotherapies can fail: the drug doesn't re-invigorate exhausted T-cells, an immune response is not strong enough for the size of the tumor, and the drug is off target. Using these factors, the researchers developed a scoring system to more accurately predict how likely it is a treatment will work. The study was published in the scientific journal Nature.


March 29, 2017

David M. Livingston, MD (Damon Runyon Board Member), of Dana-Farber Cancer Institute, Boston, has been named the 20th recipient of the Pezcoller Foundation-AACR International Award for Cancer Research. Dr. Livingston is honored for his fundamental contributions to the field of basic cancer research. His work has been pivotal to the understanding of retinoblastoma pathway of cell cycle control as well as the transcriptional co-activation function of the key regulatory proteins, p300 and CBP. He is also credited with the landmark discovery of the central functions of the tumor suppressors, BRCA1 and BRCA2, which has revolutionized the fields of breast and ovarian cancer research. He will deliver his award lecture at the AACR Annual Meeting this April in Washington, DC.


March 24, 2017

At the junction of growth and starvation stands a signaling protein called mechanistic Target of Rapamycin Complex 1 (mTORC1). Inside the cell, mTORC1 regulates metabolism, growth, protein and organelle recycling (autophagy), proliferation, and survival. When something goes wrong in the pathway, various diseases such as cancer, obesity, and type 2 diabetes, can develop. An outstanding challenge is to understand how mTORC1 becomes activated in response to a wide variety of stimuli including nutrients, growth factors, and stressors, in normal and cancer states. Roberto Zoncu, PhD (Damon Runyon-Rachleff Innovator ’16-’17), and colleagues at the University of California, Berkeley, recently identified a lipid, cholesterol, as a novel nutrient input to mTORC1. They found that when cholesterol levels in organelles known as lysosomes are high, mTORC1 activity is switched on to initiate growth signals. Lysosomes are membrane-bound compartments where waste products are broken down and recycled. Lysosomes also serve as decision-making centers, where mTORC1 is switched on or off and therefore can dictate whether cells should grow or not. The way cholesterol, an essential building block for cellular growth and proliferation, activates mTORC1 appears to be highly specific and requires dedicated cholesterol-sensing proteins that reside at the lysosome. The study was published in the prestigious journal Science.


“This work advances our understanding of how mTORC1 integrates its many inputs, and could point the way to novel therapeutic avenues in cancer, particularly pancreatic cancers, where lysosome function and potentially mTORC1 activity are intimately associated with cancer growth,” says Zoncu.


March 14, 2017

Anjana Rao, PhD (Damon Runyon Fellow ’79), and James Scott-Browne, PhD (Damon Runyon Fellow ’11-’13), at the La Jolla Institute for Allergy and Immunology, La Jolla, and colleagues, are focusing on a key issue of how tumor-fighting T cells can lose their effectiveness or become “exhausted.”  The researchers identified two proteins, NFAT and Nr4a, that can bind to the DNA of T cells and shut down their tumor-fighting activity.  Next steps will be to determine if these processes can be interfered with or reversed in order to re-motivate immune cells to eradicate a patient's tumor.  These results were published in the journal Proceedings of the National Academy of Science.


February 27, 2017

Don X. Nguyen, PhD (Damon Runyon Fellow ’05-’08), of Yale Cancer Center, New Haven, and colleagues, reported new findings that explain the propensity of latent lung adenocarcinoma (LUAD) to relapse. They showed that differential expression of extracellular matrix (ECM) molecules and their interacting proteins contributes to risk of relapse in distinct LUAD subtypes. One protein called hyaluronan receptor HMMR, when overexpressed, was associated with inflammation and poor prognosis. Blocking HMMR in LUAD cells lowered their ability to initiate lung tumors and distant metastases such as in the brain. This study reveals an important mechanism by which disseminated cancer cells can coopt the inflammatory ECM to persist, leading to brain metastases. The results were published in the journal Cancer Research.


February 23, 2017

Christine Iok In Chio, PhD (Damon Runyon Shirley Stein Fellow ’13-’17), in the laboratory of her sponsor David Tuveson, MD, PhD, and colleagues at Cold Spring Harbor Laboratory, Cold Spring Harbor, created a new 3D model of pancreatic cancer, which allowed them to identify two distinct stroma cell populations called cancer-associated fibroblasts  (CAF’s), that work together with cancer cells to protect and help the tumor grow. One reason pancreatic cancer is difficult to treat is the dense stromal tissue that envelops tumors and acts as a physical barrier that blocks drug delivery. Since CAFs secrete extracellular matrix, which surround the cancer cells and shape the stroma, CAFs are attractive targets for drug development of targeted therapies for pancreatic cancer. The findings were published in the Journal of Experimental Medicine.


January 25, 2017

Gregory L. Beatty, MD, PhD (Damon Runyon-Nadia’s Gift Foundation Innovator ’12-’15) and colleagues at the Abramson Cancer Center at University of Pennsylvania, Philadelphia, reported high levels of inflammatory compounds in mice with pancreatic tumors. These included CCL2, a signaling molecule that promotes recruitment of inflammatory white blood cells by tumors. This likely contributes to the protective tumor microenvironment that makes most pancreatic tumors resistant to treatment. CCL2 levels increased further after the mice received radiotherapy. However, treatment with chemo and a CCL2-blocking antibody resulted in dramatically slower tumor growth and reduced recruitment of inflammatory cell types. These treated mice survived roughly 25% longer than those that received radiation alone. The results were published in the journal Clinical Cancer Research.


January 24, 2017

Theodora S. Ross, MD, PhD (Damon Runyon Scholar ’01-’03), and colleagues at UT Southwestern, Dallas, reported that the BRCA1 gene is required for the survival of blood forming stem cells. This could explain why patients with BRCA1 mutations do not have an elevated risk for leukemia; the stem cells die before they have an opportunity to transform into a blood cancer. These results also suggest that these patients may be at higher risk for the serious side effects of chemotherapy. The study was published in Cell Reports.


January 23, 2017

Elaine V. Fuchs, PhD (Damon Runyon Board Member, Damon Runyon Fellow ‘77-‘79) of The Rockefeller University, New York, has been named the recipient of the 2017 McEwen Award for Innovation. The prize, given by the International Society for Stem Cell Research, recognizes groundbreaking work pertaining to stem cells or regenerative medicine. Dr. Fuchs studies adult skin stem cells, how they make and repair tissues, and how cancers develop.


January 23, 2017

Akinyemi I. Ojesina, MBBS, PhD (Damon Runyon Fellow ’08-’11), of University of Alabama at Birmingham, worked with The Cancer Genome Atlas Research Network to identify novel genomic and molecular characteristics of cervical cancer that will aid in the subclassification of the disease and may help define personalized therapies for each individual patient. The new study conducted a comprehensive analysis of the genomes of 178 primary cervical cancers, and found that more than 70 percent of the tumors had genomic alterations in either one or both of two important cell signaling pathways (PI3K/MAPK and TGF-beta). The researchers also found that a subset of tumors did not show evidence of human papillomavirus infection. Certain cervical cancers contained mutations in genes that normally put ‘brakes’ on the immune system, suggesting treatment with immunotherapy “checkpoint inhibitors” may be effective against these cancers. The report was published in the scientific journal Nature.


January 23, 2017

Pardis C. Sabeti, MD, DPhil (Damon Runyon Fellow ‘04-‘06) of Harvard University, Cambridge, will receive the 2017 Richard Lounsbery Award from the National Academy of Sciences. She is recognized for her groundbreaking contributions including the development of new methods to study evolutionary selection in humans and viruses; the creation of new collaborative models for combatting emerging diseases across disciplinary and national borders; and leadership of global efforts to increase data sharing in pandemics such as Ebola and Lassa Fever. She published landmark genomic studies describing Ebola virus transmission during the 2014 outbreak.


January 13, 2017

Elaine V. Fuchs, PhD (Damon Runyon Board Member, Damon Runyon Fellow ‘77-‘79) and Shruti Naik, PhD (Damon Runyon Fellow ’14-’18) at The Rockefeller University, New York, and colleagues, found that skin squamous cell carcinomas alter the protein-making machinery to preferentially use tumor-related mRNAs, leading to the production of proteins important for cancer progression. This switch is linked to a ribosome initiation factor called eIF2 and transition initiation factor eIF2A. The results suggest that these could represent new targets for anticancer drug development.  The study was published in the scientific journal Nature.


January 12, 2017

Trudy G. Oliver, PhD (Damon Runyon-Rachleff Innovator ’13-’15), and colleagues at the Huntsman Cancer Institute at the University of Utah, Salt Lake City, reported the generation of a new mouse model for studying small cell lung cancer (SCLC). They demonstrated that Myc oncogene expression cooperates with Rb1 and Trp53 loss in the mouse lung to promote aggressive, highly metastatic tumors that are initially sensitive to chemotherapy followed by relapse. Targeted drug screening found that SCLC with high MYC expression is vulnerable to Aurora kinase inhibition, which, combined with chemotherapy, strongly suppresses tumor progression and increases survival. This study identified molecular features for patient stratification and uncovers a potential targeted treatment approach for these specific cancers.  The study was published in Cancer Cell.


January 5, 2017

Feng Zhang, PhD (Damon Runyon-Rachleff Innovator ‘12-‘14) of the Broad Institute, Cambridge, and colleagues, reported the discovery of new types of RNA-targeting CRISPR systems, which utilize a novel Cas enzyme called Cas13b. Cas13b is capable of targeting and degrading RNA (rather than DNA, which is targeted by previous CRISPR systems), which will enable researchers to specifically manipulate RNA in a high-throughput manner and manipulate gene function more broadly. The characterization of Cas13b has the potential to create a suite of RNA manipulation tools for studying a wide-range of biological processes that could be important for understanding and treatment of cancer and other diseases. The findings were reported in the scientific journal Molecular Cell.


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