BIDMC Cancer Symposium
Mark Your Calendar for 2017 Symposium
The 10th Annual BIDMC Cancer Symposium will be held Wednesday, November 8, 2017, at the Joseph B. Martin Center at Harvard Medical School. Watch this space for additional details.
9th Annual Event Breaks All Attendance Records
Breaking all previous attendance records, the BIDMC Cancer Center’s Ninth Annual Cancer Symposium brought 500 attendees to the Joseph B. Martin Center at Harvard Medical School on November 2, 2016. Featuring 10 presentations by various leaders in the field, the daylong program, titled “Pathways to Cure,” focused on some of the newest frontiers in cancer research, including immunotherapy and cancer genomics.
“This symposium has become a fantastic forum to discuss new advances – trail-blazing advances – with a specific and particular attention on translating these advances into therapy, but importantly, into cures,” said Cancer Center Director Pier Paolo Pandolfi, MD, PhD. “We use the word ‘cure’ on purpose because we want to cure cancer and not simply treat cancer.”
David McDermott, MD, Director of the Biologic Therapy and Cutaneous Oncology programs at BIDMC’s Cancer Center, gave an historical overview of cancer immunotherapy research. BIDMC researchers James W. Mier, MD, and Michael B. Atkins, now of Georgetown University, contributed to one of the earliest cancer immunotherapy drugs, approved by the FDA in 1992. But while it produces a durable remission for a certain subset of patients, said McDermott, it is “a very toxic drug that doesn’t work for most people.”
New Immunotherapies More Tolerable
Since then, researchers have developed immunotherapies that are much more tolerable and apply to a number of different kinds of tumors, including kidney, lung, melanoma, bladder and ovarian cancers, McDermott said.
“Over the last ten to 15 years, we’ve gotten a much better understanding about the different, complex and sometimes overlapping ways in which tumors can evade and suppress the immune system,” said McDermott, who is also leader of the Dana-Farber/Harvard Cancer Center Kidney Center Cancer Program and an Associate Professor of Medicine at Harvard Medical School.
While the new treatment approach is incredibly promising, one puzzle dating back to the 1990s persists.
“Most patients don’t respond,” McDermott said. “Some do, but it’s a subset. How can we identify those patients? At BIDMC, we’re trying to focus on improving outcomes by improving patient selection.”
The C-Word Applies
“I’m going to use the word ‘cure’ unabashedly here,” said James Allison, PhD, Executive Director of the Immunotherapy Platform and Chair of the Department of Immunology at MD Anderson Cancer Center at the University of Texas. He followed McDermott’s talk by describing the mechanisms and data supporting the many new immunotherapy treatments hitting the market in recent years.
“These drugs are being approved at almost an exponential rate,” Allison said. “We got here by understanding the fundamentals of the immune system, and we did that through basic science, something that is being lost in the trend toward translational science. Translational science is important, but there won’t be anything to translate if we don’t do basic science.”
The day’s second session began with Edison T. Liu, MD, President and CEO of the Jackson Laboratory, and BIDMC’s Ralph Scully, PhD. The team talked about their collaboration uncovering the mechanisms that contribute to triple negative breast cancer. A translational scientist, Liu focuses on the functional genomics of human caners. Scully studies the basic science of BRCA1 and BRCA 2 breast cancer genes.
“We ended up coming to the same conclusions, telling the same story, but from fundamentally opposite positions,” Scully said.
Most Common Genetic Error
A pioneer in her field, Columbia University’s Carol Prives, PhD, weighed in on the P53 tumor suppressor gene—the most frequent genetic error detected in cancer. Prives described how the gene regulates the metabolic pathway responsible for lipid synthesis. She has found that the mutant form of p53 stimulates the expression of the pathway, creating more aggressive tumors. By contrast, wild type (or normal) p53 dampens this pathway. Many drugs – such as the statins developed to treat high cholesterol – already target this pathway, Prives said, and may be used to target this cancer-causing pathway.
In a talk that left the audience scrambling for the nearest glass of orange juice, Sean Morrision, PhD, of the University of Texas Southwestern Medical Center, presented his data that hematopoietic stem cells (the cells that continuously give rise to all other blood cells) soak up vast amounts of ascorbate acid, also known as vitamin C. What’s more, he said, the absence of vitamin C mimics a mutation to a leukemia suppressor gene that allows the disease progress unchecked. “This may explain the epidemiological data that people who eat more fruit get less cancer,” he said.
In the day’s last session, Celeste Simon, PhD, of the Perlman School of Medicine at the University of Pennsylvania discussed the relationship between hypoxia and tumor progression, and Howard Hughes Medical Institute investigator, George Q. Daley, MD, PhD, of Boston Children’s Hospital described the Stem Cell Pathways that drive cancer.
Other speakers also included Elaine Mardis, PhD, of Nationwide Children’s Hospital; Benjamin Ebert, MD, PhD, of Brigham and Women’s Hospital; and Irving Weissman, MD, of Stanford University.