The SWCRF Institute Without Walls™ is a network that connects more than 50 research laboratories directed by the brightest scientific minds who are collaborating throughout North America, Asia, and Europe. By working together to share their expertise along with their most recent findings, our investigators accelerate the pace toward research breakthroughs.

Since its founding in 1976, the SWCRF has mandated that investigators who receive our funding, collaborate with other investigators, often at outside research laboratories. Also, we seek to connect investigators from varying disciplines - for example, an immunologist with a geneticist - who exchange ideas and results to uncover new breakthroughs.
 

For a listing of the public and private organizations currently part of our Institute Without Wall, please visit: https://www.waxmancancer.org/our-research/partners-collaborations/ 

HIGHLIGHTS OF THE PROGRAM TO DATE

William S. Gorin Memorial Research Program for Pancreatic Cancer

Established in 2017 in memory of the inspirational business leader who died from pancreatic cancer, the SWCRF Institute Without Walls™ funded research that paired a leading investigator in immunotherapy with an equally esteemed expert in genetics.

SWCRF-funded investigator Nabeel Bardeesy, Ph.D., Associate Professor of Medicine at Harvard Medical School, and Assistant Geneticist at the Center for Cancer Research, is leading an innovative approach to pancreatic cancer, a difficult cancer to detect early.

 
Dr. Bardeesy’s work focuses on how gene alterations can affect the way that cancer cells react to particular treatments. His first grant from SWCRF was awarded in 2006 to study the role of SMAD4, a protein, in pancreatic function.
 
Mrs. Jody Gorin, the widow of Mr. Gorin, is leading efforts to raise additional support for the Program and in 2018, was appointed as a member of the SWCRF board of directors. Dr. Bardeesy sees the SWCRF Institute Without Walls™ as a way to identify new answers at a faster pace. “Most pancreatic cancers don’t respond to immunotherapy,” Dr. Bardeesy said. 

UNCOVERING PROTEINS THAT COULD MAKE GLIOBLASTOMA VULNERABLE TO THERAPY

William Weiss, M.D., Ph.D. and Kevan Shokat, Ph.D. at the Helen Diller Family Comprehensive Cancer Center at the University of California, San Francisco received funding from the SWCRF Institute Without Walls™ to study glioblastoma, the most common primary brain tumor that is currently incurable.

The SWCRF funding paired Dr. Weiss who specializes in pediatric neurology with Dr. Shokat who is a cellular and molecular pharmacologist to identify cell proteins that could be targeted by therapeutic intervention. Glioblastoma tumor cells are particularly aggressive and often grow and spread rapidly while resisting most current forms of treatments.

The research performed by Drs. Weiss and Shokat found how cancer cell proteins respond to other genetic factors to facilitate growth and tested various pharmaceutical interventions. The results of their work has led to at least one clinical trial with others expected in the coming months.

STUDYING DORMANCY IN DISSEMINATED TUMOR CELLS

Julio Aguirre-Ghiso, Ph.D. specializing in cancer biology and Dr. Emily Bernstein, Ph.D. who is a trained geneticist, collaborated on a project at the Icahn School of Medicine at Mount Sinai funded by the SWCRF Institute Without Walls™. They explored one way to prevent cancer metastasis by targeting the biology of dormant tumor cells that disperse in areas of the body outside of the original tumor site.
Their SWCRF-funded project discovered in models of head and neck, breast and prostate cancer, that restoration of vitamin A signaling could activate tumor cell dormancy. Drs. Aguirre-Ghiso and Bernstein identified the target genes that vitamin A regulates and how specific regulatory mechanisms of gene production is used to turn on mechanisms of dormancy.
They found that: 1) the dormancy program can be activated by host signals, that it is long-lived and detectable in dormant tumor cells in patients and that it overlaps with aging or senescence gene programs; 2) specific analogs of the vitamin A signaling in combination with epigenetic drugs (5-Aza-C) in the clinic “reprogram” tumor cells to enter stable dormancy, and 3) autophagy, an energy production mechanism that promotes cell survival might be responsible for the induction of dormancy. The collaborators hypothesized that understanding these mechanisms allowed the induction of residual cancer cell dormancy as well as eradicating dormant cancer cells via the activation of cell death. This approach used in the adjuvant setting may have a significant impact in preventing relapse after first-line therapies.