The UCSF Helen Diller Family Comprehensive Cancer Center hosted an afternoon event on the Mission Bay campus on May 12 to showcase recent progress and current research directions in the fight against cancer.
Plenary session speakers included UCSF Chancellor Susan Desmond-Hellmann, MD, MPH, Frank McCormick, PhD
, director of the cancer center, and James Wells, PhD
, who heads the Small Molecule Discovery Center. All three came to UCSF after driving drug development projects in industry.
Breakout sessions followed. Each was focused on specific types of cancer. The showcase event on May 12 concluded with a reception and an update on the construction of UCSF Medical Center at Mission Bay from Mark Laret, chief executive officer of UCSF Medical Center.
All three plenary speakers noted recent progress in understanding and treating cancer. But they also spoke of ongoing challenges to research and patient care, including the need to know if treatment is likely to be effective for a particular patient, and the need to know early on whether the treatment given to a patient is working.Developing New Strategies
McCormick emphasized the central role UCSF researchers play in cancer research. He noted the strong UCSF participation last month at the annual meeting of the American Association of Cancer Research (AACR) -- the nation's most prominent professional organization for researchers who aim to better understand cancers -- and the potential vulnerabilities of tumors that might be exploited in developing new treatment strategies.
McCormick touched on clinical strategies that are being explored at UCSF, including combination treatment to overcome drug resistance; emerging therapies aimed at stimulating the immune system to attack tumors; and the use of small interfering RNA (siRNA) molecules as drugs to stop the activation of genes that tumors rely on.
Wells noted that most drugs used to fight cancers inhibit proteins needed by tumors. However, Wells' latest strategy is to try instead to activate a protein. The target for activation is called caspase 3. Caspase 3 triggers a biochemical chain reaction leading to cellular suicide. Normal cells usually activate this suicide program for the greater good when they become abnormal and cannot repair themselves. Tumor cells shut down this suicide program. Wells aims to turn it back on, and already he has had success treating cells on the lab bench.
Desmond-Hellmann spoke about the need to develop more powerful and faster ways to evaluate drugs in clinical trials. She also talked about success stories - powerful new treatments for cancer developed using knowledge gained from basic research.
The drug Gleevec was among the success stories Desmond-Hellmann mentioned. Academic researchers and patient advocates played a driving role in the development of the drug, which has greatly improved the survival prospects for patients diagnosed with the blood cancer called chronic myelogenous leukemia (CML). Prior to Gleevec, most patients with this disease died. Today, most survive, she said.
But Gleevec also provides researchers and physicians with a refresher on drug resistance, which McCormick earlier described as a continual challenge to the development of successful long-term cancer therapies. Within two years of treatment, Gleevec no longer holds cancer at bay in many patients.
Fortunately, research at UCSF and elsewhere is leading to drugs that may help oncologists keep one step ahead of CML and other cancers.Making Progress on Blood Disorders
Physician-scientists who lead UCSF efforts to better understand cancers that arise in different types of cells found in blood -- leukemias, lymphomas and myelomas - described ongoing research during one of the breakout sessions.Kevin Shannon, MD
, leader of the Hematopoietic Malignancies Program for the UCSF Helen Diller Family Comprehensive Cancer Center, introduced the session by explaining how blood cancers differ from solid tumors.
Read more at Jeffrey Norris, UCSF Science Cafe