For Simon N. Powell, research and medicine have always been joint pursuits. Dr. Powell joined Memorial Sloan-Kettering in 2008 as Chair of the Department of Radiation Oncology with a joint appointment in Sloan-Kettering Institute's Molecular Biology Program. He has 18 years of experience leading basic and clinical research, first at Harvard Medical School and most recently at the Washington University School of Medicine.
Growing up in Manchester, England, I wanted to become a scientist like my brother, who now is a physicist, and my sister, who is a science teacher. Neither of our parents pursued an academic career -- very few people in England had that privilege before the Second World War.
I studied neuroscience at the University of Oxford and initially planned to pursue a PhD degree in that field. But at one point, it occurred to me that the science I was most interested in was closely connected to medicine, so I changed my mind and went to medical school instead, at the University of London.
Because of my interest in neuroscience, I initially thought I would become a neurologist. However, an elective studentship with Sir Michael Peckham, a professor of oncology at the Royal Marsden Hospital, changed my perspective. It was my first encounter with a physician who was so strongly committed to science. Inspired by his ability to combine clinical and basic research, I decided to follow in his footsteps and specialize in oncology.
Many years later, after completing my specialty training in internal medicine and oncology, plus receiving a PhD degree from the Institute for Cancer Research, in London, I gave a lecture at a teaching course for oncologists. Afterward, Herman Suit, who was the head of radiation oncology at Massachusetts General Hospital, came up to me and said, "That was a good talk. Do you want to come to Boston?" Until then, I had never considered leaving England. But I did, and never moved back.
Here in the United States, my clinical practice became more focused on radiation therapy, the principle of which is to kill cancer cells, or prevent them from dividing, by damaging their DNA. Ideally, the treatment is delivered in such a way that it damages as many cancer cells as possible while sparing the healthy tissue surrounding the tumor. My laboratory research is focused on the molecular mechanisms that underlie a cancer cell's vulnerability to DNA damage, and how these can be exploited therapeutically.
Normal cells protect their genome by repairing breaks in the DNA strands as they occur. If a cell's DNA repair functions are weakened, its genome will start to accrue alterations that may eventually lead to cancer. For example, people who inherit mutations in the genes BRCA1 or BRCA2, which are important for DNA repair, have an increased risk for developing breast or ovarian cancer. However, the same mutations can make radiation or chemotherapy more effective since they make tumors more susceptible to DNA damage.
