Oncologist Ross L. Levine had the opportunity in medical school to do laboratory research, which influenced his decision to chart a career as a physician-scientist. Now an assistant member in the Human Oncology and Pathogenesis Program and holder of a Geoffrey Beene Junior Faculty Chair, he analyzes the genetic makeup of cancer cells to identify disease pathways.
I was interested in science from a young age, growing up in the suburbs just north of New York City. I was accepted into a program at Columbia University for area high school students and spent Saturday mornings learning about biology, chemistry, math, and physics. When I entered Harvard in the early 1990s, I narrowed my focus to biology and gained exposure to clinical research, partly by shadowing physicians as they worked. This led to my decision to go to medical school.
I began medical school at The Johns Hopkins School of Medicine planning to become an academic clinical physician. One summer, to broaden my experience, I worked in the laboratory of pathologist Lora Hedrick-Ellenson, who was studying endometrial cancer. The research was fascinating, more interesting to me than any clinical experience. That brief stint in the lab caused me to consider someday becoming a physician-scientist.
Over the next four years I finished medical school and trained in internal medicine at Massachusetts General Hospital. In 2002, during my clinical fellowship in hematology/oncology at Dana-Farber Cancer Institute, I developed a specific interest in caring for patients with leukemia; however, I soon learned that most patients are not cured with existing treatments. This led me the following year to enter the laboratory of Gary Gilliland, a leader in leukemia genetics and a fantastic mentor. Our research focused on myeloproliferative neoplasms -- blood cancers -- the cause of which had eluded researchers. We hoped that by identifying the cause of these cancers we could develop better therapies.
Gary and I decided that in order to truly understand these diseases, we needed to discover the underlying genetic causes. We collected samples from patients and sequenced the DNA from their cancer cells, comparing the results to noncancerous cells from the same patients. We discovered that in two-thirds of the patients, the cancer cells had a single mutation in the gene for the signaling molecule JAK2. This suggested the JAK2 pathway was involved in several types of blood cancer.
By using patient samples as the starting point, we were able to establish evidence of what was driving these diseases. In addition to helping us understand the biological underpinnings, the finding provided targets for more-effective therapies. This experience strengthened my conviction that I wanted to work at the interface between basic research and clinical medicine.
