Professor Charles Sawyer explains that CML stands for chronic myeloid leukemia, which is a blood cancer and it is different from many cancers because it starts very slowly and patients when they're first diagnosed don't have many symptoms.

Charles Sawyer, M.D. is professor of medicine and director of the Prostate Cancer Program Area at U.C.L.A. Johnsson Comprehensive Cancer Center, and an investigator of the Howard Hughes Medical Institute. He works on therapies that target specific mutations in prostate cancer and chronic myeloid leukemia (CML). Here he describes his work developing a targeted therapy for CML patients with resistance to the anti-cancer drug Gleevec. “CML stands for chronic myeloid leukemia, which is a blood cancer. It is different from many cancers because it starts very slowly and patients when they're first diagnosed don't have many symptoms. They just have a high white blood cell count that is detected by their physician when they get a routine check up. The incidence of CML is about 5,000 new cases a year in the U.S., another 5,000 in Europe, so, 10,000 patients a year. Patients tend to have CML for five or six years and then, and it's easily controlled with oral chemotherapy drugs until it turns into an aggressive very acute leukemia called blast crisis. And then it becomes a fatal illness. CML is caused by a chromosome translocation known as the Philadelphia chromosome, which occurs in a stem cell in the bone marrow. Presumably a single cell develops that and over a period of years that cell gets a growth advantage and eventually results in a leukemia. The translocation involves two genes. The main gene is a tyrosine kinase called Abl. And the fusion of BCR from one chromosome to Abl on the other creates a kinase that's constantly on. And that enzyme causes this entire disease. We know that by putting this enzyme into a mouse model. You get essential CML in a mouse.”

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