Diagnosis, Targeted therapies: Targeting activators, Sawyer 1
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. �€œCML 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.�€�
chronic myeloid leukemia, cancer drug gleevec, prostate cancer program, hughes medical institute, howard hughes medical institute, cml patients, philadelphia chromosome, chemotherapy drugs, charles sawyer, acute leukemia, blood cell count, white blood cell, blood cancer, tyrosine kinase, high white blood cell count, blast crisis
- ID: 1013
- Source: DNALC.IC
In this section learn that tyrosine kinases are a family of activator proteins that trigger the cell signaling process leading to cell growth and division.
Conventional cancer drugs are cellular poisons that block replication or some other aspect of cell growth. These drugs affect all cells – healthy or cancerous.
Professor Charles Sawyer explains that Gleevec is a pill taken once a day and works remarkably well in all phases of CML.
Professor Charles Sawyer explains that the CML clone makes mistakes in DNA replication and generates a diverse repertoire of mutations.
Professor Charles Sawyer explains that EGF receptor happens to be the driver in at least 10% of lung cancer patients in the U.S.
CML causes an increased production of white blood cells. Bud and Yvonne talk about the breakthrough that brought Bud's white blood cell count back to normal.
15525. How Gleevec works to alleviate symptoms of myeloid leukemia, 3D animation with basic narration
View the animation to find out how the drug Gleevecâ¢ inhibits the molecular cause of chronic myeloid leukemia.
Yvonne talks about the magic pills Bud took.
Professor Vogelstein explains that the only difference between a benign tumor and a malignant tumor is not the size, it's the ability of the malignant tumor to invade, and get through the tissues.
Brian Druker talks about how the drug he designed targets the molecular cause of CML.