Friday, July 14, 2006

July 14th - Info on my special kind of AML

I have AML FLT3. Below is some info regarding FLT3 and a clinical trial that is ongoing with a new drug CEP-701. I was on CEP-701 for about 10 days, but then I became ill and had to stop the protocol. CEP-701 is something that I can use again in the future if I am unable to have the Graft versus Host Disease.

http://www.hopkinskimmelcancercenter.org/news/archive_details.cfm?documentid=256


What are the basic facts about acute myeloid leukemia?

Acute myeloid leukemia is the most common form of adult leukemia and the second most common childhood leukemia accounting for more than 10,000 cases annually in the U.S. In this type of cancer, the myeloid cells of the blood and bone marrow grow uncontrollably, crowding out and destroying normal blood cells. Standard therapies include chemotherapy and bone marrow transplantation, which replaces the diseased bone marrow with healthy marrow. Overall, AML can be cured in up to 50 percent of patients without FLT3 mutations, but FLT3 mutant AML patients have a much lower cure rate.

What are FLT3 mutations?

FLT3 gene mutations are an alteration in the DNA of certain leukemia cells. They occur in up to 40 percent of acute myeloid leukemia cases. These mutations cause the cancer to grow more aggressively and to be less amenable to cure. Researchers at the Hopkins Kimmel Cancer Center have developed a type of drug, called a tyrosine kinase inhibitor, that blocks the activity of the mutated protein. This inhibitor drug, called CEP-701, was tested on AML cells in the laboratory and in mice and found to be effective in killing FLT3-mutant AML.

What is a tyrosine kinase inhibitor?

Tyrosine kinase inhibitors are a new class of drug that have the ability to block gene signaling proteins. Mutated FLT3 genes use their tyrosine kinase portion to signal leukemia cells to grow and also to prevent them from dying. These drugs block the mutated gene’s signal and, therefore, its ability to communicate with cells. Think of someone speaking to you and requesting you to perform a function. If you were able to hear the command, you would respond. But, if you had cotton placed in your ears, it would block your ability to hear the command, and you would not respond. CEP-701 works in a similar manner with FLT3 gene signaling. The drug stops the leukemia cell from “hearing” the mutated FLT3 gene’s command to grow and spread.

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