Monday, April 19, 2010

Some notes on acute promyelocytic leukemia (APL)

In our last blog post (April 15, 2010), we discussed genetically engineered mouse cancer models, with emphasis on the work of Dr. Pier Paolo Pandolfi (Beth Israel-Deaconess Medical Center Cancer Center and the Dana-Farber/Harvard Cancer Center, Boston MA) and his colleagues. Part of that discussion was on Dr. Pandolfi’s earlier work on the construction of genetically engineered models of acute promyelocytic leukemia (APL), and the use of these models in designing therapies for that disease. As the result of these studies and the work of others, the major form of APL (in which leukemic cells express the fusion protein PML-RARĪ±) is now treated with a combination of all-trans retinoic acid (ATRA) and arsenic trioxide (As2O3). What once was an invariably fatal disease now has about a 90% survival rate.

For those of you who are interested in the mechanisms by which ATRA and As2O3 work in treatment of APL: the 9 April 2010 issue of Science has a Perspective and a research report that focus on the mechanistic basis for the action of As2O3. For the mechanistic basis of the action of ATRA in APL, you may read a November 2008 research report published in Nature Medicine.

As soon as I posted the blog article on Dr. Pandolfi’s work, I received my 9 April issue of Science with the articles on As2O3 in APL. So I am passing this information on to readers of this blog.

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