Celeryroot, I don't know the dates of this week's Cowen conference. But I came across a blurb in today's Bio Century, which is the acknowledged weekly journal of the biotech industry. In a section called, "Other Clinical News", on page B11, there appeared the following, which was submitted by Memorial Sloan Kettering Cancer Center {generally ranked the best such in the U.S.} New York, N.Y., et al, {Latin for "and others"} ;
"Product: Mice lacking gene for the PMC protein implicated in acute promelocytic leukemia.
Use: Determine role of PML in APL
Research published in Science used a mouse deficient in the PML protein to show that the protein regulates the creation of new blood cells, and allows retinoic acid to slow cell proliferation. APL is often associated with a chromosome change in which the gene for the receptor for retinoic acid fuses with the PML gene. Disruption of the retinoic acid signal is thus probably responsible for the leukemia, the researchers concluded. PML may serve as a tumor suppressor."
It seems to me, that since we are involved inrecruiting patients for a P3 trial in Europe, this finding should help us generate good results from the trial. If it is true that PML allows retinoic acid to slow cell proliferation, and unregulated cell proliferation contibutes to most cancers, the knowledge of PML's role in allowing retinoic acid to slow the proliferation of cancerous cells can only help us against cancer. Now that we know the fusion of the receptor for retinoic acid with the PML gene is probably responsible for the disruption of the retinoic acid signal, we can look to block that fusion. FInally, if it is true that PML is responsible for the regulation of the creation of new blood cells and that PML may serve as a tumor suppressor, hopefully, we haved learned how to regulate the production of PML. Bernie |
