Guest guest Posted April 22, 2009 Report Share Posted April 22, 2009 Based on surprising results from animal experiments, researchers at The University of Texas M. D. Cancer Center have revamped common beliefs about how chronic myeloid leukemia (CML) functions within bone marrow - a discovery they hope may some day lead to additional therapeutic strategies. In the least, the research demonstrates that CML is much craftier than had been suspected, he says. Before this study, no one knew that the 24p3 mouse protein (known in humans as neutrophil gelatinase-associated lipocalin, or NGAL) had any involvement in leukemia, Arlinghaus says. The protein is a normal component of cells and is believed to have a variety of functions. But the " BCR-ABL oncoprotein (encoded by the Philadelphia chromosome, a translocation of genetic material responsible for most CML) appears to hijack 24p3 and change it structurally to become a cell killer, " he says. http://www.medicalnewstoday.com/articles/23107.php __________________________________________ Scientists at the s Cancer Center at the University of California, San Diego, Stanford University School of Medicine and other centers have identified a mechanism by which a chronic form of leukemia can progress into a deadlier stage of the disease. The findings may provide physicians with an indicator of when this type of cancer - chronic myeloid leukemia (CML) - is progressing, enabling them to make more accurate prognoses for the disease and improved treatment choices. " If we can predict when a patient is moving from the chronic phase in CML to the blast crisis stage, then we can hopefully intervene before it's too late, " said Catriona H.M. son, MD, PhD, assistant professor of medicine at the UC San Diego School of Medicine and Director for Stem Cell Research at the s UCSD Cancer Center. http://www.medicalnewstoday.com/articles/139323.php __________________________________ These data demonstrate, for the first time, that the Bcr-Abl inhibitory profile of AP24534 allows it to evade resistance driven by all known Bcr-Abl mutations, " said Clackson, Ph.D., senior vice president and chief scientific officer of ARIAD. " This study highlights the potential of AP24534 to overcome clinically relevant resistance to available targeted therapies in CML. " ARIAD is conducting a Phase 1 clinical trial of AP24534 in patients with refractory CML, acute myeloid leukemia (AML) and other hematological malignancies. http://clinicaltrials.gov/ct2/show/NCT00660920?term=AP24534 & rank=1 FYI, Lottie Quote Link to comment Share on other sites More sharing options...
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