Stimulation of platelet G protein-coupled receptors results in the cleavage of phosphatidylinositol 4,5-trisphosphate (PIP(2)) into inositol 1,4,5-trisphosphate and 1,2-diacylglycerol by phospholipase C (PLCbeta). It also results in the phosphorylation of PIP2 by the gamma isoform of phosphatidylinositol 3-kinase (PI3Kgamma) to synthesize phosphatidylinositol 3,4,5-trisphosphate. To understand the role of PIP2 in platelet signaling, we evaluated knock-out mice lacking 2 isoforms of PLCbeta (PLCbeta2 and PLCbeta3) or lacking the G(betagamma)-activated isoform of PI3K (PI3Kgamma).
View Article and Find Full Text PDFFor years women have been fighting for equity in the academic work place, but this acceptance comes at a price. Balancing work and family obligations have proven to be an awkward task where maximal satisfaction and gratification in both are not easily attained. Junior-level faculty have the arduous charge of being most productive and prolific exactly during their child-raising years.
View Article and Find Full Text PDFTreatment options are limited for patients with relapsed acute myelogenous leukemia (AML), particularly when the disease is refractory to standard cytotoxic chemotherapy. Targeted drug therapy offers the advantage of delivering higher doses of non-cross resistant chemotherapy with potentially less systemic toxicity. Gemtuzumab ozogamicin (Mylotarg, Wyeth-Ayerst Laboratories) is an immunoconjugate that consists of humanized anti-CD 33 antibody linked to the potent anti-tumor antibiotic calicheamicin and has been an effective therapy for some patients with relapsed AML.
View Article and Find Full Text PDFOral Surg Oral Med Oral Pathol Oral Radiol Endod
March 2002
Acute myelogenous leukemia (AML) describes a group of related hematologic malignancies that are being approached therapeutically from several perspectives. Conventional chemotherapeutic agents, such as anthracyclines and cytosine arabinoside (Ara-C), are useful in treating AML but now appear to have reached their maximum potential. Newer therapeutic approaches to AML have recently focused on immune-based therapy through monoclonal antibodies that target and destroy malignant cells via specific cell receptors.
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