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It is a 3-in-1 reference booklet. It supplies an entire scientific dictionary overlaying thousands of phrases and expressions with regards to continual myelogenous leukemia. It additionally provides broad lists of bibliographic citations. ultimately, it presents info to clients on the best way to replace their wisdom utilizing numerous web assets. The booklet is designed for physicians, clinical scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to familiarize yourself with study devoted to continual myelogenous leukemia. in the event that your time is efficacious, this booklet is for you. First, you won't waste time looking out the web whereas lacking loads of appropriate info. moment, the ebook additionally saves you time indexing and defining entries. ultimately, you won't waste money and time printing thousands of web content.
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Additional resources for Chronic Myelogenous Leukemia - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Investigators at Emory are participating in the POG laboratory study of methotrexate metabolism by ALL cells (ALinC #16) and coordinate the study of alterations in p53 tumor-suppressor gene pathways in relapsed ALL (SIMAL #l0). Taken together, these activities of the Emory POG Program will continue to contribute to our knowledge of the biology, therapy, and prevention of neoplastic diseases in infancy, childhood and adolescence. ; Dana-Farber Cancer Institute 44 Binney St Boston, Ma 02115 Timing: Fiscal Year 2002; Project Start 30-SEP-1986; Project End 31-DEC-2002 Summary: The principal activity of this grant is to improve the care and treatment of children with cancer by participating in the Pediatric Oncology Group (POG).
Hence, in Specific Aim 1, they will use anchored PCR to clone the breakpoint. Their specific oligos will come from the known PDGFBR sequence. In Specific Aim 2, they will obtain a full length cDNA and determine the relevance of this by performing ribonuclease protection assays and mapping back to chromosome 7. Finally, for Specific Aim 3 they propose to characterize the fusion protein by determining its transforming, activity(s) and biological properties using mutational and biochemical analyses.
In Specific Aim 3, we will test the hypothesis that acute leukemia phenotypes are a collaboration between constitutively activated tyrosine kinases and transcription factor fusion genes such as AML1/ETO, AML1/EVI1 and NUP98/HOXA9. We hypothesize that coexpression of tyrosine kinase fusions and transcription factor fusions will cause an acute leukemia phenotype in murine models, and that these leukemias will retain sensitivity to specific tyrosine kinase inhibitors. This proposal will provide insights into signal transduction and target genes critical for transformation of hematopoietic cells, as well as novel therapies for leukemia.