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Acute Lymphoblastic Leukemia (ALL)

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Acute Lymphoblastic Leukemia (ALL)
Rudolf Virchow from Germany was the first to use the term leukaemia in 1847. Ehrlich had introduced staining methods, the classification into acute lymphoid leukaemia became possible in 1913, and in 1973 ALL was divided into origin from B or T-lymphocytes.Acute lymphoblastic leukemia (ALL) is a malignant neoplasm of hematopoietic stem cells, highly occurring among children with a proportion of 30% of all pediatric malignancies. The initial peak incidence of this hematologic malignancy is at 2 to 5 years of age, followed by a second peak over age 50. Acute lymphoblastic leukemia (ALL) is a condition where genetic alterations in a single lymphoblast are inherited in all the cell’s descendants. The genetic alterations lead to accumulation of these leukemic clone cells with uncontrolled proliferation, which causes dysfunction of the bone marrow leading to mono- or pancytopenia and ultimately, if not treated, death.
Multiple genetic hits to DNA are necessary to cause cancer and when cancer strikes in childhood it is probably due to only
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The ABCB1 gene is located on chromosome 7q21 and consists of 28 exons, encoding a 170-kDa membrane transport protein termed P-glycoprotein (P-gp). P-gp functions as an ATP-dependent efflux pump that transports exogenous and endogenous substrates from inside the cells to the extracellular space. Its normal expression has been identified in various human tissues, including intestinal epithelium, adrenal gland, placenta, kidney, liver, endothelial cells and testicular tissue, and P-gp naturally protects these organs against xenobiotics. P-gp substrates include adriamycin, daunorubicin, paclitaxel, vincristine, vinblastine, and imatinib. In cancer, P-gp was identified as a protein responsible for resistance to many

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