By Charles A. Schiffer (auth.), Anjali S. Advani, Hillard M. Lazarus (eds.)
The present explosion of recent components of controversy within the therapy of acute lymphocytic leukemia in adults and teenagers makes this complete ebook a miles wanted reference for hematologists and oncologists. This e-book assembles prime experts from worldwide to hide the total spectrum of ALL subtypes and their remedies. particular themes of debate comprise symptoms for allogeneic bone marrow transplant in first entire remission, the function of minimum residual ailment in making therapy judgements, the therapy of teenagers, and the therapy of Philadelphia chromosome confident ALL with the appearance of the tyrosine kinase inhibitors. this can be the 1st e-book to concentration solely at the grownup ALL sufferer. It presents an entire review of prognosis, molecular pathogenesis, evaluate, and therapy for this crucial sufferer population.
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Additional info for Adult Acute Lymphocytic Leukemia: Biology and Treatment
Besides its high prevalence in infant leukemia, it often arises in the setting of a secondary leukemia following chemotherapy (specifically following treatment with topoisomerase II inhibitors). P. Radich and O. Sala MLL gene from chromosome 11q23 to any of approximately 50 partner genes. Conceptually, and in murine models, leukemia may evolve from a gain of function, depending on the partner gene involved, or a disruption of normal MLL function. The most common translocation is the t(4;11), which fuses MLL to AF4.
Additionally, in the chimeric protein BCR-ABL1, ABL1 is capable to associate to a broader protein spectrum than wild type ABL1 through BCR protein–protein domains. 1). The activation of phosphoinositide-3 kinase (PI3K) is required for the malignant transformation by BCR-ABL . AKT is the main downstream target for PI3K, and its activation results in survival advantage through the inhibition of proapoptotic molecules BIM, TRAIL, and BAD. BCR-ABL expression also leads to constitutive activation of RAS, through adapter proteins.
British Journal Haematology, 120(1), 74–79. 87. Vidriales, M. , & San-Miguel, J. F. (2003). Immunologic monitoring in adults with acute lymphoblastic leukemia. Current Oncology Reports, 5(5), 413–418. 88. , et al. (1997). A prospective study of minimal residual disease in childhood B-lineage acute lymphoblastic leukaemia: MRD level at the end of induction is a strong predictive factor of relapse. British Journal Haematology, 98(1), 140–146. 89. van Dongen, J. , et al. (1998). Prognostic value of minimal residual disease in acute lymphoblastic leukaemia in childhood.