Read e-book online Adult Acute Lymphocytic Leukemia: Biology and Treatment PDF

By Charles A. Schiffer (auth.), Anjali S. Advani, Hillard M. Lazarus (eds.)

The present explosion of latest parts of controversy within the remedy of acute lymphocytic leukemia in adults and teenagers makes this complete publication a far wanted reference for hematologists and oncologists. This booklet assembles major professionals from worldwide to hide the total spectrum of ALL subtypes and their remedies. particular themes of debate contain symptoms for allogeneic bone marrow transplant in first whole remission, the function of minimum residual sickness in making remedy judgements, the therapy of teenagers, and the remedy of Philadelphia chromosome confident ALL with the arrival of the tyrosine kinase inhibitors. this is often the 1st e-book to concentration completely at the grownup ALL sufferer. It presents an entire evaluate of prognosis, molecular pathogenesis, assessment, and remedy for this crucial sufferer population.

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BCR-ABL activates SRC kinases in a kinase-independent manner, and the inhibition of BCR-ABL by imatinib does not decrease SRC activation [51]. At the same time, the specific inhibition of SRC kinases (without inhibition of BCR-ABL), induces apoptosis in leukemia cells and extends survival in mice with Ph+ ALL, suggesting a role for both SRC kinases and BCR-ABL in the transformation of lymphoid cells [51]. CML progression to lymphoid blast crisis may also be dependent on the activation of SRC kinases [51], as lymphoid blast crisis cells are dependent on LYN for survival (in a higher extent than myeloid blasts), [52].

The CDKIs p16INK4a/p14ARF and p15INK4b are located on chromosome 9p21, and this region is frequently deleted in both B and T-ALLs. ” The tumor suppressor genes RB1 and p53 are frequently altered in adult ALL, with RB1 deletions found in more than 50% of patients with newly diagnosed ALL, and p53 mutations occurring in 10–20% of cases [79]. In a study of patients with deletions of the above CDKI and tumor suppressor genes, 85% of cases had a lesion in one of the genes, and 33% had lesions in at least two of the genes [80].

1998). Clinical significance of cytogenetic abnormalities in adult acute lymphoblastic leukemia. Blood, 91(11), 3995–4019. 48. , et al. (2008). Impact of cytogenetics on the outcome of adult acute lymphoblastic leukemia: Results of Southwest Oncology Group 9400 study. Blood, 111(5), 2563–2572. 49. Moorman, A. , et al. (2007). Karyotype is an independent prognostic factor in adult acute lymphoblastic leukemia (ALL): Analysis of cytogenetic data from patients treated on the Medical Research Council (MRC) UKALLXII/Eastern Cooperative Oncology Group (ECOG) 2993 trial.

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