Acute Myelogenous Leukemia: Genetics, Biology and Therapy by Zeev Estrov (auth.), Lalitha Nagarajan (eds.)

By Zeev Estrov (auth.), Lalitha Nagarajan (eds.)

Acute myelogenous leukemia (AML), is the commonest kind of leukemia in adults. AML is a perilous kind of malignancy, the diagnosis for which has now not stronger within the final 20 years. extra importantly, it's a malignancy that's noticeable in older adults, for this reason the variety of situations is probably going to upward thrust because the inhabitants a long time.

Over the prior 15 years, genetic mechanisms underlying AML have all started to spread. extra study during this sector has helped determine key parts and features. hence, special treatment of AML is receiving a lot awareness. it's the wish of researchers that as with continual myelogenous leukemia (CML), and the drug, Gleevec, a exact treatment for AML can be discovered.

"The potent remedy of acute myelogenous leukemia is still a good problem. this article stories our knowing of the molecular and biologic foundation of the sickness. major investigators deal with advances in prognostication and healing options that experience major promise."

Steven T. Rosen, M.D.
Series Editor

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Extra info for Acute Myelogenous Leukemia: Genetics, Biology and Therapy

Sample text

High-dose azacitidine was toxic, however, and this approach was abandoned. In parallel, in vitro studies have shown that a lower dose of azacitidine induces cell differentiation and apoptosis by promoting the expression of genes that are silenced by hypermethylation [85]. Low-dose azacitidine has been applied to clinical settings, mostly in MDS. A phase III study where patients with MDS were randomly assigned to receive 75 mg/m2 a day of azacitidine subcutaneously for 7 days, repeated on a 28-day cycle, or supportive care only [140] yielded a response rate of 16% (CR 6%, PR 10%).

A carboxy-terminal domain of ELL is required and sufficient for immortalization of myeloid progenitors by MLL-ELL. Blood. 2000;96(12):3887–3893. 41. Djabali M, Selleri L, Parry P, Bower M, Young BD, Evans GA. A trithorax-like gene is interrupted by chromosome 11q23 translocations in acute leukaemias. Nat Genet. 1992;2 (2):113–118. 42. Durst KL, Hiebert SW. Role of RUNX family members in transcriptional repression and gene silencing. Oncogene 2004;23(24):4220–4224. 43. Eads CA, Danenberg KD, Kawakami K, Saltz LB, Danenberg PV, Laird PW.

Conclusions It is now clear that epigenetic changes play a significant role in the development and progression of AML. These epigenetic changes can be important targets of treatment, and recent clinical studies have shown the relative safety and efficacy of such epigenetic therapies. Although epigenetic modulation is effective in the treatment of AML, precise in vivo effects of these drugs have not been well described. Also, events downstream of gene expression induction such as apoptosis, senescence, and immunomodulation remain to be clarified.

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