leukemogenesis

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leukemogenesis

 [loo-ke″mo-jen´ĕ-sis]
the induction or development of leukemia.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

leu·ke·mo·gen·e·sis

(lū-kē'mō-jen'ĕ-sis),
The causation (or induction), development, and progression of a leukemic disease.
[leukemia + G. genesis, production]
Farlex Partner Medical Dictionary © Farlex 2012

leukemogenesis

A process in which successive transformational events enhance the ability of hematopoietic progenitor cells to proliferate, differentiate, and survive. See Autonomous proliferation.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

leu·ke·mo·gen·e·sis

(lū-kē'mō-jen'ĕ-sis)
The causation (or induction), development, and progression of a leukemic disease.
Synonym(s): leukaemogenesis.
[leukemia + G. genesis, production]
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
References in periodicals archive ?
Early simplified models for leukaemogenesis included the two-hit hypothesis, whereby two hits in two different mutation groups were needed [71].
(2002) demonstrated in leukaemia mice models that a single mutation in genes did not progress to leukaemogenesis, and further mutations from other classes were required [73].
The role of mutations in epigenetic modifiers such as DNMT3A is excluded from this theory, though data is increasingly proposing that these mutations have a significant contribution to leukaemogenesis. The introduction of mutations from neither Class I nor Class II has added further complexity to understanding haematological malignancies [27].
Though this may suggest a significant role for DNMT3A mutations in leukaemogenesis, the downstream consequence of the identified mutations in the enzyme remains largely underdetermined.
But what remains undetermined is the overall influence such alterations in methylation patterns have in leukaemogenesis.
In addition to this observation, the recent identification of other preleukaemic clones in individuals over the age of 70 has led to the theory that the R882 mutation is one that occurs early in the leukaemogenesis [91, 92].
This suppression of normal activity and subsequent altered methylation could be one possible mechanism of leukaemogenesis. While the hypomethylation observed in murine models carrying the R882H mutation was initially thought to produce loss-of-function function, the successful use of the hypomethylating agent decitabine in R882 patients contraindicates this theory [95].
If, however, such mutations are present, this could further support the notion of R882 mutation being a founder mutation, one which is acquired in early leukaemogenesis and leads to clonal expansion.
Mosialou et al., "Leukaemogenesis induced by an activating beta-catenin mutation in osteoblasts," Nature, vol.
(7) As such, TAM and myeloid leukaemia of Down's syndrome provides an excellent model for leukaemogenesis. (8)