PubMed · 9652724
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D Kaul. 1998. Receptor-Ck and leukemogenesis.. https://doi.org/10.1016/s0145-2126(98)00007-1
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The chromosomal translocation t(7;9) in human T-cell acute lymphoblastic leukaemia (T-ALL) results in deregulated expression of a truncated, activated form of Notch 1 (TAN1) under the control of the T-cell receptor-beta (TCRB) locus. Although TAN1 efficiently induces T-ALL in mouse models, t(7;9) is present in less than 1% of human T-ALL cases. The recent discovery of novel activating mutations in NOTCH1 in more than 50% of human T-ALL samples has made it clear that Notch 1 is far more important in human T-ALL pathogenesis than previously suspected.
The description of the molecular pathogenesis of acute myeloid leukemias (AML) has seen dramatic progress over the last years. Two major types of genetic events have been described that are crucial for leukemic transformation: alterations in myeloid transcription factors governing hematopoietic differentiation and activating mutations of signal transduction intermediates. These processes are highly interdependent, since the molecular events changing the transcriptional control in hematopoietic progenitor cells modify the composition of signal transduction molecules available for growth factor receptors, while the activating mutations in signal transduction molecules induce alterations in the activity and expression of several transcription factors that are crucial for normal myeloid differentiation. The purpose of this article is to review the current literature describing these genetic events, their biological consequences and their clinical implications. As the article will show, the recent description of several critical transforming mutations in AML may soon give rise to more efficient and less toxic molecularly targeted therapies of this deadly disease.