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Download Acute Promyelocytic Leukemia: Molecular Genetics, Mouse by P. P. Pandolfi (auth.), Pier Paolo Pandolfi MD, Ph.D., Peter PDF

By P. P. Pandolfi (auth.), Pier Paolo Pandolfi MD, Ph.D., Peter K. Vogt Ph.D. (eds.)

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PLZF may in part mediate growth suppression by these agents. PLZF was detected in the uterus in the mid and late secretory phase of the menstrual cycle but not in the proliferative phase, consistent with the general negative effect of PLZF on cell growth. Also consistent with an antiproliferative effect, PLZF overexpression in a prostate cancer cell line inhibited cell proliferation. In addition, PLZF was identified as a gene upregulated in prostate tissue by androgen treatment [39], and in breast cancer cells in response to glucocorticoids and progestins [77].

Cotylenin A is a plant growth regulator that is able to induce differentiation of human myeloid leukemia cell lines and primary AML blasts. The xenograft 24 S. C. Kogan mouse model of APL was used to show that cotylenin A can prolong survival in mice engrafted with the RA-sensitive NB4 cell line, or a RA-resistant version of NB4 (Honma et al. 2003). The possible utility of cotylenin A (or a derivative) as an antileukemic agent in humans is not yet clear. Another observation of uncertain clinical benefit is that hypoxia can facilitate differentiation of myeloid leukemic cells in vitro.

One protein identified is the kinase protein cdc2, which may play a role in the phosphorylation of PLZF. Phosphorylation of PLZF is thought be critical for its function, as treatment of PLZF with a phosphatase leads to loss of DNA-binding activity [1]. In addition, a tyrosine phosphorylation was identified at the extreme C-terminus of the PLZF protein [70]. Cdc2 was previously implicated in transcriptional repression by phosphorylation of basal transcription factors [50], another possible mechanism by which PLZF might influence repression.

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