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Article

Rac guanosine triphosphatases represent integrating molecular therapeutic targets for BCR-ABL-induced myeloproliferative disease.

Cancer cell - 1 Nov 2007

Thomas Emily K, Cancelas Jose A, Chae Hee-Don, Cox Adrienne D, Keller Patricia J, Perrotti Danilo, Neviani Paolo, Druker Brian J, Setchell Kenneth D R, Zheng Yi, Harris Chad E, Williams David A

Abstract excerpt

Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disease (MPD) initiated by expression of the p210-BCR-ABL fusion protein. We demonstrate in a murine model of p210-BCR-ABL-induced MPD that gene targeting of Rac1 and Rac2 significantly delays or abrogates disease development. Attenuation of the disease phenotype is associated with severely diminished p210-BCR-ABL-induced downstream signaling in...

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Share to Aminoquinolines
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

Share to Gene Expression Regulation, Leukemic

Share to Leukemia, Myelogenous, Chronic, BCR-ABL Positive

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Source

Identifiers

PMID: 17996650
DOI: 10.1016/j.ccr.2007.10.015

Genes

BCR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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