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Article

STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.

Oncotarget - 1 Dec 2012

Warsch Wolfgang, Grundschober Eva, Berger Angelika, Gille Lars, Cerny-Reiterer Sabine, Tigan Anca-Sarmiza, Hoelbl-Kovacic Andrea, Valent Peter, Moriggl Richard, Sexl Veronika

Abstract excerpt

We recently reported that chronic myeloid leukaemia (CML) patients harbour high levels of STAT5 when they progress to advanced phases of disease. Advanced disease is characterized by an increased incidence of BCR-ABL1 mutations. We now describe a highly significant correlation between STAT5 expression and the incidence of BCR-ABL1 mutations in primary CML. Forced expression of STAT5 in murine BCR-ABL1 transformed...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

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

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Source

Open in PubMed Open full text

Identifiers

PMID: 23458731
DOI: 10.18632/oncotarget.806
PMCID: PMC3681503

Genes

ABL1
BCR
JAK2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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