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Article

Overcoming Bcr-Abl T315I mutation by combination of GNF-2 and ATP competitors in an Abl-independent mechanism.

BMC cancer - 27 Nov 2012

Khateb Mamduh, Ruimi Nili, Khamisie Hazem, Najajreh Yousef, Mian Afsar, Metodieva Anna, Ruthardt Martin, Mahajna Jamal

Abstract excerpt

BACKGROUND: Philadelphia positive leukemias are characterized by the presence of Bcr-Abl fusion protein which exhibits an abnormal kinase activity. Selective Abl kinase inhibitors have been successfully established for the treatment of Ph (+) leukemias. Despite high rates of clinical response, Ph (+) patients can develop resistance against these kinase inhibitors mainly due to point mutations within the Abl...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Therapy, Combination

Share to Fusion Proteins, bcr-abl

Share to Genes, abl

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

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Source

Open in PubMed Open full text

Identifiers

PMID: 23186157
DOI: 10.1186/1471-2407-12-563
PMCID: PMC3561207

Genes

JAK2

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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