Publication

The two major imatinib resistance mutations E255K and T315I enhance the activity of BCR/ABL fusion kinase.

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Biochem Biophys Res Commun2004PMID 15194504stubpubmedPublished

Abstract

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Linked entities

Linked entities (6)

How each link was made (MeSH, dictionary, registry reference, curation…) and whether it has been validated. Candidate links are not counted in entity statistics.

Validated 6

cancerChronic Myeloid Leukemia, BCR-ABL1 Positivecivic_curation1.00
drugImatinibcivic_curation1.00
geneABL1civic_curation1.00
variantABL1 E255Kcivic_curation1.00
variantABL1 Fusioncivic_curation1.00
variantABL1 T315Icivic_curation1.00

Curated evidence

Evidence citing this paper (2)

civicCuratedShowing 1–2 of 2 evidence items · levels, directions and significance as curated at the source; each row links to its CIViC record.

Therapy	Cancer	Type	Level	Direction · significance	Rating (1–5)	Status	Evidence	Source
ABL1 E255K + ABL1 Fusion1
Imatinib	Chronic Myeloid Leukemia, BCR-ABL1 PositiveALIAS	Predictive	D	Supports Resistance	4	accepted	EID233 COS7 cell lines transfected with BCR-ABL constructs harboring E255K mutations were shown to be resistant to imatinib and exhibited increased kinase activity. PMID 15194504 · Yamamoto et al., 2004 · Open in CIViC	civic
ABL1 T315I + ABL1 Fusion1
Imatinib	Chronic Myeloid Leukemia, BCR-ABL1 PositiveALIAS	Predictive	D	Supports Resistance	4	accepted	EID235 COS7 cell lines transfected with BCR-ABL constructs harboring T315I mutations were shown to be resistant to imatinib and exhibited increased kinase activity. PMID 15194504 · Yamamoto et al., 2004 · Open in CIViC	civic