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Article

Three novel patient-derived BCR/ABL mutants show different sensitivity to second and third generation tyrosine kinase inhibitors.

American journal of hematology - 1 Nov 2012

Redaelli Sara, Mologni Luca, Rostagno Roberta, Piazza Rocco, Magistroni Vera, Ceccon Monica, Viltadi Michela, Flynn Daniel, Gambacorti-Passerini Carlo

Abstract excerpt

BCR/ABL (Breakpoint Cluster Region protein/Abelson tyrosine-protein kinase 1) kinase domain (KD) mutations represent the most frequently described mechanism of resistance to the treatment with tyrosine kinase inhibitors (TKI) in patients with chronic myeloid leukemia (CML). Mutations may impair T...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Fusion Proteins, bcr-abl

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

Share to Precursor Cell Lymphoblastic Leukemia-Lymphoma

Share to Protein-Tyrosine Kinases

Share to Sequence Analysis, Protein

Share to Structure-Activity Relationship

Source

Identifiers

PMID: 23044928
DOI: 10.1002/ajh.23338

Genes

BCR
DCC

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026. Prepared record publication-23044928-2026-09-04.2. Manifest publication-graph-cohort-2026-09-04.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 4 Sept 2026.

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