Resistance mechanisms for the Bruton's tyrosine kinase inhibitor ibrutinib Academic Article uri icon

Overview

MeSH Major

  • Drug Resistance, Neoplasm
  • Leukemia, Lymphocytic, Chronic, B-Cell
  • Phospholipase C gamma
  • Point Mutation
  • Protein-Tyrosine Kinases
  • Pyrazoles
  • Pyrimidines

abstract

  • Resistance to the irreversible BTK inhibitor ibrutinib often involves mutation of a cysteine residue where ibrutinib binding occurs. This finding, combined with two additional mutations in PLCĪ³2 that are immediately downstream of BTK, underscores the importance of the B-cell-receptor pathway in the mechanism of action of ibrutinib in CLL. (Funded by the National Cancer Institute and others.).

publication date

  • January 2014

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC4144824

Digital Object Identifier (DOI)

  • 10.1056/NEJMoa1400029

PubMed ID

  • 24869598

Additional Document Info

start page

  • 2286

end page

  • 94

volume

  • 370

number

  • 24