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Plasticity of Extrachromosomal and Intrachromosomal BRAF Amplifications in Overcoming Targeted Therapy Dosage Challenges.

Kai SongJenna K MinamiArthur HuangSiavash R DehkordiShirley H LomeliJens LuebeckMark H GoodmanGatien MoriceauOscar KrijgsmanPrashanthi DharanipragadaTrevor RidgleyWilliam P CrossonJesus SalazarEli PazolGabriel KarinRachana JayaramanNikolas G BalanisSalwan AlhaniKyle SheuJohanna Ten HoeveAmelia PalermoStephen E MotikaT Niroshi SenaratneKim H ParaisoPaul J HergenrotherP Nagesh RaoAsha S MultaniDaniel S PeeperVineet BafnaRoger S LoThomas Glen Graeber
Published in: Cancer discovery (2022)
Understanding the structure and dynamics of oncogene amplifications is critical for overcoming tumor relapse. BRAF amplifications are highly plastic under MAPKi dosage challenges in melanoma, through involvement of de novo genomic alterations, even in the HSR mode. Moreover, BRAF FA-driven, dual MAPKi-resistant cells extend the spectrum of resistance-linked ferroptosis sensitivity. This article is highlighted in the In This Issue feature, p. 873.
Keyphrases
  • metastatic colorectal cancer
  • wild type
  • induced apoptosis
  • cell death
  • cell cycle arrest
  • machine learning
  • deep learning
  • copy number
  • oxidative stress
  • gene expression
  • cell proliferation
  • dna methylation