KRAS-Mutant Lung Cancers in the Era of Targeted Therapy. Review uri icon

Overview

abstract

  • KRAS-mutant lung cancers account for approximately 25% of non-small cell lung carcinomas, thus representing an enormous burden of cancer worldwide. KRAS mutations are clear drivers of tumor growth and are characterized by a complex biology involving the interaction between mutant KRAS, various growth factor pathways, and tumor suppressor genes. While KRAS mutations are classically associated with a significant smoking history, they are also identified in a substantial proportion of never-smokers. These mutations are found largely in lung adenocarcinomas with solid growth patterns and tumor-infiltrating lymphocytes. A variety of tools are available for diagnosis including Sanger sequencing, multiplex mutational hotspot profiling, and next-generation sequencing. The prognostic and predictive roles of KRAS status remain controversial. It has become increasingly clear, however, that KRAS mutations drive primary resistance to EGFR tyrosine kinase inhibition. Until recently, mutant KRAS was not thought of as a clinically-targetable driver in lung cancers. With the expansion of our knowledge regarding the biology of KRAS-mutant lung cancers and the role of MEK and PI3K/mTOR inhibition, the face of targeted therapeutics for this genomic subset of patients is slowly beginning to change.

publication date

  • January 1, 2016

Research

keywords

  • Lung Neoplasms
  • Molecular Targeted Therapy
  • Mutation
  • Proto-Oncogene Proteins p21(ras)

Identity

Scopus Document Identifier

  • 84950349713

Digital Object Identifier (DOI)

  • 10.1007/978-3-319-24223-1_8

PubMed ID

  • 26667343

Additional Document Info

volume

  • 893