The RasGEFs SOS1 and SOS2 are Potential Therapeutic Targets in RAS-Driven Cancers

Abstract

The RAS family of genes HRAS, NRAS, and KRAS are mutated in about a third of human cancers, with limited treatment options available. Wild-type RAS isoforms cooperate with mutant RAS to promote oncogenic signaling to downstream effectors, proliferation, and transformation. Activation of wild-type RAS involves the RAS guanine nucleotide exchange factors (RasGEFs) SOS1 and SOS2, creating a dependence on upstream signaling despite constitutive activation of mutant RAS.

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Document Details

Document Type
Technical Report
Publication Date
Mar 17, 2020
Accession Number
AD1182848

Entities

People

  • Erin Sheffels

Organizations

  • Uniformed Services University of the Health Sciences

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Amino Acids
  • Blood
  • Cancer
  • Carcinoma
  • Cell Line
  • Cell Physiological Processes
  • Cells
  • Chemical Synthesis
  • Chemistry
  • Colon Cancer
  • Crystal Structure
  • Culture Media
  • Culture Techniques
  • Cytoskeleton
  • Genetics
  • Lymphocytes
  • Medical Genetics
  • Neoplasms
  • Oncology
  • Peptide Growth Factors
  • Three Dimensional
  • Tumor Cell Line

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