Targeting KRAS in gynecological malignancies

FASEB J. 2024 Oct 15;38(19):e70089. doi: 10.1096/fj.202401734R.

Abstract

Cervical, endometrial, and ovarian cancers stand prominently as the leading gynecological malignancies of the female reproductive system. The conventional therapeutic modalities for gynecological malignancies have predominantly encompassed surgery, chemotherapy, and radiotherapy. However, efficacy of these approaches remains limited in cases of relapse or drug resistance. KRAS is one of the most frequently mutated oncogenes in human cancers. The KRAS gene encodes a small guanosine triphosphatase protein that acts as a molecular switch for crucial intracellular signaling pathways. KRAS mutations are deeply involved in the occurrence and development of gynecological malignancies. The present review aims to expound upon the role of oncogenic KRAS as a biomarker, elucidating various therapeutic approaches under investigation targeting the KRAS pathway in gynecological tumors.

Keywords: KRAS; cervical cancer; endometrial cancer; gynecological malignancy; ovarian cancer.

Publication types

  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Female
  • Genital Neoplasms, Female* / drug therapy
  • Genital Neoplasms, Female* / genetics
  • Genital Neoplasms, Female* / metabolism
  • Humans
  • Molecular Targeted Therapy / methods
  • Mutation
  • Proto-Oncogene Proteins p21(ras)* / antagonists & inhibitors
  • Proto-Oncogene Proteins p21(ras)* / genetics
  • Proto-Oncogene Proteins p21(ras)* / metabolism
  • Signal Transduction

Substances

  • Proto-Oncogene Proteins p21(ras)
  • KRAS protein, human
  • Antineoplastic Agents