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The Ras Gene

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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Related Experiment Video

Updated: Sep 6, 2025

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Fully Processed Recombinant KRAS4b: Isolating and Characterizing the Farnesylated and Methylated Protein

Published on: January 16, 2020

Synthetic Vulnerabilities in the KRAS Pathway.

Marta Roman¹, Elizabeth Hwang¹, E Alejandro Sweet-Cordero¹

¹Department of Pediatrics, University of California San Francisco, San Francisco, CA 94158, USA.

|June 24, 2022

Summary

Targeting KRAS-mutant cancers requires new strategies. This review explores synthetic lethal vulnerabilities and stress response pathways for novel therapeutic approaches in KRAS-driven cancers.

Keywords:

KRAS cancer synthetic lethality

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Area of Science:

Oncology
Molecular Biology
Genetics

Background:

KRAS mutations are common in human cancers, driving oncogenesis through sustained signaling.
Targeted therapies for KRAS-mutant cancers are emerging but remain an unmet clinical need.
Synthetic lethality offers a promising avenue for developing novel cancer treatments.

Purpose of the Study:

To review the concept of synthetic lethal vulnerabilities in KRAS-mutant cancers.
To discuss the role of stress response pathways in KRAS-driven oncogenesis.
To highlight the potential of exploiting these pathways for therapeutic benefit.

Main Methods:

Review of current literature on KRAS mutations and targeted therapies.
Analysis of functional genomics data and cancer models.
Exploration of molecular pathways involved in KRAS signaling and stress responses.

Main Results:

KRAS-driven cancers exhibit unique vulnerabilities exploitable through synthetic lethality.
Stress response pathways are activated in KRAS-mutant cells, presenting therapeutic targets.
Advances in genomics and modeling reveal new synthetic lethal interactions.

Conclusions:

Synthetic lethal interactions represent a promising strategy for treating KRAS-mutant cancers.
Targeting stress response pathways offers a novel therapeutic approach.
Further research into these vulnerabilities could lead to effective clinical treatments.