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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
The Ras Gene02:38

The Ras Gene

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.
Ras is a superfamily...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
The Ras Gene02:38

The Ras Gene

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.
Ras is a superfamily...

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Related Experiment Video

Updated: May 10, 2026

Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT
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Gene Regulation and Targeted Therapy in Gastric Cancer Peritoneal Metastasis: Radiological Findings from Dual Energy CT and PET/CT

Published on: January 22, 2018

Targeting RAS in gastrointestinal malignancies.

Oluseyi Abidoye1, Celine Hoyek1, Tanios Bekaii-Saab1

  • 1Department of Hematology and Oncology, Mayo Clinic, Arizona.

Clinical Advances in Hematology & Oncology : H&O
|March 28, 2025
PubMed
Summary

Targeting Kirsten rat sarcoma virus (KRAS) mutations, especially KRAS G12C, shows promise for gastrointestinal cancers. New small-molecule inhibitors offer hope against these prevalent oncogenic drivers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gastrointestinal Oncology

Background:

  • Kirsten rat sarcoma virus (KRAS) mutations are key drivers in gastrointestinal (GI) cancers like pancreatic and colorectal cancer.
  • The KRAS protein, a GTPase, regulates critical survival pathways, making it a significant therapeutic target.

Purpose of the Study:

  • To review the molecular basis of KRAS mutations in GI cancers.
  • To explore current and emerging therapeutic strategies targeting KRAS mutations.
  • To discuss challenges, clinical trials, and future directions in KRAS-targeted therapy.

Main Methods:

  • Literature review of KRAS molecular biology.
  • Analysis of prevalence data for KRAS mutations in GI malignancies.
  • Examination of current and investigational KRAS-targeted therapies.

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  • Review of clinical trial outcomes and resistance mechanisms.

    • Main Results:

    • KRAS mutations are prevalent oncogenic drivers in GI cancers.
    • Small-molecule inhibitors targeting KRAS G12C mutations demonstrate therapeutic potential.
    • Ongoing clinical trials are evaluating the efficacy of these novel agents.

    Conclusions:

    • Targeting KRAS mutations, particularly G12C, represents a significant advancement in GI cancer treatment.
    • Further research is needed to overcome resistance and optimize KRAS-targeted therapies.