Related Experiment Video

Updated: May 20, 2026

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
06:51

Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer

Published on: July 21, 2018

The genetics and biology of KRAS in lung cancer

Peter M K Westcott1, Minh D To

  • 1Pharmaceutical Sciences and Pharmacogenomics Program, Helen Diller Comprehensive Cancer Center, University of California San Francisco, San Francisco, CA 94115, USA.

Chinese Journal of Cancer
|July 11, 2012
PubMed

Insights

Mutational activation of KRAS is a common cause of cancer, but therapies targeting it remain largely unsuccessful. Further research into KRAS mutations is crucial for developing effective treatments for KRAS-driven cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Mutational activation of KRAS is a frequent oncogenic event in lung and other epithelial cancers.
  • Cancers driven by mutant KRAS are notoriously difficult to treat with current therapies.
  • Decades of research have illuminated the clinical significance of KRAS mutations in lung cancer.

Purpose of the Study:

  • To review the current understanding of KRAS mutations in cancer.
  • To highlight the challenges in developing targeted therapies for KRAS-driven cancers.
  • To emphasize the need for deeper insights into KRAS functions for future therapeutic strategies.

Main Methods:

  • Review of existing literature on KRAS mutations in cancer.
  • Analysis of data from mutant Kras-driven mouse models.
  • Integration of cellular and molecular studies on KRAS function in tumorigenesis.

Main Results:

  • KRAS mutations are a significant driver in various epithelial cancers, particularly lung cancer.
  • Despite extensive research, effective therapies against mutant KRAS remain elusive.
  • Studies have revealed the complex roles of KRAS in tumor development.

Conclusions:

  • Targeting mutant KRAS in cancer therapy presents substantial challenges.
  • A comprehensive understanding of KRAS in tumorigenesis is essential for clinical advancement.
  • Further investigation is required to overcome therapeutic resistance in KRAS-driven malignancies.

More Related Videos

Detection of Lung Tumor Progression in Mice by Ultrasound Imaging04:43

Detection of Lung Tumor Progression in Mice by Ultrasound Imaging

Published on: February 27, 2020

Related Concept Videos

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...
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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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,...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...