Related Experiment Video

Updated: May 28, 2026

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
08:12

Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans

Published on: October 5, 2020

Inhibition of Ras for cancer treatment: the search continues

Antonio T Baines1, Dapeng Xu, Channing J Der

  • 1Department of Biology and the Cancer Research Program, JLC-Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, NC 27707, USA.

Future Medicinal Chemistry
|October 19, 2011
PubMed

Insights

Developing effective cancer treatments targeting RAS oncogenes (HRAS, NRAS, KRAS) remains challenging. While direct inhibition failed, indirect strategies blocking Ras signaling show promise, with new avenues emerging from genetic screens.

Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Discovery

Background:

  • RAS oncogenes (HRAS, NRAS, KRAS) are the most frequently mutated oncogenes in human cancers, present in 33% of cases.
  • Despite their prevalence, no effective anti-RAS therapies have reached clinical application.

Purpose of the Study:

  • To provide an overview of current and past strategies for inhibiting oncogenic RAS in cancer treatment.
  • To highlight novel directions for anti-RAS drug discovery.

Main Methods:

  • Review of past and ongoing research on RAS inhibition strategies.
  • Analysis of indirect approaches targeting Ras membrane association and downstream effector signaling.
  • Consideration of findings from genome-wide genetic screens.

Main Results:

  • Direct targeting of mutant RAS has proven unsuccessful.
  • Indirect strategies focusing on blocking Ras membrane association or downstream effector signaling are under clinical evaluation.
  • Genome-wide genetic screens have identified novel therapeutic targets.

Conclusions:

  • Effective inhibition of oncogenic RAS remains a critical unmet need in cancer therapy.
  • Indirect targeting strategies and novel targets identified through genetic screens offer promising avenues for future drug development.

More Related Videos

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies09:29

Development and Maintenance of a Preclinical Patient Derived Tumor Xenograft Model for the Investigation of Novel Anti-Cancer Therapies

Published on: September 30, 2016

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...
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:
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 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,...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...