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The Ras Gene

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...

The Ras Gene

The Ras Gene

Small GTPases - Ras and Rho

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:

Targeted Cancer Therapies

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...

Abnormal Proliferation

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...

MAPK Signaling Cascades

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

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Related Experiment Video

Updated: Mar 19, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Therapeutic Approaches to RAS Mutation.

Aaron J Scott¹, Christopher H Lieu, Wells A Messersmith

¹From the Division of Medical Oncology, University of Colorado Denver Anschutz Medical Campus, and University of Colorado Cancer Center, Aurora, CO.

Cancer Journal (Sudbury, Mass.)

|June 25, 2016

Summary

Targeting oncogenic RAS mutations, common in cancer, remains challenging. This review explores RAS biology, inhibition strategies, and new complexities in developing effective cancer therapies.

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Area of Science:

Oncology
Molecular Biology
Cancer Genetics

Background:

Oncogenic RAS mutations are key drivers in human cancers.
These mutations have significantly advanced cancer molecular biology understanding and targeted therapy development.
Despite progress, effective inhibitors for RAS mutations remain elusive, earning them the "undruggable" moniker.

Purpose of the Study:

To review current knowledge of RAS biology.
To explore strategies for inhibiting RAS oncoproteins and their downstream targets.
To discuss recent complexities influencing the development of RAS-targeted cancer therapies.

Main Methods:

Literature review of RAS biology and targeted therapy research.
Analysis of current and emerging strategies for RAS oncoprotein inhibition.
Discussion of recent findings and complexities in the field.

Main Results:

RAS mutations are prevalent oncogenic drivers.
Targeting RAS has been historically difficult, necessitating novel approaches.
Recent discoveries are providing new insights into RAS biology and potential therapeutic avenues.

Conclusions:

Understanding RAS biology is crucial for cancer treatment.
Developing effective RAS inhibitors is an ongoing, complex challenge.
Emerging strategies and complexities offer new hope for targeting RAS-mutated cancers.