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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...
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...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...

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Updated: May 19, 2026

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Interactions between wild-type and mutant Ras genes in lung and skin carcinogenesis.

M D To1, R D Rosario, P M K Westcott

  • 1Thoracic Oncology Program, Department of Surgery, University of California San Francisco, San Francisco, CA 94115, USA.

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|September 5, 2012
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Wild-type Ras proteins can suppress cancer, particularly when their own gene is mutated. Interactions between different Ras family members show complex, context-dependent effects on tumor development in vivo.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ras oncogenes (Hras, Kras, Nras) are key drivers of cancer.
  • Wild-type (WT) Ras alleles are often lost in tumors, suggesting a tumor suppressor role.
  • In vitro studies indicate WT Ras can suppress alternate mutant Ras family members, but in vivo evidence is limited.

Purpose of the Study:

  • To investigate in vivo genetic interactions between mutant and WT Ras alleles.
  • To determine the heterologous interactions of Ras family members in carcinogenesis.
  • To elucidate the context-dependent roles of Ras proto-oncogenes and oncogenes.

Main Methods:

  • Carcinogen-induced lung and skin carcinogenesis models in mice.
  • Targeted deletion of different Ras family members (Hras, Kras, Nras).
  • Analysis of tumor development in mice with various combinations of mutant and WT Ras alleles.

Main Results:

  • WT Kras showed a major suppressor effect in Kras-mutant lung carcinogenesis.
  • WT Hras suppressed progression from skin papillomas to squamous carcinomas.
  • Interactions between different Ras family members (e.g., Kras and Hras) exhibited context-dependent effects on tumor promotion or suppression.

Conclusions:

  • The strongest tumor suppressor effects of WT Ras are observed when its cognate allele is mutated.
  • Ras family members interact in complex, context-dependent ways during tumor development.
  • WT Ras proteins can act as suppressors of carcinogenesis, particularly in relation to their own mutations.