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Related Concept Videos

The Ras Gene02:38

The Ras Gene

7.4K
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...
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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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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:
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Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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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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Rous Sarcoma Virus (RSV) and Cancer01:03

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The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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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,...
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Abnormal Proliferation02:23

Abnormal Proliferation

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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...
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Related Experiment Video

Updated: Mar 14, 2026

RhoC GTPase Activation Assay
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RhoC GTPase Activation Assay

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Variegated RHOA mutations in human cancers.

Keisuke Kataoka1, Seishi Ogawa1

  • 1Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Yoshida Konoe-cho, Sakyo-ku, Kyoto, Japan.

Experimental Hematology
|October 4, 2016
PubMed
Summary

Frequent mutations in the RHOA gene are found across many human cancers. These genetic alterations in RHOA may influence cancer development, but their precise role remains complex and debated.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The Rho GTPase family protein, RHOA, is a known factor in cancer development, invasion, and metastasis.
  • Recent advancements in sequencing technology have identified recurrent RHOA mutations in diverse human malignancies.
  • Specific RHOA mutations vary by cancer type, suggesting distinct functional impacts.

Purpose of the Study:

  • To provide an overview of current knowledge regarding RHOA mutations in human cancers.
  • To highlight the complex genetic and biological properties of RHOA mutations.
  • To discuss the controversial role of RHOA mutations in tumor development.

Main Methods:

  • Review of recent scientific literature on RHOA mutations in cancer.
  • Analysis of mutation data from various human cancer types.

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  • Synthesis of findings on the functional and biological implications of RHOA mutations.
  • Main Results:

    • RHOA mutations are frequently observed in hematological malignancies (e.g., angio-immunoblastic T-cell lymphoma) and solid tumors (e.g., gastric cancer).
    • The location and type of amino acid substitutions in RHOA mutations differ across cancer types.
    • Evidence suggests that RHOA mutations possess unique functional and biological characteristics specific to each cancer context.

    Conclusions:

    • RHOA mutations represent a significant genetic event in a broad spectrum of human cancers.
    • The functional consequences and oncogenic roles of RHOA mutations are complex and context-dependent.
    • Further research is needed to fully elucidate the impact of RHOA mutations on tumorigenesis and metastasis.