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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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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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Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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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...
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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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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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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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.
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Clinical and Genomic Landscape of RAS Mutations in Gynecologic Cancers.

Ji Son1, Yingao Zhang1, Heather Lin2

  • 1Department of Gynecologic Oncology and Reproductive Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|April 30, 2024
PubMed
Summary

RAS mutations are found in 15.7% of gynecologic cancers and are linked to poorer survival. Targeted therapies show promise but require further investigation in this patient population.

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Area of Science:

  • Oncology
  • Genomics
  • Cancer Research

Background:

  • RAS mutations are prevalent in various cancers, but their role in gynecologic malignancies requires further elucidation.
  • Understanding the clinicopathologic and genomic landscape of RAS mutations is crucial for developing targeted treatment strategies.

Purpose of the Study:

  • To investigate the frequency, clinicopathologic correlations, genomic features, and survival impact of RAS mutations in gynecologic cancers.
  • To explore the therapeutic implications of RAS mutations and associated co-alterations in this patient cohort.

Main Methods:

  • Retrospective analysis of 3,328 gynecologic cancer cases with somatic molecular profiling data.
  • Kaplan-Meier method for overall survival estimation and Cox proportional hazard model for multivariable analysis.

Main Results:

  • RAS mutations were identified in 15.7% of cases, associated with younger age, higher endometriosis prevalence, and lower tumor grade.
  • KRAS mutations were most common, particularly in mesonephric-like endometrial and ovarian cancers, and mucinous and low-grade serous ovarian subtypes.
  • RAS mutation was linked to worse overall survival (HR=1.3, P=0.001). Actionable co-mutations (PIK3CA, PTEN, ARID1A) were frequent (64.7%).

Conclusions:

  • RAS mutations exhibit a distinct distribution in gynecologic cancers and are associated with adverse survival outcomes.
  • PIK3CA, PTEN, and ARID1A represent actionable co-alterations in RAS-mutated gynecologic cancers.
  • Consideration of RAS pathway-targeted therapies is warranted for patients with RAS-mutated gynecologic cancers.