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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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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.
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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

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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.
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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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Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Wild-type RAS: keeping mutant RAS in CHK.

Theonie Anastassiadis1, Eric J Brown1

  • 1Abramson Family Cancer Research Institute, Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, 421 Curie Boulevard, Philadelphia, PA 19104, USA.

Cancer Cell
|February 15, 2014
PubMed
Summary
This summary is machine-generated.

Wild-type RAS isoforms play a crucial role in cancer development, contrary to previous beliefs. Their loss impacts oncogenic signaling and DNA repair, influencing tumor growth and response to chemotherapy.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Mutant RAS proteins are key drivers of tumorigenesis.
  • Wild-type RAS isoforms were historically considered uninvolved in RAS-driven cancers.
  • Emerging evidence suggests a role for wild-type RAS in cancer development.

Purpose of the Study:

  • To investigate the role of wild-type RAS isoforms in mutant RAS-driven tumorigenesis.
  • To understand how loss of wild-type RAS affects oncogenic signaling pathways.
  • To determine the impact of wild-type RAS on DNA-damage response and chemosensitivity.

Main Methods:

  • Analysis of oncogenic signaling pathways in the presence and absence of wild-type RAS.
  • Assessment of DNA-damage response mechanisms.
  • Evaluation of tumor progression and chemosensitivity in relevant models.

Main Results:

  • Loss of wild-type RAS significantly alters oncogenic signaling.
  • The DNA-damage response is dampened upon loss of wild-type RAS.
  • Altered signaling and DNA repair impact tumor progression and chemosensitivity.

Conclusions:

  • Wild-type RAS isoforms are involved in mutant RAS-driven tumorigenesis.
  • Loss of wild-type RAS creates vulnerabilities in cancer cells.
  • Understanding this interaction may reveal new therapeutic strategies for RAS-driven cancers.