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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.
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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...
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.
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...
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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:
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...

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RASSF1 Polymorphisms in Cancer.

Marilyn Gordon1, Mohamed El-Kalla, Shairaz Baksh

  • 1Department of Pediatrics, Faculty of Medicine and Dentistry, University of Alberta, 3-055 Katz Group Centre for Pharmacy and Health Research, 113 Street 87 Avenue, Edmonton, AB, Canada T6G 2E1.

Molecular Biology International
|June 16, 2012
PubMed
Summary
This summary is machine-generated.

Ras association domain family 1A (RASSF1A) is a tumor suppressor silenced in cancers. Polymorphisms and epigenetic silencing of RASSF1A contribute to cancer development by impairing its tumor-suppressive functions.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ras association domain family 1A (RASSF1A) is a key tumor suppressor gene.
  • RASSF1A is frequently epigenetically silenced in various human cancers.
  • Its functions include regulation of cell cycle, apoptosis, and autophagy.

Purpose of the Study:

  • To summarize the origins of RASSF1A polymorphisms in cancer patients.
  • To elucidate how these polymorphisms and epigenetic silencing impact RASSF1A's tumor suppressor role.
  • To understand the biological significance of RASSF1A in cancer development.

Main Methods:

  • Review of existing literature on RASSF1A polymorphisms and epigenetic silencing.
  • Analysis of studies investigating the functional consequences of RASSF1A alterations.
  • Correlation of genetic changes with epigenetic silencing in cancer tissues.

Main Results:

  • RASSF1A is frequently epigenetically silenced via promoter methylation in cancers.
  • Somatic nucleotide changes (polymorphisms) in RASSF1A are observed in cancer patients.
  • Both epigenetic silencing and polymorphisms are hypothesized to lead to loss of tumor suppressor function.

Conclusions:

  • Combined epigenetic silencing and polymorphisms in RASSF1A contribute to its loss of function.
  • This loss of function promotes tumor growth and cancer progression.
  • Understanding RASSF1A alterations is crucial for cancer research.