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Related Concept Videos

Cancers Originate from Somatic Mutations in a Single Cell02:21

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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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.
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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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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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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.
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BRAF Mutations in Canine Cancers.

Hiroyuki Mochizuki1, Katherine Kennedy1, Susan G Shapiro1

  • 1Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, United States of America.

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|June 9, 2015
PubMed
Summary
This summary is machine-generated.

BRAF gene mutations, common in human cancers, were identified in canine tumors. This discovery opens avenues for canine cancer diagnostics and targeted therapies.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Activating BRAF mutations constitutively activate the MAPK pathway, a common event in human cancers.
  • BRAF mutations are not yet characterized in canine cancers, despite shared molecular abnormalities between human and canine cancers.

Purpose of the Study:

  • To investigate the presence and frequency of BRAF gene mutations in canine primary tumors.
  • To determine if canine BRAF mutations mirror those found in human cancers, specifically the V600E mutation.

Main Methods:

  • Sequencing of exon 15 of the BRAF gene, a known mutation hotspot.
  • Analysis of 667 canine primary tumors and 38 control tissues.

Main Results:

  • A BRAF mutation (T1349A, V450E) was identified in 9.6% (64/667) of canine tumors.
  • High frequencies were observed in prostatic carcinoma (80%) and urothelial carcinoma (67%).
  • The canine V450E mutation corresponds to the human V600E BRAF mutation.

Conclusions:

  • The BRAF V450E mutation is present in canine cancers, analogous to the human V600E mutation.
  • This finding underscores the significance of MAPK pathway activation in canine neoplasia.
  • Identified mutations offer potential for developing molecular diagnostics and targeted therapeutics for canine cancers.