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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

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...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...

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Comparative Lesions Analysis Through a Targeted Sequencing Approach
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Published on: November 5, 2019

Oncogenic activating mutations are associated with local copy gain.

Barmak Modrek1, Lin Ge, Ajay Pandita

  • 1Department of Bioinformatics, Genentech, Inc., South San Francisco, California, USA.

Molecular Cancer Research : MCR
|August 13, 2009
PubMed
Summary

KRAS copy gains are more common in non-small cell lung cancer with activating mutations, leading to increased KRAS expression. These gains are more focal in mutated tumors, suggesting a link between mutation and copy number alterations.

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Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells
12:04

Engineering Oncogenic Heterozygous Gain-of-Function Mutations in Human Hematopoietic Stem and Progenitor Cells

Published on: March 10, 2023

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Activating mutations and copy number gains are crucial for oncogene activation.
  • The interplay between these mechanisms, particularly for KRAS in non-small cell lung cancer (NSCLC), remains unclear.

Purpose of the Study:

  • To investigate the relationship between KRAS copy number gains and activating mutations in NSCLC.
  • To explore the impact of copy gains on KRAS expression levels and tumor characteristics.

Main Methods:

  • Analysis of KRAS copy number and mutations in NSCLC tumors.
  • Fluorescence in situ hybridization (FISH) to assess copy number alterations.
  • Correlation analysis between mutation status, copy gain frequency, and gene expression.

Main Results:

  • KRAS copy gains were more frequent in NSCLC tumors with activating KRAS mutations.
  • Copy gains were associated with significant increases in KRAS expression.
  • Focality of copy gains differed between tumors with and without activating KRAS mutations.
  • Similar associations were observed for EGFR in NSCLC and BRAF/NRAS in melanoma, but not for KRAS in colorectal cancer.

Conclusions:

  • Activating mutations and copy number gains are linked mechanisms of oncogene activation in certain cancers.
  • The relationship is locus-specific and cancer-type dependent.
  • Further research is needed to fully elucidate the complex interactions between oncogene activation mechanisms.