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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...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
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...
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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Related Experiment Video

Updated: Jul 5, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Oncogene addiction.

I Bernard Weinstein1, Andrew Joe

  • 1Herbert Irving Comprehensive Cancer Center, Department of Medicine, Columbia University Medical Center, New York, New York 10032-2704, USA. ibw1@columbia.edu

Cancer Research
|May 3, 2008
PubMed
Summary
This summary is machine-generated.

Cancer cells rely on single oncogenes for survival, a state known as oncogene addiction. Identifying this Achilles heel through advanced genomics and systems biology is crucial for effective targeted cancer therapies.

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Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
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Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

Related Experiment Videos

Last Updated: Jul 5, 2026

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line
06:24

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • Cancer complexity arises from numerous genetic and epigenetic alterations.
  • Despite complexity, cancer cells often depend on single oncogenes for growth and survival.
  • This dependency, termed oncogene addiction, underpins molecular targeted therapy.

Purpose of the Study:

  • To explore the concept of oncogene addiction in cancer.
  • To highlight the need for advanced methods to identify oncogene addiction states.
  • To discuss the potential of combination therapy to overcome treatment resistance.

Main Methods:

  • Integrative genomics approaches.
  • Systems biology methodologies.
  • Analysis of cancer cell dependency on specific oncogenes.

Main Results:

  • Oncogene addiction represents a critical vulnerability in cancer cells.
  • Identifying the specific oncogene addiction state is key to effective therapy.
  • Cancer cells can develop resistance to targeted therapies over time.

Conclusions:

  • Oncogene addiction provides a strong rationale for developing targeted cancer therapies.
  • Novel methods like integrative genomics and systems biology are essential for identifying these addiction states.
  • Combination therapies may be necessary to prevent or overcome therapeutic resistance in oncogene-addicted cancers.