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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...
Cancer02:18

Cancer

Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...

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Updated: Jun 2, 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

Cancer therapy based on oncogene addiction.

Frank McCormick1

  • 1UCSF Helen Diller Family Comprehensive Cancer Center, University of California-San Francisco, San Francisco, California 94158-9001, USA. mccormick@cc.ucsf.edu

Journal of Surgical Oncology
|April 12, 2011
PubMed
Summary
This summary is machine-generated.

Targeting cancer-driving oncoproteins offers dramatic responses but often fails due to drug resistance. Understanding signaling complexity, like in the Ras-MAPK pathway, is key for future targeted therapies.

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Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Tumor cells harbor numerous mutations but frequently rely on specific oncoproteins for survival.
  • Targeted therapies focusing on these critical oncoproteins have shown significant initial success in cancer treatment.

Purpose of the Study:

  • To examine the mechanisms of resistance that limit the long-term efficacy of targeted cancer therapies.
  • To investigate the role of the Ras-MAPK pathway in oncogene addiction and adaptive resistance.
  • To derive lessons from the Ras-MAPK pathway's successes and failures for improving future targeted therapy strategies.

Main Methods:

  • Review of existing literature on targeted cancer therapy and resistance mechanisms.
  • Analysis of signaling network reprogramming in response to oncogene-targeted drugs.
  • Case study focusing on the Ras-MAPK pathway as a model for oncogene addiction and resistance.

Main Results:

  • Targeted therapies can induce dramatic initial tumor regression.
  • Acquired resistance, through drug resistance or adaptive reprogramming of signaling networks, is a common cause of treatment failure.
  • The Ras-MAPK pathway exemplifies both the potential and limitations of targeting single oncoproteins, highlighting complex signaling interactions.

Conclusions:

  • Despite initial successes, targeted therapies face significant challenges due to resistance mechanisms.
  • Understanding oncogene addiction and pathway plasticity, particularly within networks like Ras-MAPK, is crucial for overcoming resistance.
  • Future targeted therapies must account for signaling complexity and adaptive resistance to achieve durable clinical responses.