Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes

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-oncogenes

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 Stem Cells and Tumor Maintenance

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...

Cancer Stem Cells and Tumor Maintenance

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

A novel drug series optimized to address cystic fibrosis and other CFTR deficiency diseases of human airways.

npj drug discovery·2026

Same author

Elexacaftor-Tezacaftor-Ivacaftor for Individuals with Residual CFTR Activity: An Open-Label, Nonrandomized Clinical Trial.

Annals of the American Thoracic Society·2026

Same author

Broadening activity of checkpoint blockade agents by intratumoral nucleoside cleavage.

JCI insight·2026

Same author

Large variations in total and allele-specific transcript expression in a disease mutation-independent manner.

Scientific reports·2026

Same author

Reconstitution of CFTR ubiquitination identifies lysine-420 as a regulator of cell surface residence and current.

Biochemistry and biophysics reports·2025

Same author

Barriers to the Pharmacologic Rescue of W1282X CFTR.

Biochemistry·2025

Search research articles

Related Experiment Video

Updated: Jul 4, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Evolutionary maintenance of oncogenesis.

Steven M Sorscher¹, Aubrey Hill, Eric J Sorscher

¹Internal Medicine/Oncology Section, Washington University, Campus Box 8056, St. Louis, MO, 63110, USA. ssorsche@im.wustl.edu

Journal of Cancer Research and Clinical Oncology

|May 31, 2008

Summary

This summary is machine-generated.

Tumor suppressor genes (TSGs) are preserved to help cells survive carcinogen exposure. However, mutations in these genes can paradoxically lead to cancer, causing host death.

More Related Videos

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

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

Published on: January 7, 2019

Related Experiment Videos

Last Updated: Jul 4, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

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

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

Published on: January 7, 2019

Area of Science:

Cellular Biology
Genetics
Cancer Research

Background:

Malignant transformation involves the loss of tumor suppressor gene (TSG) function.
Carcinogen exposure is a primary cause of TSG dysfunction.

Purpose of the Study:

To propose an evolutionary explanation for the preservation of mutation-susceptible TSGs.
To elucidate the dual role of TSGs in cellular survival and oncogenesis.

Main Methods:

Evolutionary genetic analysis (proposed).
Comparative genomics (proposed).
Functional assays of TSGs (proposed).

Main Results:

TSGs are evolutionarily maintained to promote cell survival against mutagenic insults.
Mutations in TSGs confer cellular persistence, preventing apoptosis.
This cellular persistence, while protective, can lead to oncogenesis.

Conclusions:

The study proposes that TSGs are evolutionarily conserved to enable cell survival post-carcinogen exposure.
Mutations in TSGs lead to apoptosis evasion and cellular persistence, ultimately causing cancer.
Proto-oncogenes may also be evolutionarily maintained with sequences prone to mutations that paradoxically lead to host death via malignancy.