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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...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Tumor Progression02:07

Tumor Progression

Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

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Related Experiment Video

Updated: Jun 6, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

[Colorectal oncogenesis].

P Laurent-Puig1, J Agostini, K Maley

  • 1Université Paris-Descartes, UMR-S775, Pôle de Biologie, Hôpital Européen Georges-Pompidou AP-HP, Paris, France. pierre.laurent-puig@parisdescartes.fr

Bulletin Du Cancer
|December 1, 2010
PubMed
Summary
This summary is machine-generated.

Colorectal cancer (CRC) arises from distinct molecular pathways, including chromosomal instability (CIN) and microsatellite instability (MSI). Despite differences, these pathways converge on similar signaling alterations driving tumor growth.

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Area of Science:

  • Molecular biology
  • Genetics
  • Oncology

Background:

  • Colorectal cancer (CRC) exhibits significant molecular heterogeneity.
  • Two primary molecular mechanisms, chromosomal instability (CIN) and microsatellite instability (MSI), drive CRC development.
  • A third phenotype involving gene promoter hypermethylation is also recognized.

Purpose of the Study:

  • To elucidate the molecular mechanisms underlying colorectal carcinogenesis.
  • To compare the signaling pathway alterations associated with different CRC molecular phenotypes.
  • To understand how genetic heterogeneity leads to common downstream effects in CRC.

Main Methods:

  • Analysis of genetic alterations in CRC tumors, including allelic losses and gene mutations (e.g., TP53, APC, SMAD2, SMAD4, BRAF).
  • Investigation of mismatch repair (MMR) deficiency and its consequences in MSI tumors.
  • Examination of gene promoter hypermethylation patterns.
  • Comparative analysis of signaling pathway activation (Wnt, TGFβ, RAS-MAPK, p53) across different CRC phenotypes.

Main Results:

  • CIN phenotype (80% of sporadic CRC) is linked to allelic losses and mutations in key genes.
  • MSI phenotype (12-15% of CRC) results from MMR deficiency, causing mutations in cell cycle and apoptosis genes.
  • Convergent alterations in Wnt, TGFβ, RAS-MAPK, and p53 pathways are observed across CIN and MSI phenotypes, despite distinct initiating events.

Conclusions:

  • Colorectal cancer displays significant genetic heterogeneity but converges on similar signaling pathway dysregulation.
  • Understanding these molecular pathways is crucial for targeted therapies in CRC.
  • The identification of distinct molecular phenotypes aids in classifying CRC and predicting treatment responses.