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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Epigenetic Regulation01:46

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Related Experiment Video

Updated: Jul 19, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

Epigenetics in colorectal cancer.

Lanlan Shen1, Jean-Pierre J Issa

  • 1The University of Texas at MD Anderson Cancer Center, Houston, Texas 77030, USA.

Current Opinion in Gastroenterology
|October 13, 2006
PubMed
Summary

Epigenetic changes, like DNA methylation, drive cancer development, particularly in the colon. These changes, especially the CpG island methylator phenotype (CIMP), are crucial in sporadic colorectal neoplasia.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Malignant transformation involves molecular alterations in growth factor response, cell-cycle control, and invasion.
  • Genetic changes are traditionally seen as the primary drivers of hereditary cancers.
  • Epigenetic changes, altering gene expression without DNA sequence modification, are increasingly recognized as drivers of neoplastic transformation.

Purpose of the Study:

  • To highlight the role of epigenetic changes, specifically DNA methylation, in cancer development.
  • To discuss the significance of the CpG island methylator phenotype (CIMP) in sporadic colorectal neoplasia.
  • To explore the implications of epigenetic alterations for cancer research and clinical applications.

Main Methods:

  • Review of molecular alterations in malignant transformation.

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Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

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Related Experiment Videos

Last Updated: Jul 19, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
07:33

In vitro Organoid Culture of Primary Mouse Colon Tumors

Published on: May 17, 2013

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
07:50

Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer

Published on: September 18, 2020

Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres
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Discovery of Driver Genes in Colorectal HT29-derived Cancer Stem-Like Tumorspheres

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  • Focus on DNA methylation and histone acetylation as epigenetic mediators.
  • Analysis of aberrant methylation in early colorectal neoplasia and its association with CIMP.

    • Main Results:

    • Epigenetic changes, particularly DNA methylation, are key drivers in neoplastic transformation.
    • Aberrant DNA methylation occurs early in colorectal neoplasia, potentially contributing to a field defect.
    • The CpG island methylator phenotype (CIMP) is a critical event in approximately half of sporadic colon tumors, influencing distinct clinical and epidemiological features and causing microsatellite instability via hMLH1 inactivation.

    Conclusions:

    • Epigenetic alterations are significant driving forces in colorectal neoplasia.
    • CIMP is a defining characteristic of a subset of sporadic colon cancers with unique features.
    • Understanding epigenetic changes opens new avenues for cancer epidemiology, risk assessment, screening, and treatment.