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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
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...
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...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
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 28, 2026

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy
05:21

Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy

Published on: October 6, 2014

Period 2 mutation accelerates ApcMin/+ tumorigenesis.

Patricia A Wood1, Xiaoming Yang, Andrew Taber

  • 1Medical Chronobiology Laboratory, Dorn Research Institute, Columbia, South Carolina, USA. patricia.wood2@va.gov

Molecular Cancer Research : MCR
|November 18, 2008
PubMed
Summary

The Period 2 (Per2) gene, crucial for the circadian clock, suppresses colorectal cancer development by regulating beta-catenin. Inactivating Per2 accelerates tumor formation, highlighting its potential in cancer prevention.

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Real-time Imaging of Myeloid Cells Dynamics in ApcMin/+ Intestinal Tumors by Spinning Disk Confocal Microscopy
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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

Area of Science:

  • Chronobiology
  • Molecular Biology
  • Oncology

Background:

  • Circadian disruption, common in shift work, is linked to increased colorectal cancer risk.
  • The circadian clock regulates intestinal epithelial cell proliferation, with Period 2 (Per2) being a key gene.
  • Per2 mutations in mice lead to lymphomas and altered expression of proliferation-controlling genes like cyclin D and c-Myc.

Purpose of the Study:

  • To investigate if Per2 clock gene inactivation accelerates intestinal and colonic tumorigenesis.
  • To determine the role of PER2 in regulating cell proliferation and beta-catenin in colon cancer.
  • To examine the in vivo effects of Per2 inactivation on beta-catenin, polyp formation, and tumorigenesis in mice.

Main Methods:

  • Studied PER2's effect on cell proliferation and beta-catenin in colon cancer cell lines (HCT116, SW480) via RNA interference.
  • Analyzed Per2 mutant mice (Per2(m/m)) for colonic polyps and beta-catenin/cyclin D levels.
  • Crossed Per2 mutant mice with polyp-prone Apc(Min/+) mice to assess combined effects on tumorigenesis.

Main Results:

  • Down-regulation of PER2 in colon cell lines increased beta-catenin, cyclin D, and cell proliferation.
  • Simultaneous down-regulation of beta-catenin and Per2 inhibited these increases.
  • Per2(m/m) mice developed colonic polyps and elevated beta-catenin/cyclin D in intestinal mucosa.
  • Apc(Min/+)Per2(m/m) mice exhibited a twofold increase in polyps and exacerbated anemia/splenomegaly compared to Apc(Min/+) mice.

Conclusions:

  • The Per2 gene product acts as a tumor suppressor in the small intestine and colon.
  • Per2 likely functions by down-regulating beta-catenin and its target genes.
  • Per2, a core circadian clock gene, represents a potential novel target for colorectal cancer prevention and control.