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Related Concept Videos

The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
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...
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...
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...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...

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Related Experiment Video

Updated: May 27, 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

Is KRAS mutation associated with interval colorectal cancers?

Aasma Shaukat1, Mustafa Arain, Ruth Anway

  • 1Division of Gastroenterology, VA Medical Center, University of Minnesota, One-Veterans Drive, 111-D, Minneapolis, MN 55417, USA. shaukat@umn.edu

Digestive Diseases and Sciences
|December 6, 2011
PubMed
Summary

KRAS mutations are less common in interval colorectal cancers, which are often rapidly growing and linked to microsatellite instability (MSI). This suggests KRAS mutations indicate a different, slower tumor growth pathway.

Related Experiment Videos

Last Updated: May 27, 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

Area of Science:

  • Oncology
  • Molecular Biology
  • Gastroenterology

Background:

  • Interval colorectal cancers (ICCs) are diagnosed after a negative colonoscopy, potentially due to rapid tumor growth.
  • ICCs are frequently associated with microsatellite instability (MSI).

Purpose of the Study:

  • To investigate the relationship between KRAS mutations, MSI, and ICCs.
  • To understand the molecular pathways distinguishing ICCs from non-interval cancers.

Main Methods:

  • Retrospective analysis of ICCs and non-interval colorectal cancers from institutional cancer registry.
  • Evaluation of KRAS mutations (codons 12 and 13) and MSI status using sequencing.
  • Multivariable logistic regression and Cox proportional hazards models to assess associations.

Main Results:

  • KRAS mutations were less frequent in ICCs (12.9%) compared to non-interval cancers (28.9%) (P=0.03).
  • KRAS mutation showed an inverse association with interval cancers (OR 0.36).
  • No significant association was found between KRAS mutation and 5-year survival after adjusting for clinical factors and MSI status.

Conclusions:

  • KRAS mutation is inversely associated with ICCs and MSI, indicating a distinct molecular pathway.
  • This suggests KRAS mutations are linked to slower-growing tumors, contrasting with MSI-associated rapid growth.
  • Molecular profiling aids in understanding colorectal cancer pathways and guiding therapy.