Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

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...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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...

You might also read

Related Articles

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

Sort by
Same author

Metabolic and Laboratory Biomarkers in Early-Onset Versus Late-Onset Colorectal Cancer: A Case-Control Study.

Cancers·2026
Same author

Pharmacological and non-pharmacological therapies for chronic pancreatitis pain: a narrative review.

Frontiers in physiology·2026
Same author

Younger age at colorectal cancer diagnosis in hereditary gastrointestinal cancer predisposition syndromes and Lynch syndrome: a nationwide analysis.

Journal of gastrointestinal oncology·2026
Same author

Risk of Myeloproliferative Neoplasms in Patients With Inflammatory Bowel Disease and Impact on Outcomes: A Multi-Centre Matched Analysis.

Alimentary pharmacology & therapeutics·2026
Same author

Normalizing Catastrophe: Learning From Responses to Cancer Diagnosis.

JCO oncology practice·2026
Same author

Association of proximal adenomas with high-grade dysplasia with increased cumulative incidence of postpolypectomy colon cancer: A Surveillance, Epidemiology, and End Results-Medicare analysis.

Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract·2026

Related Experiment Video

Updated: Jun 14, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Is BRAF mutation associated with interval colorectal cancers?

Aasma Shaukat1, Mustafa Arain, Bharat Thaygarajan

  • 1Division of Gastroenterology, VA Medical Center, Minneapolis, MN 55417, USA. shaukat@umn.edu

Digestive Diseases and Sciences
|March 20, 2010
PubMed
Summary

BRAF V600E mutation is not linked to interval colorectal cancers. However, this mutation indicates a poor 5-year survival, especially in microsatellite stable cancers.

More Related Videos

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells
06:44

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells

Published on: March 1, 2024

Related Experiment Videos

Last Updated: Jun 14, 2026

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells
06:44

Bioluminescence Resonance Energy Transfer (BRET)-Based Assay for Measuring Interactions of CRAF with 14-3-3 Proteins in Live Cells

Published on: March 1, 2024

Area of Science:

  • Oncology
  • Gastroenterology
  • Molecular Diagnostics

Background:

  • Interval colorectal cancers arise after a complete colonoscopy, potentially due to screening limitations or rapid tumor progression.
  • Understanding the molecular drivers of interval cancers is crucial for improving early detection and patient outcomes.

Purpose of the Study:

  • To investigate the association between BRAF V600E mutation and interval colorectal cancers.
  • To evaluate the relationship between BRAF mutation status and 5-year survival in colorectal cancer patients.

Main Methods:

  • A case-control study comparing 63 interval cancers with 131 non-interval cancers.
  • BRAF V600E mutation and microsatellite instability (MSI) testing on archived tumor specimens.
  • Multivariable logistic regression analysis to identify independent predictors of interval cancers.

Main Results:

  • BRAF V600E mutation was observed in 28% of interval cancers versus 19% of non-interval cancers (P=0.18).
  • Proximal location and MSI were significantly associated with interval cancers, but BRAF mutation was not.
  • BRAF mutation was a significant predictor of poor 5-year survival, particularly in microsatellite stable (MSS) colorectal cancers.

Conclusions:

  • BRAF V600E mutation is not associated with the development of interval colorectal cancers.
  • BRAF mutation serves as a prognostic marker for reduced 5-year survival, especially in microsatellite stable colorectal cancers.