Related Experiment Video
Updated: Jun 14, 2026
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
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.
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.
Related Concept Videos
02:38The 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...
Ras is a superfamily...
01:20The 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 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,...
01:20The 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 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,...
03:03mTOR 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...
The mTOR pathway or the...
02:21Cancers 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...
02:07Tumor 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...
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...