Related Experiment Video
Updated: May 5, 2026

28:15
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 29, 2010
15.7K
High frequency of K-ras mutations in human colorectal hyperplastic polyps
1Investigative Treatment Division, National Cancer Center Research Institute, Chiba, Japan.
Gut
|May 1, 1997
Summary
Common hyperplastic polyps may transform into cancerous colorectal neoplasms. Genetic analysis revealed K-ras mutations in nearly half of these polyps, suggesting they are neoplastic lesions.
Area of Science:
- Gastroenterology
- Molecular Biology
- Oncology
Background:
- Hyperplastic polyps are common benign colorectal growths.
- Traditionally considered low-risk, some evidence suggests they can become neoplastic.
Purpose of the Study:
- To investigate genetic alterations in colorectal hyperplastic polyps.
- To determine if hyperplastic polyps possess neoplastic potential.
Main Methods:
- Endoscopic resection of 28 colorectal polyps with serrated features.
- Analysis of K-ras gene mutations (codons 12 and 13) using PCR-RFLP.
- Immunohistochemical staining for intranuclear p53 protein.
Main Results:
- K-ras gene mutations were found in 47% of hyperplastic polyps and 56% of adenomas.
- p53 protein nuclear accumulation was observed in 22% of adenomas but not in hyperplastic polyps.
- Serrated polyps with K-ras mutations indicate neoplastic potential.
Conclusions:
- Certain hyperplastic polyps exhibit genetic alterations characteristic of neoplastic lesions.
- These findings suggest hyperplastic polyps can be precursors to colorectal cancer.
Related Concept Videos
Abnormal Proliferation
4.0K
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...
4.0K
Cancers Originate from Somatic Mutations in a Single Cell
12.6K
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...
12.6K
Tumor Progression
6.2K
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...
6.2K
Cancer-Critical Genes I: Proto-oncogenes
9.1K
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...
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...
9.1K
The Ras Gene
5.7K
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...
Ras is a...
5.7K
Small GTPases - Ras and Rho
4.4K
Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
Three regulatory proteins control their activity:
4.4K

