Related Experiment Video
Updated: Jan 15, 2026

28:15
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
12.7K
Clinicopathological Characteristics With the Status of Mismatch Repair Deficient Invasive Colorectal Cancer With
Fumiya Okano1, Naohisa Yoshida2, Yukiko Morinaga3
1Department of Gastroenterology National Hospital Organization Maizuru Medical Center Kyoto Japan.
DEN Open
|October 8, 2025
Summary
Spontaneous regression of colorectal cancer (CRC) after biopsy is rare. This study found three cases of endoscopically invasive CRC that regressed after biopsy, with two showing mismatch repair deficiency (MMR-d).
Area of Science:
- Gastroenterology
- Oncology
- Pathology
Background:
- Spontaneous regression of endoscopically invasive colorectal cancer (CRC) following biopsy is exceptionally rare.
- Mismatch repair deficiency (MMR-d) is a known factor in some cancers, but its role in CRC regression is not fully understood.
Purpose of the Study:
- To report three novel cases of endoscopically invasive CRC that underwent spontaneous regression after biopsy.
- To review the literature for similar cases of CRC with spontaneous regression, particularly those associated with MMR deficiency.
Main Methods:
- Case series reporting three patients with endoscopically invasive CRC.
- Literature review of studies investigating spontaneous regression of CRC and MMR status.
- Analysis of lesion characteristics, including location and morphology, and MMR status.
Main Results:
- Three patients with endoscopically invasive CRC experienced complete regression of their lesions after biopsy.
- Two of the three patients had tumors with mismatch repair deficiency (MMR-d).
- A literature review identified 12 cases (including these three) of spontaneously regressing CRC, with 11 showing MMR-d and all 12 lesions having a depressed morphology.
Conclusions:
- Spontaneous regression of endoscopically invasive colorectal cancer after biopsy can occur, particularly in cases with MMR deficiency.
- Depressed morphology and proximal colon location appear to be associated with spontaneously regressing CRC.
- Further research is warranted to understand the mechanisms behind MMR-d-associated CRC regression.
Related Concept Videos
Mismatch Repair
6.3K
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...
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...
6.3K
Mismatch Repair
43.5K
Overview
43.5K
Tumor Progression
7.2K
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...
7.2K
Restarting Stalled Replication Forks
6.3K
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
6.3K
Abnormal Proliferation
5.1K
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...
5.1K
Cancers Originate from Somatic Mutations in a Single Cell
14.6K
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...
14.6K

