Mismatch repair deficient colorectal cancer in the era of personalized treatment
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Updated: Jun 16, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
Published on: July 28, 2010
Madeleine Hewish1, Christopher J Lord, Sarah A Martin
1Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK.
Abstract:
The molecular and genetic subtyping of cancer has allowed the emergence of individualized therapies. This approach could potentially deliver treatments that have both increased efficacy as well as reduced toxicity. A well-defined subtype of colorectal cancer (CRC) is characterized by a deficiency in the mismatch repair (MMR) pathway. MMR deficiency not only contributes to the pathogenesis of a large proportion of CRC, but also determines the response to many of the drugs that are frequently used to treat this disease. In this Review we describe the MMR deficient phenotype and discuss how a deficiency in this DNA repair process may impact on the management of CRC, including surgery, adjuvant chemotherapy and the choice of systemic agents for the palliation of advanced disease. We also discuss how the DNA repair defect in MMR deficient CRC could be exploited in the development of novel therapeutic strategies.
Insights
Mismatch repair (MMR) deficiency is a key subtype of colorectal cancer (CRC). Understanding MMR deficiency impacts CRC management and offers potential for novel therapeutic strategies.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Molecular and genetic subtyping enables individualized cancer therapies with improved efficacy and reduced toxicity.
- A significant subset of colorectal cancer (CRC) exhibits a deficiency in the mismatch repair (MMR) pathway.
- MMR deficiency plays a role in CRC development and influences patient response to common treatments.
Purpose of the Study:
- To describe the MMR deficient phenotype in colorectal cancer.
- To discuss the impact of MMR deficiency on CRC management, including surgery, chemotherapy, and palliative care.
- To explore the potential of exploiting the DNA repair defect in MMR-deficient CRC for novel therapeutic development.
Main Methods:
- Review of existing literature on MMR deficiency in colorectal cancer.
- Analysis of the role of MMR pathway in CRC pathogenesis.
- Discussion of clinical implications for treatment strategies.
Main Results:
- MMR deficiency is a critical determinant in colorectal cancer.
- This deficiency affects treatment responses and management strategies across different stages of CRC.
- The DNA repair defect presents opportunities for innovative therapeutic approaches.
Conclusions:
- MMR deficiency is a crucial factor in colorectal cancer management and treatment.
- Targeting the DNA repair defect in MMR-deficient CRC holds promise for future therapies.
- Individualized treatment strategies based on MMR status can optimize CRC patient outcomes.
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