Distinctive Tumor Biology of MSI-High Colorectal Cancer

Neil Majithia; Benjamin R. Kipp; Axel F Grothey

doi:10.1007/s11888-015-0283-4

Distinctive Tumor Biology of MSI-High Colorectal Cancer

Neil Majithia, Benjamin R. Kipp, Axel F Grothey

Medical Oncology

Research output: Contribution to journal › Article › peer-review

1 Scopus citations

Abstract

High-frequency microsatellite instability (MSI-H) accounts for roughly 15 % of all cases of colorectal cancer (CRC) and results from pathogenic mutations or epigenetic changes in mismatch repair (MMR) proteins, primarily MLH1, MSH2, MSH6, and PMS2. These alterations can be inherited, as in the case of Lynch syndrome, or can be acquired sporadically, including cases of epigenetic alteration along crucial regulatory sequences. Cancers that develop in the setting of MSI-H possess a unique clinicopathologic phenotype, with a high degree of mutation resulting in potential recognition by the immune system. These features have directed therapeutic investigation in recent years to involve consideration of immune-stimulating agents, which might exploit the inherent immunogenicity of these tumors.

Original language	English (US)
Pages (from-to)	281-287
Number of pages	7
Journal	Current Colorectal Cancer Reports
Volume	11
Issue number	5
DOIs	https://doi.org/10.1007/s11888-015-0283-4
State	Published - Jul 23 2015

Keywords

Chromosomal instability
Colorectal cancer
Microsatellite instability
Mismatch repair deficiency

ASJC Scopus subject areas

Oncology
Gastroenterology
Hepatology

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abstract = "High-frequency microsatellite instability (MSI-H) accounts for roughly 15 % of all cases of colorectal cancer (CRC) and results from pathogenic mutations or epigenetic changes in mismatch repair (MMR) proteins, primarily MLH1, MSH2, MSH6, and PMS2. These alterations can be inherited, as in the case of Lynch syndrome, or can be acquired sporadically, including cases of epigenetic alteration along crucial regulatory sequences. Cancers that develop in the setting of MSI-H possess a unique clinicopathologic phenotype, with a high degree of mutation resulting in potential recognition by the immune system. These features have directed therapeutic investigation in recent years to involve consideration of immune-stimulating agents, which might exploit the inherent immunogenicity of these tumors.",

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