Distinctive Tumor Biology of MSI-High Colorectal Cancer

Neil Majithia, Benjamin R. Kipp, Axel F Grothey

Research output: Contribution to journalArticle

1 Citation (Scopus)

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 languageEnglish (US)
Pages (from-to)281-287
Number of pages7
JournalCurrent Colorectal Cancer Reports
Volume11
Issue number5
DOIs
StatePublished - Jul 23 2015

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Epigenomics
Colorectal Neoplasms
Hereditary Nonpolyposis Colorectal Neoplasms
Microsatellite Instability
Mutation
DNA Mismatch Repair
Immune System
Neoplasms
Phenotype
N-methylsuccinimide
Therapeutics
MutL Protein Homolog 1

Keywords

  • Chromosomal instability
  • Colorectal cancer
  • Microsatellite instability
  • Mismatch repair deficiency

ASJC Scopus subject areas

  • Oncology
  • Gastroenterology
  • Hepatology

Cite this

Distinctive Tumor Biology of MSI-High Colorectal Cancer. / Majithia, Neil; Kipp, Benjamin R.; Grothey, Axel F.

In: Current Colorectal Cancer Reports, Vol. 11, No. 5, 23.07.2015, p. 281-287.

Research output: Contribution to journalArticle

Majithia, Neil ; Kipp, Benjamin R. ; Grothey, Axel F. / Distinctive Tumor Biology of MSI-High Colorectal Cancer. In: Current Colorectal Cancer Reports. 2015 ; Vol. 11, No. 5. pp. 281-287.
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