TY - JOUR
T1 - Distinctive Tumor Biology of MSI-High Colorectal Cancer
AU - Majithia, Neil
AU - Kipp, Benjamin R.
AU - Grothey, Axel
N1 - Funding Information:
Axel Grothey has received support through research grants to the Mayo Foundation from Genentech, Bayer, Eisai, BBI, and Eli Lilly.
Funding Information:
Benjamin R. Kipp has received support through a grant from Abbott Molecular, Inc.
Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2015/10/28
Y1 - 2015/10/28
N2 - 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.
AB - 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.
KW - Chromosomal instability
KW - Colorectal cancer
KW - Microsatellite instability
KW - Mismatch repair deficiency
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U2 - 10.1007/s11888-015-0283-4
DO - 10.1007/s11888-015-0283-4
M3 - Review article
AN - SCOPUS:84940452530
VL - 11
SP - 281
EP - 287
JO - Current Colorectal Cancer Reports
JF - Current Colorectal Cancer Reports
SN - 1556-3790
IS - 5
ER -