Commentaries

Foxp3 and microsatellite stability phenotype in colorectal cancer

Christoph Loddenkemper¹, Dirk Nagorsen², Martin Zeitz³

¹ Institute of Pathology/Research Center ImmunoSciences (RCIS), Charité–Universitätsmedizin Berlin, Berlin, Germany
² Medical Clinic for Hematology and Oncology, Charité–Universitätsmedizin Berlin, Berlin, Germany
³ Medical Clinic for Gastroenterology, Rheumatology and Infectiology, Charité–Universitätsmedizin Berlin, Berlin, Germany

Correspondence to:
Professor C Loddenkemper, Institut für Pathologie, Campus Benjamin Franklin, Charité–Universitätsmedizin Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany; christoph.loddenkemper@charite.de

The first 150 words of the full text of this article appear below.

Colorectal tumourigenesis is in the majority of cases regarded as a multistep process resulting in chromosomal instability.¹ High-frequency microsatellite instability (MSI-H) can be detected in 15–20% of all sporadic colorectal cancers (CRCs) and represents the hallmark of the hereditary non-polyposis colorectal cancer (HNPCC) syndrome. CRCs with MSI-H are caused by inactivation of DNA mismatch repair (MMR) genes leading to hundreds of insertion or deletion mutations in short segments of repeated nucleotide sequences, but no chromosomal instability. It has been speculated that abnormal peptides are generated as a consequence of these frameshift mutations, and one would expect a stimulation of the antitumour response by these tumour-associated antigens (TAAs).^{2 3} In fact, CRCs with MSI-H are associated with a markedly increased number of tumour-infiltrating lymphocytes (TILs) as compared with microsatellite-stable (MSS) tumours, and the favourable prognosis of patients with MSI-H cancer has been attributed to the high content of cytotoxic T cells.⁴

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