% IMPORTANT: The following is UTF-8 encoded. This means that in the presence % of non-ASCII characters, it will not work with BibTeX 0.99 or older. % Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or % “biber”. @ARTICLE{Echterdiek:125748, author = {F. Echterdiek and J. Janikovits$^*$ and L. Staffa$^*$ and M. Müller$^*$ and B. Lahrmann and M. Frühschütz$^*$ and B. Hartog$^*$ and N. Nelius$^*$ and A. Benner$^*$ and M. Tariverdian and M. von Knebel Doeberitz$^*$ and N. Grabe and M. Kloor$^*$}, title = {{L}ow density of {FOXP}3-positive {T} cells in normal colonic mucosa is related to the presence of beta2-microglobulin mutations in {L}ynch syndrome-associated colorectal cancer.}, journal = {OncoImmunology}, volume = {5}, number = {2}, issn = {2162-402X}, address = {Austin, Tex.}, publisher = {Landes Bioscience}, reportid = {DKFZ-2017-01874}, pages = {e1075692 -}, year = {2016}, abstract = {Microsatellite instability (MSI-H) is caused by DNA mismatch repair deficiency and occurs in $15\%$ of colorectal cancers. MSI-H cancers generate highly immunogenic frameshift peptide (FSP) antigens, which elicit pronounced local immune responses. A subset of MSI-H colorectal cancers develops in frame of Lynch syndrome, which represents an ideal human model for studying the concept of immunoediting. Immunoediting describes how continuous anti-tumoral immune surveillance of the host eventually leads to the selection of tumor cells that escape immune cell recognition and destruction. Between 30 and $40\%$ of Lynch syndrome-associated colorectal cancers display loss of HLA class I antigen expression as a result of Beta2-microglobulin (B2M) mutations. Whether B2M mutations result from immunoediting has been unknown. To address this question, we related B2M mutation status of Lynch syndrome-associated colorectal cancer specimens (n = 30) to CD3-positive, CD8-positive and FOXP3-positive T cell infiltration in both tumor and normal mucosa. No significant correlation between B2M mutations and immune cell infiltration was observed in tumor tissue. However, FOXP3-positive T cell infiltration was significantly lower in normal mucosa adjacent to B2M-mutant (mt) compared to B2M-wild type (wt) tumors (mean: $0.98\%$ FOXP3-positive area/region of interest (ROI) in B2M-wt vs. $0.52\%$ FOXP3-positive area/ROI in B2M-mt, p = 0.023). Our results suggest that in the absence of immune-suppressive regulatory T cells (Treg), the outgrowth of less immunogenic B2M-mt tumor cells is favored. This finding supports the immunoediting concept in human solid cancer development and indicates a critical role of the immune milieu in normal colonic mucosa for the course of disease.}, cin = {G105 / C060}, ddc = {610}, cid = {I:(DE-He78)G105-20160331 / I:(DE-He78)C060-20160331}, pnm = {317 - Translational cancer research (POF3-317)}, pid = {G:(DE-HGF)POF3-317}, typ = {PUB:(DE-HGF)16}, pubmed = {pmid:27057447}, pmc = {pmc:PMC4801455}, doi = {10.1080/2162402X.2015.1075692}, url = {https://inrepo02.dkfz.de/record/125748}, }