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000125748 0247_ $$2ISSN$$a2162-402X
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000125748 041__ $$aeng
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000125748 1001_ $$aEchterdiek, Fabian$$b0
000125748 245__ $$aLow density of FOXP3-positive T cells in normal colonic mucosa is related to the presence of beta2-microglobulin mutations in Lynch syndrome-associated colorectal cancer.
000125748 260__ $$aAustin, Tex.$$bLandes Bioscience$$c2016
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000125748 520__ $$aMicrosatellite 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.
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000125748 7001_ $$0P:(DE-HGF)0$$aJanikovits, Jonas$$b1
000125748 7001_ $$0P:(DE-HGF)0$$aStaffa, Laura$$b2
000125748 7001_ $$0P:(DE-HGF)0$$aMüller, Meike$$b3
000125748 7001_ $$aLahrmann, Bernd$$b4
000125748 7001_ $$0P:(DE-HGF)0$$aFrühschütz, Monika$$b5
000125748 7001_ $$0P:(DE-HGF)0$$aHartog, Benjamin$$b6
000125748 7001_ $$0P:(DE-He78)af4b1091bd23a160b527ee39101ed100$$aNelius, Nina$$b7$$udkfz
000125748 7001_ $$0P:(DE-He78)e15dfa1260625c69d6690a197392a994$$aBenner, Axel$$b8$$udkfz
000125748 7001_ $$aTariverdian, Mirjam$$b9
000125748 7001_ $$0P:(DE-He78)11747cd1dc061b9333c0e3a3ff31bf2f$$avon Knebel Doeberitz, Magnus$$b10$$udkfz
000125748 7001_ $$aGrabe, Niels$$b11
000125748 7001_ $$0P:(DE-HGF)0$$aKloor, Matthias$$b12$$eLast author
000125748 773__ $$0PERI:(DE-600)2645309-5$$a10.1080/2162402X.2015.1075692$$gVol. 5, no. 2, p. e1075692 -$$n2$$pe1075692 -$$tOncoImmunology$$v5$$x2162-402X$$y2016
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