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000182209 1001_ $$0P:(DE-He78)07eef6d38a91f4642c810745c5bf5000$$aAhadova, Aysel$$b0$$eFirst author$$udkfz
000182209 245__ $$aIs HLA type a possible cancer risk modifier in Lynch syndrome?
000182209 260__ $$aBognor Regis$$bWiley-Liss$$c2023
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000182209 500__ $$a#EA:F210#LA:F210# / 2023 May 15;152(10):2024-2031
000182209 520__ $$aLynch syndrome (LS) is the most common inherited cancer syndrome. It is inherited via a monoallelic germline variant in one of the DNA mismatch repair (MMR) genes. LS carriers have a broad 30% to 80% risk of developing various malignancies, and more precise, individual risk estimations would be of high clinical value, allowing tailored cancer prevention and surveillance. Due to MMR deficiency, LS cancers are characterized by the accumulation of frameshift mutations leading to highly immunogenic frameshift peptides (FSPs). Thus, immune surveillance is proposed to inhibit the outgrowth of MMR-deficient cell clones. Recent studies have shown that immunoediting during the evolution of MMR-deficient cancers leads to a counter-selection of highly immunogenic antigens. The immunogenicity of FSPs is dependent on the antigen presentation. One crucial factor determining antigen presentation is the HLA genotype. Hence, a LS carrier's HLA genotype plays an important role in the presentation of FSP antigens to the immune system, and may influence the likelihood of progression from precancerous lesions to cancer. To address the challenge of clarifying this possibility including diverse populations with different HLA types, we have established the INDICATE initiative (Individual cancer risk by HLA type, http://indicate-lynch.org/), an international network aiming at a systematic evaluation of the HLA genotype as a possible cancer risk modifier in LS. Here we summarize the current knowledge on the role of HLA type in cancer risk and outline future research directions to delineate possible association in the scenario of LS with genetically defined risk population and highly immunogenic tumors.
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000182209 650_7 $$2Other$$aHLA genotype
000182209 650_7 $$2Other$$aLynch syndrome
000182209 650_7 $$2Other$$acancer immunoediting
000182209 650_7 $$2Other$$aimmune surveillance
000182209 650_7 $$2Other$$apersonalized cancer risk
000182209 7001_ $$0P:(DE-HGF)0$$aWitt, Johannes$$b1
000182209 7001_ $$aHaupt, Saskia$$b2
000182209 7001_ $$aGallon, Richard$$b3
000182209 7001_ $$aHüneburg, Robert$$b4
000182209 7001_ $$aNattermann, Jacob$$b5
000182209 7001_ $$aTen Broeke, Sanne$$b6
000182209 7001_ $$0P:(DE-He78)a7f54298fcba548e34453b02202e6519$$aBohaumilitzky, Lena$$b7$$udkfz
000182209 7001_ $$0P:(DE-HGF)0$$aHernandez-Sanchez, Alejandro$$b8
000182209 7001_ $$aSantibanez-Koref, Mauro$$b9
000182209 7001_ $$aJackson, Michael S$$b10
000182209 7001_ $$aAhtiainen, Maarit$$b11
000182209 7001_ $$aPylvänäinen, Kirsi$$b12
000182209 7001_ $$aAndini, Katarina$$b13
000182209 7001_ $$aGrolmusz, Vince Kornel$$b14
000182209 7001_ $$aMöslein, Gabriela$$b15
000182209 7001_ $$00000-0001-7856-0057$$aDominguez-Valentin, Mev$$b16
000182209 7001_ $$aMøller, Pål$$b17
000182209 7001_ $$aFürst, Daniel$$b18
000182209 7001_ $$aSijmons, Rolf$$b19
000182209 7001_ $$aBorthwick, Gillian M$$b20
000182209 7001_ $$aBurn, John$$b21
000182209 7001_ $$aMecklin, Jukka-Pekka$$b22
000182209 7001_ $$aHeuveline, Vincent$$b23
000182209 7001_ $$0P:(DE-He78)11747cd1dc061b9333c0e3a3ff31bf2f$$avon Knebel Doeberitz, Magnus$$b24$$udkfz
000182209 7001_ $$aSeppälä, Toni$$b25
000182209 7001_ $$0P:(DE-He78)3121b75683af3772ca9289d447889ed9$$aKloor, Matthias$$b26$$eLast author
000182209 773__ $$0PERI:(DE-600)1474822-8$$a10.1002/ijc.34312$$gp. ijc.34312$$n10$$p2024-2031$$tInternational journal of cancer$$v152$$x0020-7136$$y2023
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