% 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{TenBroeke:148599, author = {S. W. Ten Broeke and H. M. van der Klift and C. M. J. Tops and S. Aretz and I. Bernstein and D. D. Buchanan and A. de la Chapelle and G. Capella and M. Clendenning and C. Engel and S. Gallinger and E. Gomez Garcia and J. C. Figueiredo and R. Haile and H. L. Hampel and J. L. Hopper and N. Hoogerbrugge and M. von Knebel Doeberitz$^*$ and L. Le Marchand and T. G. W. Letteboer and M. A. Jenkins and A. Lindblom and N. M. Lindor and A. R. Mensenkamp and P. Møller and P. A. Newcomb and T. A. M. van Os and R. Pearlman and M. Pineda and N. Rahner and E. J. W. Redeker and M. J. W. Olderode-Berends and C. Rosty and H. K. Schackert and R. Scott and L. Senter and L. Spruijt and V. Steinke-Lange and M. Suerink and S. Thibodeau and Y. J. Vos and A. Wagner and I. Winship and F. J. Hes and H. F. A. Vasen and J. T. Wijnen and M. Nielsen and A. K. Win}, title = {{C}ancer {R}isks for {PMS}2-{A}ssociated {L}ynch {S}yndrome.}, journal = {Journal of clinical oncology}, volume = {36}, number = {29}, issn = {1527-7755}, address = {Alexandria, Va.}, publisher = {American Society of Clinical Oncology}, reportid = {DKFZ-2019-03147}, pages = {2961 - 2968}, year = {2018}, abstract = {Lynch syndrome due to pathogenic variants in the DNA mismatch repair genes MLH1, MSH2, and MSH6 is predominantly associated with colorectal and endometrial cancer, although extracolonic cancers have been described within the Lynch tumor spectrum. However, the age-specific cumulative risk (penetrance) of these cancers is still poorly defined for PMS2-associated Lynch syndrome. Using a large data set from a worldwide collaboration, our aim was to determine accurate penetrance measures of cancers for carriers of heterozygous pathogenic PMS2 variants.A modified segregation analysis was conducted that incorporated both genotyped and nongenotyped relatives, with conditioning for ascertainment to estimates corrected for bias. Hazard ratios (HRs) and corresponding $95\%$ CIs were estimated for each cancer site for mutation carriers compared with the general population, followed by estimation of penetrance.In total, 284 families consisting of 4,878 first- and second-degree family members were included in the analysis. PMS2 mutation carriers were at increased risk for colorectal cancer (cumulative risk to age 80 years of $13\%$ $[95\%$ CI, $7.9\%$ to $22\%]$ for males and $12\%$ $[95\%$ CI, $6.7\%$ to $21\%]$ for females) and endometrial cancer $(13\%$ $[95\%$ CI, $7.0\%-24\%]),$ compared with the general population $(6.6\%,$ $4.7\%,$ and $2.4\%,$ respectively). There was no clear evidence of an increased risk of ovarian, gastric, hepatobiliary, bladder, renal, brain, breast, prostate, or small bowel cancer.Heterozygous PMS2 mutation carriers were at small increased risk for colorectal and endometrial cancer but not for any other Lynch syndrome-associated cancer. This finding justifies that PMS2-specific screening protocols could be restricted to colonoscopies. The role of risk-reducing hysterectomy and bilateral salpingo-oophorectomy for PMS2 mutation carriers needs further discussion.}, keywords = {PMS2 protein, human (NLM Chemicals) / Mismatch Repair Endonuclease PMS2 (NLM Chemicals)}, cin = {G105}, ddc = {610}, cid = {I:(DE-He78)G105-20160331}, pnm = {316 - Infections and cancer (POF3-316)}, pid = {G:(DE-HGF)POF3-316}, typ = {PUB:(DE-HGF)16}, pubmed = {pmid:30161022}, pmc = {pmc:PMC6349460}, doi = {10.1200/JCO.2018.78.4777}, url = {https://inrepo02.dkfz.de/record/148599}, }