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@ARTICLE{Papadimitriou:288088,
      author       = {N. Papadimitriou and C. Qu and T. A. Harrison and A. M.
                      Bever and R. M. Martin and K. K. Tsilidis and P. A. Newcomb
                      and S. N. Thibodeau and C. C. Newton and C. Y. Um and M.
                      Obón-Santacana and V. Moreno and H. Brenner$^*$ and M.
                      Mandic$^*$ and J. Chang-Claude$^*$ and M. Hoffmeister$^*$
                      and A. J. Pellatt and R. E. Schoen and S. Harlid and S.
                      Ogino and T. Ugai and D. D. Buchanan and B. M. Lynch and S.
                      B. Gruber and Y. Cao and L. Hsu and J. R. Huyghe and Y. Lin
                      and R. S. Steinfelder and W. Sun and B. Van Guelpen and S.
                      H. Zaidi and A. E. Toland and S. I. Berndt and W.-Y. Huang
                      and E. K. Aglago and D. A. Drew and A. J. French and P.
                      Georgeson and M. Giannakis and M. Hullar and J. A. Nowak and
                      C. E. Thomas and L. Le Marchand and I. Cheng and S.
                      Gallinger and M. A. Jenkins and M. J. Gunter and P. T.
                      Campbell and U. Peters and M. Song and A. I. Phipps and N.
                      Murphy},
      title        = {{B}ody size and risk of colorectal cancer molecular defined
                      subtypes and pathways: {M}endelian randomization analyses.},
      journal      = {EBioMedicine},
      volume       = {101},
      issn         = {2352-3964},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-00342},
      pages        = {105010},
      year         = {2024},
      abstract     = {Obesity has been positively associated with most molecular
                      subtypes of colorectal cancer (CRC); however, the magnitude
                      and the causality of these associations is uncertain.We used
                      Mendelian randomization (MR) to examine potential causal
                      relationships between body size traits (body mass index
                      [BMI], waist circumference, and body fat percentage) with
                      risks of Jass classification types and individual subtypes
                      of CRC (microsatellite instability [MSI] status, CpG island
                      methylator phenotype [CIMP] status, BRAF and KRAS
                      mutations). Summary data on tumour markers were obtained
                      from two genetic consortia (CCFR, GECCO).A 1-standard
                      deviation (SD:5.1 kg/m2) increment in BMI levels was found
                      to increase risks of Jass type
                      1MSI-high,CIMP-high,BRAF-mutated,KRAS-wildtype (odds ratio
                      [OR]: 2.14, $95\%$ confidence interval [CI]: 1.46, 3.13;
                      p-value = 9 × 10-5) and Jass type
                      2non-MSI-high,CIMP-high,BRAF-mutated,KRAS-wildtype CRC (OR:
                      2.20, $95\%$ CI: 1.26, 3.86; p-value = 0.005). The magnitude
                      of these associations was stronger compared with Jass type
                      4non-MSI-high,CIMP-low/negative,BRAF-wildtype,KRAS-wildtype
                      CRC (p-differences: 0.03 and 0.04, respectively). A 1-SD
                      (SD:13.4 cm) increment in waist circumference increased risk
                      of Jass type
                      3non-MSI-high,CIMP-low/negative,BRAF-wildtype,KRAS-mutated
                      (OR 1.73, $95\%$ CI: 1.34, 2.25; p-value = 9 × 10-5) that
                      was stronger compared with Jass type 4 CRC (p-difference:
                      0.03). A higher body fat percentage $(SD:8.5\%)$ increased
                      risk of Jass type 1 CRC (OR: 2.59, $95\%$ CI: 1.49, 4.48;
                      p-value = 0.001), which was greater than Jass type 4 CRC
                      (p-difference: 0.03).Body size was more strongly linked to
                      the serrated (Jass types 1 and 2) and alternate (Jass type
                      3) pathways of colorectal carcinogenesis in comparison to
                      the traditional pathway (Jass type 4).Cancer Research UK,
                      National Institute for Health Research, Medical Research
                      Council, National Institutes of Health, National Cancer
                      Institute, American Institute for Cancer Research, Brigham
                      and Women's Hospital, Prevent Cancer Foundation, Victorian
                      Cancer Agency, Swedish Research Council, Swedish Cancer
                      Society, Region Västerbotten, Knut and Alice Wallenberg
                      Foundation, Lion's Cancer Research Foundation,
                      Insamlingsstiftelsen, Umeå University. Full funding details
                      are provided in acknowledgements.},
      keywords     = {Colorectal cancer (Other) / Mendelian randomization (Other)
                      / Molecular subtypes (Other) / Obesity (Other)},
      cin          = {C070 / C120 / HD01 / C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C070-20160331 / I:(DE-He78)C120-20160331 /
                      I:(DE-He78)HD01-20160331 / I:(DE-He78)C020-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38350331},
      doi          = {10.1016/j.ebiom.2024.105010},
      url          = {https://inrepo02.dkfz.de/record/288088},
}