The effect on melanoma risk of genes previously associated with telomere length.

OA: gold CC-BY-4.0
AI-generated summary by qwen3.7-flash, 2026-08-14

This study found that a genetic score predicting telomere length is strongly associated with melanoma risk, demonstrating that germline determinants of telomere length influence cancer risk.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by qwen3.7-flash, 2026-08-14 · read from full text

The provided text consists exclusively of funding acknowledgments and grant information for the GenoMEL study, Wellcome Trust Case Control Consortium, and various international research centers. It lists specific financial support from organizations such as the European Commission, Cancer Research UK, and multiple national health institutes across Europe, North America, and Australia. The document details the monetary contributions and fellowship awards that supported data collection and analysis for melanoma genetics and related conditions like endometriosis and inflammatory bowel disease. Relevance to endometriosis: listed as a funded condition within the QIMR Endometriosis study section, though the paper's main focus is melanoma risk and telomere length genes.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Telomere length has been associated with risk of many cancers, but results are inconsistent. Seven single nucleotide polymorphisms (SNPs) previously associated with mean leukocyte telomere length were either genotyped or well-imputed in 11108 case patients and 13933 control patients from Europe, Israel, the United States and Australia, four of the seven SNPs reached a P value under .05 (two-sided). A genetic score that predicts telomere length, derived from these seven SNPs, is strongly associated (P = 8.92x10(-9), two-sided) with melanoma risk. This demonstrates that the previously observed association between longer telomere length and increased melanoma risk is not attributable to confounding via shared environmental effects (such as ultraviolet exposure) or reverse causality. We provide the first proof that multiple germline genetic determinants of telomere length influence cancer risk.
Full text 5,364 characters · extracted from pmc-nxml · 1 sections · click to expand

Funding

The GenoMEL study ( http://www.genomel.org/ ) was funded by the European Commission under the 6 th Framework Programme (contract no. LSHC-CT-2006–018702), by Cancer Research UK Programme Awards (C588/A4994 and C588/A10589), by a Cancer Research UK Project Grant (C8216/A6129), and by a grant from the US National Institutes of Health ( NIH ; CA83115 ). This research was also supported by the intramural Research Program of the NIH, National Cancer Institute (NCI), Division of Cancer Epidemiology and Genetics. Funding for the Wellcome Trust Case Control Consortium project was provided by the Wellcome Trust under award 076113. Funding specific to particular centers is given below: Stockholm: Swedish Cancer Society, Karolinska Institutet’s research funds. Lund: Swedish Cancer Society, Gunnar Nilsson Foundation and European Research Council Advanced Grant (ERC-2011–294576).Genoa: Italian Ministry of Education, University and Research PRIN 2008, IMI and Mara Naum foundation. University of Genoa (PRA 2012 D31J13000000005 to PG). Intergruppo Melanoma Italiano and Mara Naum foundation to GBS Emilia Romagna: Intramural Research Program of National Institutes of Health, National Cancer Institute, Division of Cancer Epidemiology and Genetics. Paris: Grants from Institut National du Cancer (INCa-PL016) and Ligue Nationale Contre Le Cancer (PRE05/FD and PRE 09/FD) to FD, Programme Hospitalier de Recherche Clinique (AOM-07-195) to MFA and FD. Ligue Nationale Contre Le Cancer doctoral fellowship to MB. Leiden: Grant provided by European Biobanking and Biomolecular Resources Research Infrastructure (BBMRI)−Netherlands hub (CO18). Spain: The research at the Melanoma Unit in Barcelona is partially funded by Grants from Fondo de Investigaciones Sanitarias PI, 09/01393, Spain; by the CIBER de Enfermedades Raras of the Instituto de Salud Carlos III, Spain; by the AGAUR 2009 SGR 1337 of the Catalan Government, Spain. Norway: Grants from the Comprehensive Cancer Center, Oslo University Hospital (SE0728), and the Norwegian Cancer Society (71512-PR-2006-0356). Houston (MD Anderson): Support by the National Institutes of Health/National Cancer Institute (2P50CA093459 and P30CA023108), and by the Marit Peterson Fund for Melanoma Research. Australian Melanoma Family Study (AMFS): AMFS is supported by the National Health and Medical Research Council of Australia (NHMRC) (project grants 566946, 107359, 211172 and program grant number 402761 to GJM and RFK); the Cancer Council New South Wales (project grant 77/00, 06/10), the Cancer Council Victoria and the Cancer Council Queensland (project grant 371); the US National Institutes of Health (via NIH RO1 grant CA-83115-01A2 to the International Melanoma Genetics Consortium - GenoMEL) and a Victorian Cancer Agency Early Career Seed Grant (ECSG07_010). AEC is supported by fellowships from the Cancer Institute NSW (10/ECF/2–06) and NHMRC (520018). Brisbane: SM is supported by fellowships from the Australian National Health and Medical Research Council and the Australian Research Council. MHL is supported by Cancer Australia grant 1011143. Western Australian Melanoma Health Study (WAMHS): The WAMHS gratefully acknowledges all study participants for their time and contributions, and the Western Australian DNA Bank and the Ark at the University of Western Australia for biospecimen and bioinformatics related support. The Western Australian Cancer Registry, the WAMHS study team and the WAMHS Management Committee are also gratefully acknowledged for their assistance, as well as the Scott Kirkbride Melanoma Research Centre for funding the establishment of the WAMHS resource and related salaries and PhD stipends. Q-MEGA and QTWIN: The Q-MEGA/QTWIN studies were supported by the Melanoma Research Alliance, the NIH NCI (CA88363, CA83115, CA122838, CA87969, CA055075, CA100264, CA133996, and CA49449), the National Health and Medical Research Council of Australia (NHMRC) (200071, 241944, 339462, 380385, 389927, 389875, 389891, 389892, 389938, 443036, 442915, 442981, 496610, 496675, 496739, 552485, 552498), the Cancer Councils New South Wales, Victoria and Queensland, the Cancer Institute New South Wales, the Cooperative Research Centre for Discovery of Genes for Common Human Diseases (CRC), Cerylid Biosciences (Melbourne), the Australian Cancer Research Foundation, the Wellcome Trust (WT084766/Z/08/Z), and donations from Neville and Shirley Hawkins. QIMR Endometriosis study: The QIMR Study was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia ( 496610 ), the Cooperative Research Centre for Discovery of Genes for Common Human Diseases (CRC) and Cerylid Biosciences (Melbourne). Endometriosis sample genotyping was funded by grants from the NHMRC ( 496610 ) and Wellcome Trust (WT084766/Z/08/Z). GWM was supported by an NHMRC Fellowship ( 339446 , 619667 ). Study of Digestive Health (SDH): The SDH was supported by the National Cancer Institute ( 5 RO1 CA 001833-02 ). Inflammatory Bowel Disease study (IBD): This research was supported by the United States National Cancer Institute (grant number CA 001833-03 ). DCW is a Senior Research Fellow of the National Health and Medical Research Council of Australia. NP was supported by a PhD scholarship from the National Health and Medical Research Council of Australia.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: pmc-nxml

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

europepmc
last seen: 2026-08-16T09:21:09.727480+00:00
License: CC-BY-4.0 · commercial use OK · attribution required
Per Europe PMC