David J Hunter

Durham University, Durham, England, United Kingdom

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Publications (572)6287.86 Total impact

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    ABSTRACT: Background: Epidemiological studies have linked adult height with breast cancer risk in women. However, the magnitude of the association, particularly by subtypes of breast cancer, has not been established. Furthermore, the mechanisms of the association remain unclear. Methods: We performed a meta-analysis to investigate associations between height and breast cancer risk using data from 159 prospective cohorts totaling 5216302 women, including 113178 events. In a consortium with individual-level data from 46325 case patients and 42482 control patients, we conducted a Mendelian randomization analysis using a genetic score that comprised 168 height-associated variants as an instrument. This association was further evaluated in a second consortium using summary statistics data from 16003 case patients and 41335 control patients. Results: The pooled relative risk of breast cancer was 1.17 (95% confidence interval [CI] = 1.15 to 1.19) per 10cm increase in height in the meta-analysis of prospective studies. In Mendelian randomization analysis, the odds ratio of breast cancer per 10cm increase in genetically predicted height was 1.22 (95% CI = 1.13 to 1.32) in the first consortium and 1.21 (95% CI = 1.05 to 1.39) in the second consortium. The association was found in both premenopausal and postmenopausal women but restricted to hormone receptor-positive breast cancer. Analyses of height-associated variants identified eight new loci associated with breast cancer risk after adjusting for multiple comparisons, including three loci at 1q21.2, DNAJC27, and CCDC91 at genome-wide significance level P < 5×10(-8). Conclusions: Our study provides strong evidence that adult height is a risk factor for breast cancer in women and certain genetic factors and biological pathways affecting adult height have an important role in the etiology of breast cancer.
    Journal of the National Cancer Institute 08/2015; 107(11). DOI:10.1093/jnci/djv219 · 12.58 Impact Factor
  • David J Hunter · Ralph B D'Agostino
    New England Journal of Medicine 08/2015; 373(8):691-3. DOI:10.1056/NEJMp1508144 · 55.87 Impact Factor
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    ABSTRACT: Considerable resources are spent on research to establish what works to improve the nation’s health. If the findings from this research are used, better health outcomes can follow, but we know that these findings are not always used. In public health, evidence of what works may not ‘fit’ everywhere, making it difficult to know what to do locally. Research suggests that evidence use is a social and dynamic process, not a simple application of research findings. It is unclear whether it is easier to get evidence used via a legal contracting process or within unified organisational arrangements with shared responsibilities. Objective To work in cocreation with research participants to investigate how research is utilised and knowledge mobilised in the commissioning and planning of public health services to reduce alcohol-related harms. Design, setting and participants Two in-depth, largely qualitative, cross-comparison case studies were undertaken to compare real-time research utilisation in commissioning across a purchaser–provider split (England) and in joint planning under unified organisational arrangements (Scotland) to reduce alcohol-related harms. Using an overarching realist approach and working in cocreation, case study partners (stakeholders in the process) picked the topic and helped to interpret the findings. In Scotland, the topic picked was licensing; in England, it was reducing maternal alcohol consumption. Methods Sixty-nine interviews, two focus groups, 14 observations of decision-making meetings, two local feedback workshops ( n = 23 and n = 15) and one national workshop ( n = 10) were undertaken. A questionnaire ( n = 73) using a Behaviourally Anchored Rating Scale was issued to test the transferability of the 10 main findings. Given the small numbers, care must be taken in interpreting the findings. Findings Not all practitioners have the time, skills or interest to work in cocreation, but when there was collaboration, much was learned. Evidence included professional and tacit knowledge, and anecdotes, as well as findings from rigorous research designs. It was difficult to identify evidence in use and decisions were sometimes progressed in informal ways and in places we did not get to see. There are few formal evidence entry points. Evidence (prevalence and trends in public health issues) enters the process and is embedded in strategic documents to set priorities, but local data were collected in both sites to provide actionable messages (sometimes replicating the evidence base). Conclusions Two mid-range theories explain the findings. If evidence has saliency (relates to ‘here and now’ as opposed to ‘there and then’) and immediacy (short, presented verbally or visually and with emotional appeal) it is more likely to be used in both settings. A second mid-range theory explains how differing tensions pull and compete as feasible and acceptable local solutions are pursued across stakeholders. Answering what works depends on answering for whom and where simultaneously to find workable (if temporary) ‘blends’. Gaining this agreement across stakeholders appeared more difficult across the purchaser–provider split, because opportunities to interact were curtailed; however, more research is needed. Funding This study was funded by the Health Services and Delivery Research programme of the National Institute for Health Research.
    08/2015; 3(33):1-182. DOI:10.3310/hsdr03330
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    ABSTRACT: BACKGROUND: Caffeine has been shown to prevent ultraviolet radiation-induced carcinogenesis and to inhibit growth of melanoma cells in experimental studies. We evaluated the association among caffeine intake, coffee consumption, and melanoma risk among three large cohort studies. METHODS: The analysis used data from 89,220 women in the Nurses' Health Study II (1991-2009), 74,666 women in the Nurses' Health Study (1980-2008), and 39,424 men in the Health Professionals Follow-up Study (1986-2008). We used Cox proportional hazards models to estimate the hazard ratios (HR) with 95% confidence intervals (CIs) of melanoma associated with dietary intakes. RESULTS: We documented 2,254 melanoma cases over 4 million person-years of follow-up. After adjustment for other risk factors, higher total caffeine intake was associated with a lower risk of melanoma (≥393 mg/day vs. <60 mg/day: HR = 0.78, 95% CI = 0.64, 0.96; Ptrend = 0.048). The association was more apparent in women (≥393 mg/day vs. <60 mg/day: HR = 0.70, 95% CI = 0.58, 0.85; Ptrend = 0.001) than in men (HR = 0.94, 95% CI = 0.75, 1.2; Ptrend = 0.81), and more apparent for melanomas occurring on body sites with higher continuous sun exposure (head, neck, and extremities; ≥393 mg/day vs. <60 mg/day: HR = 0.71, 95% CI = 0.59, 0.86; Ptrend = 0.001) than for melanomas occurring on body sites with lower continuous sun exposure (trunk including shoulder, back, hip, abdomen, and chest; HR = 0.90, 95% CI = 0.70, 1.2; Ptrend = 0.60). This pattern of association was similar to that for caffeinated coffee consumption, whereas no association was found for decaffeinated coffee consumption and melanoma risk. CONCLUSIONS: Increasing caffeine intake and caffeinated coffee consumption is associated with decreased risk of cutaneous malignant melanomas.
    Epidemiology 07/2015; DOI:10.1097/EDE.0000000000000360 · 6.20 Impact Factor
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    ABSTRACT: Introduction: Previous studies have identified common germline variants nominally associated with breast cancer survival. These associations have not been widely replicated in further studies. The purpose of this study was to evaluate the association of previously reported SNPs with breast cancer-specific survival using data from a pooled analysis of eight breast cancer survival genome-wide association studies (GWAS) from the Breast Cancer Association Consortium. Methods: A literature review was conducted of all previously published associations between common germline variants and three survival outcomes: breast cancer-specific survival, overall survival and disease-free survival. All associations that reached the nominal significance level of P value <0.05 were included. Single nucleotide polymorphisms that had been previously reported as nominally associated with at least one survival outcome were evaluated in the pooled analysis of over 37,000 breast cancer cases for association with breast cancer-specific survival. Previous associations were evaluated using a one-sided test based on the reported direction of effect. Results: Fifty-six variants from 45 previous publications were evaluated in the meta-analysis. Fifty-four of these were evaluated in the full set of 37,954 breast cancer cases with 2,900 events and the two additional variants were evaluated in a reduced sample size of 30,000 samples in order to ensure independence from the previously published studies. Five variants reached nominal significance (P <0.05) in the pooled GWAS data compared to 2.8 expected under the null hypothesis. Seven additional variants were associated (P <0.05) with ER-positive disease. Conclusions: Although no variants reached genome-wide significance (P <5 x 10(-8)), these results suggest that there is some evidence of association between candidate common germline variants and breast cancer prognosis. Larger studies from multinational collaborations are necessary to increase the power to detect associations, between common variants and prognosis, at more stringent significance levels.
    Breast Cancer Research 04/2015; 17(1). DOI:10.1186/s13058-015-0570-7 · 5.49 Impact Factor
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    David J Hunter · Julio Frenk
    JAMA The Journal of the American Medical Association 03/2015; 313(11):1105-1106. DOI:10.1001/jama.2015.1595 · 35.29 Impact Factor
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    ABSTRACT: Purpose – The purpose of this paper is to examine a bold and ambitious scheme known as the North East transformation system (NETS). The principal aim of the NETS is the achievement of a step-change in the quality of health services delivered to people living in the North East region of England. The paper charts the origins of the NETS and its early journey before describing what happened to it when the UK coalition government published its proposals for unexpected major structural change in the NHS. This had a profound impact on the leadership and direction of the NETS and resulted in it taking a different direction from that intended. Design/methodology/approach – The research design took the form of a mixed methods, longitudinal 3.5-year study aimed at exploring transformational change in terms of content, context, process and outcomes. The sample of study sites comprised 14 NHS trusts in the North East region chosen to provide geographical coverage of the area and to reflect the scale, scope and variety of the bodies that formed part of the NETS programme. The qualitative component of the research, which the paper draws upon, included 68 semi-structured interviews, observational studies and focus groups. Data analysis made use of both deductive and inductive frameworks. The deductive framework adopted was Pettigrew et al.’s “receptive contexts for change” and four of the eight factors stood out as especially important and form the basis of the paper. Findings – The fate of the NETS was shaped and influenced by the eight factors comprising the Pettigrew et al. receptive contexts for change framework but four factors in particular stood out as being especially significant: environmental pressure, quality and coherence of policy, key people leading change, supportive organisational culture. Perhaps the most significant lesson from the NETS is that achieving whole systems change is particularly vulnerable to the vicissitudes of politics especially where that system, like the UK NHS, is itself subject to those very same pressures. Yet, despite having an enormous influence on health policy, the political context is frequently avoided in research or not regarded as instrumental in determining the outcomes in respect of transformational change. Research limitations/implications – The chief limitation is the credibility and authenticity of the interviews captured at particular points in time. These formed the datebase for subsequent analysis. The authors sought to guard against possible bias by supplementing interviews with observational studies and focus groups as well as running two dissemination events at which emerging findings from the study were subjected to independent external scrutiny and comment. These events provided a form of validation for the key study findings. Practical implications – The research findings demonstrate the importance of context for the likely outcome and success of complex transformational change initiatives. These require time to become embedded and demonstrate results especially when focused on changing culture and behaviour. But, in practice, allowing sufficient time during which the organisation may remain sufficiently stable to allow the change intervention to run its course and become embedded and sustainable is highly problematic. The consequence is that bold and ambitious efforts like the NETS are not given the space and stability to prove themselves. Too often, politics and external environmental pressures intrude in ways that may prove dysfunctional and negative. Social implications – Unless a different approach to transformational change and its leadership and management is adopted, then changing the NHS to enable it to appear more responsive to changing health care needs and expectations will remain a cause for concern. Ultimately the public will be the losers if the NHS remains insensitive to changing needs and expectations. The patient experience was at the centre of the NETS programme. Originality/value – The study is original insofar as no other has sought to evaluate the NETS independently and over a reasonable time period. The research design, based on a mixed-methods approach, is unusual in evaluations of this nature. The study’s conclusions are not so original but their value lies in largely confirming and reinforcing the findings from other studies. It perhaps goes further in stressing the impact of politics on health policy and the negative consequences of constant organisational change on attempts to achieve deep change in the way the NHS is organised and led.
    Journal of Health Organisation and Management 03/2015; 29(1):10-24. DOI:10.1108/JHOM-01-2014-0019 · 0.36 Impact Factor
  • David J Hunter
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    ABSTRACT: Rather than exclude politics from health, David Hunter argues that we must embrace it if we are to improve our complex health systems
    BMJ Clinical Research 03/2015; 350(mar09 5):h1214. DOI:10.1136/bmj.h1214 · 14.09 Impact Factor
  • Lorelei A Mucci · David J Hunter · Michelle Williams
    Cancer Epidemiology Biomarkers & Prevention 03/2015; 24(3):483. DOI:10.1158/1055-9965.EPI-14-1412 · 4.13 Impact Factor
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    Julio Frenk · David J Hunter · Ian Lapp
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    ABSTRACT: We are transforming the educational strategy at the Harvard T. H. Chan School of Public Health guided by 5 principles: (1) development of T-shaped competencies (breadth across fields, depth in primary fields), (2) flexible and modular design accommodating different needs through the lifecycle, (3) greater experiential learning, (4) 3 levels of education (informative, formative, and transformative learning), and (5) integrated instructional design (online, in person, and in the field). We aim to create an arc of education resulting in continuous learning. We seek to bridge the research versus education dichotomy and create research-teaching congruence, adapting the values of peer review and quality assessment that we routinely accept for grant and article review to education.
    American Journal of Public Health 03/2015; 105(S1):S109-S113. DOI:10.2105/AJPH.2014.302468 · 4.55 Impact Factor
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    ABSTRACT: Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 x 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms.
    Nature 02/2015; 518(7538-7538):187-96. DOI:10.1038/nature14132 · 41.46 Impact Factor
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    ABSTRACT: Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis
    Nature 02/2015; 518(7538). DOI:10.1038/nature14177 · 41.46 Impact Factor
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    ABSTRACT: We recently identified a novel susceptibility variant, rs865686, for estrogen-receptor positive breast cancer at 9q31.2. Here, we report a fine-mapping analysis of the 9q31.2 susceptibility locus using 43,160 cases and 42,600 controls of European ancestry ascertained from 52 studies and a further 5,795 cases and 6,624 controls of Asian ancestry from nine studies. Single nucleotide polymorphism (SNP) rs676256 was most strongly associated with risk in Europeans (OR=0.90 [0.88-0.92]; P-value=1.58 x 10(-25)). This SNP is one of a cluster of highly correlated variants, including rs865686, that spans approximately 14.5 Kb. We identified two additional independent association signals demarcated by SNPs rs10816625 (OR=1.12 [1.08-1.17]; P-value=7.89 x 10(-09)) and rs13294895 (OR=1.09 [1.06-1.12]; P-value=2.97 x 10(-11)). SNP rs10816625, but not rs13294895, was also associated with risk of breast cancer in Asian individuals (OR=1.12 [1.06-1.18]; P-value=2.77 x 10(-05)). Functional genomic annotation using data derived from breast cancer cell-line models indicates that these SNPs localise to putative enhancer elements that bind known drivers of hormone dependent breast cancer, including ER-α, FOXA1 and GATA-3. In vitro analyses indicate that rs10816625 and rs13294895 have allele-specific effects on enhancer activity and suggest chromatin interactions with the KLF4 gene locus. These results demonstrate the power of dense genotyping in large studies to identify independent susceptibility variants. Analysis of associations using subjects with different ancestry, combined with bioinformatic and genomic characterisation, can provide strong evidence for the likely causative alleles and their functional basis. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.
    Human Molecular Genetics 02/2015; 24(10). DOI:10.1093/hmg/ddv035 · 6.39 Impact Factor
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    David J. Hunter · Ian Lapp · Julio Frenk
    American Journal of Preventive Medicine 11/2014; 47(5):S286–S287. DOI:10.1016/j.amepre.2014.07.047 · 4.53 Impact Factor
  • Jane Beenstock · Sarah Sowden · David J Hunter · Martin White
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    ABSTRACT: Background: Since 1 April 2013, local authority (LA) health and well-being boards (HWBs) in England are required to publish a health and well-being strategy (HWS). HWSs should identify how population health needs are to be addressed. The extent to which this has been achieved is not known. We analysed HWSs to assess how LAs have interpreted statutory guidance, how evidence has been used within HWSs and the relationship of HWSs to Joint Strategic Needs Assessments (JSNAs). Methods: Qualitative thematic content analysis of a random sample of one-third of upper tier LA HWSs in 2013-14. Results: Fifty out of 152 LAs were sampled and 47 HWSs analysed. Strategies varied in timescale, length and structure. The term 'evidence' was used most commonly referring to local need, rather than evidence of effectiveness. All, except two, referred to JSNAs. Conclusions: HWSs are dominated by evidence of need and could be strengthened by greater use of evidence of effectiveness for public health interventions. Public health agencies and academics can support the development of effective HWSs by improving the accessibility of evidence and conducting research when evidence is absent. To strengthen HWSs' impact, the statutory guidance should clarify the distinction between evidence of need and evidence of effectiveness.
    Journal of Public Health 10/2014; 37(3). DOI:10.1093/pubmed/fdu073 · 2.04 Impact Factor
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    ABSTRACT: Using genome-wide data from 253,288 individuals, we identified 697 variants at genome-wide significance that together explained one-fifth of the heritability for adult height. By testing different numbers of variants in independent studies, we show that the most strongly associated approximately 2,000, approximately 3,700 and approximately 9,500 SNPs explained approximately 21%, approximately 24% and approximately 29% of phenotypic variance. Furthermore, all common variants together captured 60% of heritability. The 697 variants clustered in 423 loci were enriched for genes, pathways and tissue types known to be involved in growth and together implicated genes and pathways not highlighted in earlier efforts, such as signaling by fibroblast growth factors, WNT/beta-catenin and chondroitin sulfate-related genes. We identified several genes and pathways not previously connected with human skeletal growth, including mTOR, osteoglycin and binding of hyaluronic acid. Our results indicate a genetic architecture for human height that is characterized by a very large but finite number (thousands) of causal variants.
    Nature Genetics 10/2014; DOI:10.1038/ng.3097 · 29.35 Impact Factor
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    ABSTRACT: Genome-wide association studies (GWAS) have identified 76 variants associated with prostate cancer risk predominantly in populations of European ancestry. To identify additional susceptibility loci for this common cancer, we conducted a meta-analysis of >10 million SNPs in 43,303 prostate cancer cases and 43,737 controls from studies in populations of European, African, Japanese and Latino ancestry. Twenty-three new susceptibility loci were identified at association P < 5 × 10(-8); 15 variants were identified among men of European ancestry, 7 were identified in multi-ancestry analyses and 1 was associated with early-onset prostate cancer. These 23 variants, in combination with known prostate cancer risk variants, explain 33% of the familial risk for this disease in European-ancestry populations. These findings provide new regions for investigation into the pathogenesis of prostate cancer and demonstrate the usefulness of combining ancestrally diverse populations to discover risk loci for disease.
    Nature Genetics 09/2014; 46(10). DOI:10.1038/ng.3094 · 29.35 Impact Factor
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    ABSTRACT: Striking differences exist in outcomes for cancer between developed countries with comparable healthcare systems. We compare the healthcare systems of 3 countries (Denmark, Norway, Sweden), 3 UK jurisdictions (England, Wales and Northern Ireland), 3 Canadian provinces (British Columbia, Manitoba, Ontario) and 2 Australian states (New South Wales, Victoria) using a framework which assesses the possible contribution of primary care systems to a range of health outcomes, drawing on key characteristics influencing population health. For many of the characteristics we investigated there are no significant differences between those countries with poorer cancer outcomes (England and Denmark) and the rest. In particular, regulation, financing, the existence of patient lists, the GP gatekeeping role, direct access to secondary care, the degree of comprehensiveness of primary care services, the level of cost sharing and the type of primary care providers within healthcare systems were not specifically and consistently associated with differences between countries. Factors that could have an influence on patient and professional behaviour, and consequently contribute to delays in cancer diagnosis and poorer cancer outcomes in some countries, include centralisation of services, free movement of patients between primary care providers, access to secondary care, and the existence of patient list systems. It was not possible to establish a causal correlation between healthcare system characteristics and cancer outcomes. Further studies should explore in greater depth the associations between single health system factors and cancer outcomes, recognising that in complex systems where context is all-important, it will be difficult to establish causal relationships. Better understanding of the interaction between healthcare system variables and patient and professional behaviour may generate new hypotheses for further research.
    Social Science & Medicine 09/2014; DOI:10.1016/j.socscimed.2014.06.030 · 2.89 Impact Factor
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    ABSTRACT: Previous studies have suggested that polymorphisms in CASP8 on chromosome 2 are associated with breast cancer risk. To clarify the role of CASP8 in breast cancer susceptibility, we carried out dense genotyping of this region in the Breast Cancer Association Consortium (BCAC). Single-nucleotide polymorphisms (SNPs) spanning a 1 Mb region around CASP8 were genotyped in 46 450 breast cancer cases and 42 600 controls of European origin from 41 studies participating in the BCAC as part of a custom genotyping array experiment (iCOGS). Missing genotypes and SNPs were imputed and, after quality exclusions, 501 typed and 1232 imputed SNPs were included in logistic regression models adjusting for study and ancestry principal components. The SNPs retained in the final model were investigated further in data from nine genome-wide association studies (GWAS) comprising in total 10 052 case and 12 575 control subjects. The most significant association signal observed in European subjects was for the imputed intronic SNP rs1830298 in ALS2CR12 (telomeric to CASP8), with per allele odds ratio and 95% confidence interval [OR (95% confidence interval, CI)] for the minor allele of 1.05 (1.03–1.07), P = 1 × 10−5. Three additional independent signals from intronic SNPs were identified, in CASP8 (rs36043647), ALS2CR11 (rs59278883) and CFLAR (rs7558475). The association with rs1830298 was replicated in the imputed results from the combined GWAS (P = 3 × 10−6), yielding a combined OR (95% CI) of 1.06 (1.04–1.08), P = 1 × 10−9. Analyses of gene expression associations in peripheral blood and normal breast tissue indicate that CASP8 might be the target gene, suggesting a mechanism involving apoptosis.
    Human Molecular Genetics 08/2014; 24(1). DOI:10.1093/hmg/ddu431 · 6.39 Impact Factor
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    ABSTRACT: Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10−39; Region 3: rs2853677, P = 3.30 × 10−36 and PConditional = 2.36 × 10−8; Region 4: rs2736098, P = 3.87 × 10−12 and PConditional = 5.19 × 10−6, Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10−6; and Region 6: rs10069690, P = 7.49 × 10−15 and PConditional = 5.35 × 10−7) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 × 10−18 and PConditional = 7.06 × 10−16). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.
    Human Molecular Genetics 07/2014; DOI:10.1093/hmg/ddu363 · 6.39 Impact Factor

Publication Stats

51k Citations
6,287.86 Total Impact Points


  • 2001–2015
    • Durham University
      • Centre for Public Policy and Health "CPPH"
      Durham, England, United Kingdom
  • 1990–2015
    • Harvard University
      • • Department of Nutrition
      • • Department of Epidemiology
      Cambridge, Massachusetts, United States
    • Harvard Medical School
      • • Department of Medicine
      • • Division of Nutrition
      Boston, Massachusetts, United States
  • 2014
    • Universität Regensburg
      Ratisbon, Bavaria, Germany
    • University of Aberdeen
      Aberdeen, Scotland, United Kingdom
    • Newcastle University
      • Institute of Health and Society
      Newcastle-on-Tyne, England, United Kingdom
  • 2011
    • Brown University
      • Department of Epidemiology
      Providence, Rhode Island, United States
  • 2010–2011
    • University of Sydney
      • Northern Clinical School
      Sydney, New South Wales, Australia
    • University of Exeter
      • Peninsula College of Medicine and Dentistry
      Exeter, ENG, United Kingdom
    • Mayo Clinic - Rochester
      • Department of Health Science Research
      Rochester, MN, United States
    • Kaiser Permanente
      Oakland, California, United States
  • 2008–2011
    • National Institutes of Health
      • Division of Cancer Epidemiology and Genetics
      Bethesda, MD, United States
    • Boston Children's Hospital
      Boston, Massachusetts, United States
  • 2007–2011
    • New England Baptist Hospital
      Boston, Massachusetts, United States
    • Broad Institute of MIT and Harvard
      • Program in Medical and Population Genetics
      Cambridge, Massachusetts, United States
    • University of Groningen
      Groningen, Groningen, Netherlands
  • 2001–2010
    • Beverly Hospital, Boston MA
      BVY, Massachusetts, United States
  • 2000–2010
    • Royal North Shore Hospital
      Sydney, New South Wales, Australia
  • 1992–2010
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, Massachusetts, United States
  • 2008–2009
    • National Cancer Institute (USA)
      • Division of Cancer Epidemiology and Genetics
      베서스다, Maryland, United States
  • 2004–2009
    • Boston University
      Boston, Massachusetts, United States
  • 2005–2006
    • Muhimbili University of Health and Allied Sciences
      Dār es Salām, Dar es Salaam, Tanzania
    • University of Toronto
      Toronto, Ontario, Canada
    • Population Health Research Institute
      Hamilton, Ontario, Canada
    • Umeå University
      • Department of Public Health and Clinical Medicine
      Umeå, Västerbotten, Sweden
  • 2004–2006
    • Massachusetts Department of Public Health
      Boston, Massachusetts, United States
  • 2002–2004
    • Dana-Farber Cancer Institute
      • Department of Medical Oncology
      Boston, MA, United States
    • Maastricht University
      Maestricht, Limburg, Netherlands
    • Simmons College
      • Program in Nutrition and Dietetics
      Boston, Massachusetts, United States
  • 2003
    • Icahn School of Medicine at Mount Sinai
      • Department of Microbiology
      Manhattan, New York, United States
  • 1991–1995
    • University of Dar es Salaam
      Dār es Salām, Dar es Salaam, Tanzania