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Stocks, Tanja
Publications (10 of 46) Show all publications
Fritz, J., Bjorge, T., Nagel, G., Concin, H., Manjer, J., Häggström, C., . . . Ulmer, H. (2019). Insulin resistance measured by the triglyceride-glucose index and risk of obesity-related cancers: An epidemiological investigation in more than 500,000 individuals.. Paper presented at Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), MAY 31-JUN 04, 2019, Chicago, IL. Journal of Clinical Oncology, 37(15), 1552-1552
Open this publication in new window or tab >>Insulin resistance measured by the triglyceride-glucose index and risk of obesity-related cancers: An epidemiological investigation in more than 500,000 individuals.
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2019 (English)In: Journal of Clinical Oncology, ISSN 0732-183X, E-ISSN 1527-7755, Vol. 37, no 15, p. 1552-1552Article in journal, Meeting abstract (Other academic) Published
Abstract [en]

Background: The role of insulin resistance as a mediator in the association of body mass index (BMI) with site-specific cancer risk has, to our knowledge, never been systematically quantified. We aimed to determine to what extent insulin resistance measured as the logarithmized triglyceride glucose product (TyG index) mediates the effect of BMI on risk of obesity-related cancers. Methods: A total of 510,471 individuals from six European cohorts with a mean age of 43.1 years were included in the study. We fitted Cox models, adjusted for relevant confounders, to investigate associations of TyG index with ten common obesity-related cancer sites, and quantified the proportion of the effect of BMI mediated through TyG index. Results: During a median follow-up of 17.2 years, 16 052 individuals developed obesity-related cancers. TyG index was associated with the risk of cancers of the kidney (hazard ratio (HR) per one standard deviation increase 1.13, 95% confidence interval: 1.07-1.20), liver (1.13, 1.04-1.23), pancreas (1.12, 1.06-1.19), colon (1.07, 1.03-1.10), and rectum (1.09, 1.04-1.14). Substantial proportions of the effect of BMI were mediated by TyG index for cancers of the pancreas (42%), rectum (34%), and colon (20%); smaller proportions for kidney (15%) and liver (11%); none for endometrium, ovary and breast (postmenopausal). Conclusions: In this pooled cohort study including more than 500,000 individuals, insulin resistance measured as the logarithmized triglyceride glucose product significantly mediated the effect of overweight and obesity on risk of cancers of the kidney, liver, pancreas, colon, and rectum. In contrast, insulin resistance did not mediate the risk for cancers of the endometrium, ovary and breast. Our results confirm a promoting role of insulin resistance in the pathogenesis of gastrointestinal cancers. Although often claimed, insulin resistance does not appear to connect excess body weight with cancers of the female reproductive organs.

Place, publisher, year, edition, pages
American Society of Clinical Oncology, 2019
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-164084 (URN)10.1200/JCO.2019.37.15_suppl.1552 (DOI)000487345804348 ()
Conference
Annual Meeting of the American-Society-of-Clinical-Oncology (ASCO), MAY 31-JUN 04, 2019, Chicago, IL
Note

Supplement: S (May 20, 2019)

Meeting Abstract: 1552

Available from: 2019-10-14 Created: 2019-10-14 Last updated: 2019-10-14Bibliographically approved
Häggström, C., Stattin, P., Stocks, T., Garmo, H., Holmberg, L. & Van Hemelrijck, M. (2016). Interpretation of conventional survival analysis and competing-risk analysis: an example of hypertension and prostate cancer. BJU International, 118(6), 850-852
Open this publication in new window or tab >>Interpretation of conventional survival analysis and competing-risk analysis: an example of hypertension and prostate cancer
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2016 (English)In: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 118, no 6, p. 850-852Article in journal, Editorial material (Refereed) Published
National Category
Public Health, Global Health, Social Medicine and Epidemiology Urology and Nephrology
Identifiers
urn:nbn:se:umu:diva-128544 (URN)10.1111/bju.13494 (DOI)000388479100007 ()27037631 (PubMedID)
Available from: 2016-12-07 Created: 2016-12-07 Last updated: 2018-06-09Bibliographically approved
Rukh, G., Ahmad, S., Ericson, U., Hindy, G., Stocks, T., Renström, F., . . . Orho-Melander, M. (2016). Inverse relationship between a genetic risk score of 31 BMI loci and weight change before and after reaching middle age. International Journal of Obesity, 40(2), 252-259
Open this publication in new window or tab >>Inverse relationship between a genetic risk score of 31 BMI loci and weight change before and after reaching middle age
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2016 (English)In: International Journal of Obesity, ISSN 0307-0565, E-ISSN 1476-5497, Vol. 40, no 2, p. 252-259Article in journal (Refereed) Published
Abstract [en]

BACKGROUND/OBJECTIVE: Genome-wide-association studies have identified numerous body mass index (BMI)-associated variants, but it is unclear how these relate to weight gain in adults at different ages.

METHODS: We examined the association of a genetic risk score (GRS), consisting of 31 BMI-associated variants, with an annual weight change (AWC) and a substantial weight gain (SWG) of 10% by comparing self-reported weight at 20 years (y) with baseline weight (mean: 58 y; s.d.: 8 y) in 21407 participants from the Malmö Diet and Cancer Study (MDCS), and comparing baseline weight to weight at follow-up (mean: 73 y; s.d.: 6 y) among 2673 participants. Association between GRS and AWG and SWG was replicated in 4327 GLACIER (Gene x Lifestyle interactions And Complex traits Involved in Elevated disease Risk) participants (mean: 45 y; s.d.: 7 y) with 10 y follow-up. Cohort-specific results were pooled by fixed-effect meta-analyses.

RESULTS: In MDCS, the GRS was associated with increased AWC (β: 0.003; s.e: 0.01; P: 7 × 10(-8)) and increased odds for SWG (odds ratio (OR) 1.01 (95% confidence interval (CI): 1.00, 1.02); P: 0.013) per risk-allele from age 20y, but unexpectedly with decreased AWC (β: -0.006; s.e: 0.002; P: 0.009) and decreased odds for SWG OR 0.96 (95% CI: 0.93, 0.98); P: 0.001) between baseline and follow-up. Effect estimates from age 20 y to baseline differed significantly from those from baseline to follow-up (P: 0.0002 for AWC and P: 0.0001 for SWG). Similar to MDCS, the GRS was associated with decreased odds for SWG OR 0.98 (95% CI: 0.96, 1.00); P: 0.029) from baseline to follow-up in GLACIER. In meta-analyses (n=7000), the GRS was associated with decreased AWC (β: -0.005; s.e.m. 0.002; P: 0.002) and decreased odds for SWG OR 0.97 (95% CI: 0.96, 0.99); P: 0.001) per risk-allele.

CONCLUSIONS: Our results provide convincing evidence for a paradoxical inversed relationship between a high number of BMI-associated risk-alleles and less weight gain during and after middle-age, in contrast to the expected increased weight gain seen in younger age.

National Category
Endocrinology and Diabetes Medical Genetics
Identifiers
urn:nbn:se:umu:diva-116976 (URN)10.1038/ijo.2015.180 (DOI)000369691500010 ()26374450 (PubMedID)
Note

Special Issue: All roads lead to the brain

Available from: 2016-02-16 Created: 2016-02-16 Last updated: 2018-06-07Bibliographically approved
Wozniak, M. B., Brennan, P., Brenner, D. R., Overvad, K., Olsen, A., Tjonneland, A., . . . Scelo, G. (2015). Alcohol consumption and the risk of renal cancers in the European prospective investigation into cancer and nutrition (EPIC). International Journal of Cancer, 137(8), 1953-1966
Open this publication in new window or tab >>Alcohol consumption and the risk of renal cancers in the European prospective investigation into cancer and nutrition (EPIC)
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2015 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 137, no 8, p. 1953-1966Article in journal (Refereed) Published
Abstract [en]

Epidemiologic studies have reported that moderate alcohol consumption is inversely associated with the risk of renal cancer. However, there is no information available on the associations in renal cancer subsites. From 1992 through to 2010, 477,325 men and women in the European Prospective Investigation into Cancer and Nutrition cohort were followed for incident renal cancers (n=931). Baseline and lifetime alcohol consumption was assessed by country-specific, validated dietary questionnaires. Information on past alcohol consumption was collected by lifestyle questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox proportional hazard models. In multivariate analysis, total alcohol consumption at baseline was inversely associated with renal cancer; the HR and 95% CI for the increasing categories of total alcohol consumption at recruitment versus the light drinkers category were 0.78 (0.62-0.99), 0.82 (0.64-1.04), 0.70 (0.55-0.90), 0.91 (0.63-1.30), respectively, (p(trend)=0.001). A similar relationship was observed for average lifetime alcohol consumption and for all renal cancer subsites combined or for renal parenchyma subsite. The trend was not observed in hypertensive individuals and not significant in smokers. In conclusion, moderate alcohol consumption was associated with a decreased risk of renal cancer. What's new? Previous studies have indicated that environmental or lifestyle factors may be involved in the etiology of renal cancer, and that moderate alcohol consumption may reduce the risk of this type of cancer. In this very large European study (nearly 500,000 subjects), the authors found that, indeed, total alcohol consumption was inversely associated with renal cancer overall (for all subsites combined), and also with cancers of the renal parenchyma.

Keywords
kidney cancer, renal cell carcinoma, risk factors, alcohol consumption, EPIC, cohort study
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-108119 (URN)10.1002/ijc.29559 (DOI)000359350600023 ()25866035 (PubMedID)
Available from: 2015-09-23 Created: 2015-09-04 Last updated: 2018-06-07Bibliographically approved
Kelly, R. S., Roulland, S., Morgado, E., Sungalee, S., Jouve, N., Tumino, R., . . . Vineis, P. (2015). Determinants of the t(14;18) translocation and their role in t(14;18)-positive follicular lymphoma. Cancer Causes and Control, 26(12), 1845-1855
Open this publication in new window or tab >>Determinants of the t(14;18) translocation and their role in t(14;18)-positive follicular lymphoma
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2015 (English)In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 26, no 12, p. 1845-1855Article in journal (Refereed) Published
Abstract [en]

Purpose: The strong association between t(14;18) translocation and follicular lymphoma (FL) is well known. However, the determinants of this chromosomal aberration and their role in t(14;18) associated FL remain to be established.

Methods: t(14;18) frequency within the B cell lymphoma 2 major breakpoint region was determined for 135 incident FL cases and 251 healthy controls as part of a nested case–control study within the European Prospective Investigation into Cancer cohort. Quantitative real-time PCR was performed in DNA extracted from blood samples taken at recruitment. The relationship between prevalence and frequency of the translocation with baseline anthropometric, lifestyle, and dietary factors in cases and controls was determined. Unconditional logistic regression was used to explore whether the risk of FL associated with these factors differed in t(14;18)+ as compared to t(14;18) cases.

Results: Among incident FL cases, educational level (χ 2 p = 0.021) and height (χ 2 p = 0.025) were positively associated with t(14;18) prevalence, and cases with high frequencies [t(14;18)HF] were significantly taller (t test p value = 0.006). These findings were not replicated in the control population, although there were a number of significant associations with dietary variables. Further analyses revealed that height was a significant risk factor for t(14;18)+ FL [OR 6.31 (95 % CI 2.11, 18.9) in the tallest versus the shortest quartile], but not t(14;18) cases.

Conclusions: These findings suggest a potential role for lifestyle factors in the prevalence and frequency of the t(14;18) translocation. The observation that the etiology of FL may differ by t(14;18) status, particularly with regard to height, supports the subdivision of FL by translocation status.

Place, publisher, year, edition, pages
Springer Netherlands, 2015
Keywords
Follicular lymphoma, Translocation, t(14, 18), Height
National Category
Cancer and Oncology Public Health, Global Health, Social Medicine and Epidemiology Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-111988 (URN)10.1007/s10552-015-0677-2 (DOI)000363956100014 ()26424368 (PubMedID)
Available from: 2015-12-03 Created: 2015-11-30 Last updated: 2018-06-07Bibliographically approved
Obon-Santacana, M., Peeters, P. H. M., Freisling, H., Dossus, L., Clavel-Chapelon, F., Baglietto, L., . . . Duell, E. J. (2015). Dietary Intake of Acrylamide and Epithelial Ovarian Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) Cohort. Cancer Epidemiology, Biomarkers and Prevention, 24(1), 291-297
Open this publication in new window or tab >>Dietary Intake of Acrylamide and Epithelial Ovarian Cancer Risk in the European Prospective Investigation into Cancer and Nutrition (EPIC) Cohort
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2015 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 24, no 1, p. 291-297Article in journal (Refereed) Published
Abstract [en]

Acrylamide, classified in 1994 by the International Agency for Research on Cancer (IARC) as "probably carcinogenic" to humans, was discovered in 2002 in some heat-treated, carbohydrate-rich foods. The association between dietary acrylamide intake and epithelial ovarian cancer risk (EOC) has been previously studied in one case-control and three prospective cohort studies which obtained inconsistent results and could not further examine histologic subtypes other than serous EOC. The present study was carried out in the European Prospective Investigation into Cancer and Nutrition (EPIC) subcohort of women (n = 325,006). Multivariate Cox proportional hazards models were used to assess the association between questionnaire-based acrylamide intake and EOC risk. Acrylamide was energy-adjusted using the residual method and was evaluated both as a continuous variable (per 10 mu g/d) and in quintiles; when subgroups by histologic EOC subtypes were analyzed, acrylamide intake was evaluated in quartiles. During a mean follow-up of 11 years, 1,191 incident EOC cases were diagnosed. At baseline, the median acrylamide intake in EPIC was 21.3 mu g/d. No associations and no evidence for a dose-response were observed between energy-adjusted acrylamide intake and EOC risk (HR10 mu(g/d), 1.02; 95% CI, 0.96-1.09; HRQ5vsQ1, 0.97; 95% CI, 0.76-1.23). No differences were seen when invasive EOC subtypes (582 serous, 118 endometrioid, and 79 mucinous tumors) were analyzed separately. This study did not provide evidence that acrylamide intake, based on food intake questionnaires, was associated with risk for EOC in EPIC. Additional studies with more reliable estimates of exposure based on biomarkers may be needed.

National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-100136 (URN)10.1158/1055-9965.EPI-14-0636 (DOI)000348030700035 ()25300475 (PubMedID)
Available from: 2015-03-02 Created: 2015-02-24 Last updated: 2018-06-07Bibliographically approved
Stocks, T., Björge, T., Ulmer, H., Manjer, J., Häggström, C., Nagel, G., . . . Stattin, P. (2015). Metabolic risk score and cancer risk: pooled analysis of seven cohorts. International Journal of Epidemiology, 44(4), 1353-1387
Open this publication in new window or tab >>Metabolic risk score and cancer risk: pooled analysis of seven cohorts
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2015 (English)In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 44, no 4, p. 1353-1387Article in journal (Refereed) Published
Abstract [en]

Background: There are few data on the joint influence of metabolic factors on risk of separate cancers. Methods: We analysed data on body mass index, blood pressure and plasma levels of glucose, total cholesterol and triglycerides from seven European cohorts comprising 564 596 men and women with a mean age of 44 years. We weighted those factors equally into a standardized metabolic risk score [MRS, mean = 0, standard deviation (SD) = 1], with an individual's level indicated as SDs from the sex-and cohort-specific means. Cancer hazard ratios were calculated by Cox regression with age as timescale and with relevant adjustments including smoking status. All statistical tests were two-sided. Results: During a mean follow-up of 12 years, 21 593 men and 14 348 women were diagnosed with cancer. MRS was linearly and positively associated with incident cancer in total and at sites (P<0.05). In men, risk per SD MRS was increased by 43% (95% confidence interval: 27-61) for renal cell cancer, 43% (16-76) for liver cancer, 29% (20-38) for colon cancer, 27% (5-54) for oesophageal cancer, 20% (9-31) for rectal cancer, 19% (4-37) for leukaemias, 15% (1-30) for oral cancer and 10% (2-19) for bladder cancer. In women, risk increases per SD MRS were 56% (42-70) for endometrial cancer, 53% (29-81) for pancreatic cancer, 40% (16-67) for renal cell cancer, 27% (9-47) for cervical cancer and 17% (3-32) for rectal cancer. Conclusion: This largest study to date on the joint influence of metabolic factors on risk of separate cancers showed increased risks for several cancers, in particular renal cell and liver cancer in men and endometrial and pancreatic cancer in women.

Keywords
cohort studies, metabolic syndrome x, neoplasms
National Category
Cancer and Oncology Urology and Nephrology
Identifiers
urn:nbn:se:umu:diva-111509 (URN)10.1093/ije/dyv001 (DOI)000363061500031 ()25652574 (PubMedID)
Available from: 2015-12-08 Created: 2015-11-13 Last updated: 2018-08-31Bibliographically approved
Borena, W., Edlinger, M., Bjørge, T., Häggström, C., Lindkvist, B., Nagel, G., . . . Ulmer, H. (2014). A prospective study on metabolic risk factors and gallbladder cancer in the metabolic syndrome and cancer (Me-Can) collaborative study. PLoS ONE, 9(2), e89368
Open this publication in new window or tab >>A prospective study on metabolic risk factors and gallbladder cancer in the metabolic syndrome and cancer (Me-Can) collaborative study
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2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 2, p. e89368-Article in journal (Refereed) Published
Abstract [en]

Objective: To investigate the association between metabolic risk factors (individually and in combination) and risk of gallbladder cancer (GBC). Methods: The metabolic syndrome and cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden with data on 578,700 men and women. We used Cox proportional hazard regression models to calculate relative risks of GBC by body mass index (BMI), blood pressure, and plasma levels of glucose, cholesterol, and triglycerides as continuous standardised variables and their standardised sum of metabolic syndrome (MetS) z-score. The risk estimates were corrected for random error in measurements. Results: During an average follow-up of 12.0 years (SD = 7.8), 184 primary gallbladder cancers were diagnosed. Relative risk of gallbladder cancer per unit increment of z-score adjusted for age, smoking status and BMI (except for BMI itself) and stratified by birth year, sex and sub-cohorts, was for BMI 1.31 (95% confidence interval 1.11, 1.57) and blood glucose 1.76 (1.10, 2.85). Further analysis showed that the effect of BMI on GBC risk is larger among women in the premenopausal age group (1.84 (1.23, 2.78)) compared to those in the postmenopausal age group (1.29 (0.93, 1.79)). For the other metabolic factors no significant association was found (mid blood pressure 0.96 (0.71, 1.31), cholesterol 0.84 (0.66, 1.06) and serum triglycerides 1.16 (0.82, 1.64)). The relative risk per one unit increment of the MetS z-score was 1.37 (1.07, 1.73). Conclusion: This study showed that increasing BMI and impaired glucose metabolism pose a possible risk for gallbladder cancer. Beyond the individual factors, the results also showed that the metabolic syndrome as an entity presents a risk constellation for the occurrence of gallbladder cancer.

National Category
Cancer and Oncology Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-87646 (URN)10.1371/journal.pone.0089368 (DOI)000331717900084 ()
Available from: 2014-04-09 Created: 2014-04-07 Last updated: 2018-06-08Bibliographically approved
Ankarfeldt, M. Z., Ängquist, L., Stocks, T., Jakobsen, M. U., Overvad, K., Halkjær, J., . . . Sørensen, T. I. A. (2014). Body characteristics, dietary protein and body weight regulation. Reconciling conflicting results from intervention and observational studies?. PLoS ONE, 9(7), e101134
Open this publication in new window or tab >>Body characteristics, dietary protein and body weight regulation. Reconciling conflicting results from intervention and observational studies?
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2014 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, no 7, p. e101134-Article in journal (Refereed) Published
Abstract [en]

Background/Objectives: Physiological evidence indicates that high-protein diets reduce caloric intake and increase thermogenic response, which may prevent weight gain and regain after weight loss. Clinical trials have shown such effects, whereas observational cohort studies suggest an association between greater protein intake and weight gain. In both types of studies the results are based on average weight changes, and show considerable diversity in both directions. This study investigates whether the discrepancy in the evidence could be due to recruitment of overweight and obese individuals into clinical trials. Subjects/Methods: Data were available from the European Diet, Obesity and Genes (DiOGenes) post-weight-loss weight-maintenance trial and the Danish Diet, Cancer and Health (DCH) cohort. Participants of the DCH cohort were matched with participants from the DiOGenes trial on gender, diet, and body characteristics. Different subsets of the DCH-participants, comparable with the trial participants, were analyzed for weight maintenance according to the randomization status (high or low protein) of the matched trial participants. Results: Trial participants were generally heavier, had larger waist circumference and larger fat mass than the participants in the entire DCH cohort. A better weight maintenance in the high-protein group compared to the low protein group was observed in the subgroups of the DCH cohort matching body characteristics of the trial participants. Conclusion: This modified observational study, minimized the differences between the RCT and observational data with regard to dietary intake, participant characteristics and statistical analysis. Compared with low protein diet the high protein diet was associated with better weight maintenance when individuals with greater body mass index and waist circumference were analyzed. Selecting subsets of large-scale observational cohort studies with similar characteristics as participants in clinical trials may reconcile the otherwise conflicting results.

Place, publisher, year, edition, pages
Public library science, 2014
National Category
Nutrition and Dietetics
Identifiers
urn:nbn:se:umu:diva-94166 (URN)10.1371/journal.pone.0101134 (DOI)000341253400045 ()
Available from: 2014-10-06 Created: 2014-10-06 Last updated: 2018-06-07Bibliographically approved
Lindkvist, B., Johansen, D., Stocks, T., Concin, H., Bjorge, T., Almquist, M., . . . Manjer, J. (2014). Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580 000 subjects within the Me-Can project. BMC Cancer, 14, 103
Open this publication in new window or tab >>Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580 000 subjects within the Me-Can project
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2014 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 14, p. 103-Article in journal (Refereed) Published
Abstract [en]

Background: Obesity is associated with an increased risk of esophageal adenocarcinoma (EAC) and a decreased risk of esophageal squamous cell carcinoma (ESCC). However, little is known about the risk of EAC and ESCC related to other metabolic risk factors. We aimed to examine the risk of EAC and ESCC in relation to metabolic risk factors, separately and combined in a prospective cohort study. Methods: The Metabolic Syndrome and Cancer cohort includes prospective cohorts in Austria, Norway and Sweden, with blood pressure, lipids, glucose and BMI available from 578 700 individuals. Relative risk (RR) for EAC and ESCC was calculated using Cox's proportional hazards analysis for metabolic risk factors categorized into quintiles and transformed into z-scores. The standardized sum of all z-scores was used as a composite score for the metabolic syndrome (MetS). Results: In total, 324 histologically verified cases of esophageal cancer were identified (114 EAC, 184 ESCC and 26 with other histology). BMI was associated with an increased risk of EAC (RR 7.34 (95% confidence interval, 2.88-18.7) top versus bottom quintile) and negatively associated with the risk of ESCC (RR 0.38 (0.23-0.62)). The mean value of systolic and diastolic blood pressure (mid blood pressure) was associated with the risk of ESCC (RR 1.77 (1.37-2.29)). The composite MetS score was associated with the risk of EAC (RR 1.56 (1.19-2.05) per one unit increase of z-score) but not ESCC. Conclusions: In accordance with previous studies, high BMI was associated with an increased risk of EAC and a decreased risk of ESCC. An association between high blood pressure and risk of ESCC was observed but alcohol consumption is a potential confounding factor that we were not able to adjust for in the analysis. The MetS was associated with EAC but not ESCC. However this association was largely driven by the strong association between BMI and EAC. We hypothesize that this association is more likely to be explained by factors directly related to obesity than the metabolic state of the MetS, considering that no other metabolic factor than BMI was associated with EAC.

Place, publisher, year, edition, pages
London: BioMed Central, 2014
Keywords
Esophageal cancer, Esophageal adenocarcinoma, Esophageal squamous cell carcinoma, Obesity, Hypertension
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-87881 (URN)10.1186/1471-2407-14-103 (DOI)000332523500002 ()
Available from: 2014-04-14 Created: 2014-04-14 Last updated: 2018-06-08Bibliographically approved
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