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Blood glucose and risk of incident and fatal cancer in the metabolic syndrome and cancer project (me-can): analysis of six prospective cohorts.

https://arctichealth.org/en/permalink/ahliterature98549
Source
PLoS Med. 2009 Dec;6(12):e1000201
Publication Type
Article
Date
Dec-2009
Author
Tanja Stocks
Kilian Rapp
Tone Bjørge
Jonas Manjer
Hanno Ulmer
Randi Selmer
Annekatrin Lukanova
Dorthe Johansen
Hans Concin
Steinar Tretli
Göran Hallmans
Håkan Jonsson
Pär Stattin
Author Affiliation
Department of Surgical and Perioperative sciences, Urology and Andrology, Umeå University, Umeå, Sweden. tanja.stocks@urologi.umu.se
Source
PLoS Med. 2009 Dec;6(12):e1000201
Date
Dec-2009
Language
English
Publication Type
Article
Keywords
Adult
Blood Glucose - analysis
Body mass index
Cohort Studies
Europe - epidemiology
Female
Follow-Up Studies
Humans
Male
Metabolic Syndrome X - blood - epidemiology
Middle Aged
Neoplasms - blood - epidemiology
Prospective Studies
Risk assessment
Abstract
BACKGROUND: Prospective studies have indicated that elevated blood glucose levels may be linked with increased cancer risk, but the strength of the association is unclear. We examined the association between blood glucose and cancer risk in a prospective study of six European cohorts. METHODS AND FINDINGS: The Metabolic syndrome and Cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden; the current study included 274,126 men and 275,818 women. Mean age at baseline was 44.8 years and mean follow-up time was 10.4 years. Excluding the first year of follow-up, 18,621 men and 11,664 women were diagnosed with cancer, and 6,973 men and 3,088 women died of cancer. We used Cox regression models to calculate relative risk (RR) for glucose levels, and included adjustment for body mass index (BMI) and smoking status in the analyses. RRs were corrected for regression dilution ratio of glucose. RR (95% confidence interval) per 1 mmol/l increment of glucose for overall incident cancer was 1.05 (1.01-1.10) in men and 1.11 (1.05-1.16) in women, and corresponding RRs for fatal cancer were 1.15 (1.07-1.22) and 1.21 (1.11-1.33), respectively. Significant increases in risk among men were found for incident and fatal cancer of the liver, gallbladder, and respiratory tract, for incident thyroid cancer and multiple myeloma, and for fatal rectal cancer. In women, significant associations were found for incident and fatal cancer of the pancreas, for incident urinary bladder cancer, and for fatal cancer of the uterine corpus, cervix uteri, and stomach. CONCLUSIONS: Data from our study indicate that abnormal glucose metabolism, independent of BMI, is associated with an increased risk of cancer overall and at several cancer sites. Our data showed stronger associations among women than among men, and for fatal cancer compared to incident cancer. Please see later in the article for the Editors' Summary.
PubMed ID
20027213 View in PubMed
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Blood pressure and other metabolic syndrome factors and risk of brain tumour in the large population-based Me-Can cohort study.

https://arctichealth.org/en/permalink/ahliterature128682
Source
J Hypertens. 2012 Feb;30(2):290-6
Publication Type
Article
Date
Feb-2012
Author
Michael Edlinger
Susanne Strohmaier
Håkan Jonsson
Tone Bjørge
Jonas Manjer
Wegene T Borena
Christel Häggström
Anders Engeland
Steinar Tretli
Hans Concin
Gabriele Nagel
Randi Selmer
Dorthe Johansen
Tanja Stocks
Göran Hallmans
Pär Stattin
Hanno Ulmer
Author Affiliation
Department of Medical Statistics, Informatics and Health Economics, Medical University Innsbruck, Innsbruck, Austria.
Source
J Hypertens. 2012 Feb;30(2):290-6
Date
Feb-2012
Language
English
Publication Type
Article
Keywords
Adult
Austria - epidemiology
Blood pressure
Brain Neoplasms - epidemiology - physiopathology
Cohort Studies
Female
Humans
Male
Metabolic Syndrome X - physiopathology
Middle Aged
Norway - epidemiology
Sweden - epidemiology
Abstract
Brain tumour has few established determinants. We assessed to which extent risk of brain tumour was related to metabolic syndrome factors in adults.
In the Me-Can project, 580?000 individuals from Sweden, Austria, and Norway were followed for a median of 10 years after baseline measurement. Data on brain tumours were obtained from national cancer registries. The factors of metabolic syndrome (BMI, SBP and DBP, and blood levels of glucose, cholesterol, and triglycerides), separately and combined, were analysed in quintiles and for transformed z-scores (mean transformed to 0 and standard deviation to 1). Cox proportional hazards multivariate regression models were used, with corrections for measurement error.
During follow-up, 1312 primary brain tumours were diagnosed, predominantly meningioma (n?=?348) and high-grade glioma (n?=?436). For meningioma, the hazard ratio was increased for z-scores of SBP [hazard ratio?=?1.27 per unit standard deviation, 95% confidence interval (CI) 1.03-1.57], of DBP (hazard ratio?=?1.29, 95% CI 1.04-1.58), and of the combined metabolic syndrome score (hazard ratio?=?1.31, 95% CI 1.11-1.54). An increased risk of high-grade glioma was found for DBP (hazard ratio?=?1.23, 95% CI 1.01-1.50) and triglycerides (hazard ratio?=?1.35, 95% CI 1.05-1.72). For both meningioma and high-grade glioma, the risk was more than double in the fifth quintiles of DBP compared to the lowest quintile. For meningioma this risk was even larger for SBP.
Increased blood pressure was associated with risk of brain tumours, especially of meningiomas.
PubMed ID
22179083 View in PubMed
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Blood pressure and risk of cancer incidence and mortality in the Metabolic Syndrome and Cancer Project.

https://arctichealth.org/en/permalink/ahliterature126806
Source
Hypertension. 2012 Apr;59(4):802-10
Publication Type
Article
Date
Apr-2012
Author
Tanja Stocks
Mieke Van Hemelrijck
Jonas Manjer
Tone Bjørge
Hanno Ulmer
Göran Hallmans
Björn Lindkvist
Randi Selmer
Gabriele Nagel
Steinar Tretli
Hans Concin
Anders Engeland
Håkan Jonsson
Pär Stattin
Author Affiliation
Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden. tanja.stocks@urologi.umu.se
Source
Hypertension. 2012 Apr;59(4):802-10
Date
Apr-2012
Language
English
Publication Type
Article
Keywords
Adult
Austria - epidemiology
Blood Pressure - physiology
Cohort Studies
Female
Humans
Hypertension - complications - epidemiology - physiopathology
Incidence
Longitudinal Studies
Male
Middle Aged
Neoplasms - epidemiology - mortality
Norway - epidemiology
Retrospective Studies
Sex Characteristics
Survival Rate
Sweden - epidemiology
Abstract
Observational studies have shown inconsistent results for the association between blood pressure and cancer risk. We investigated the association in 7 cohorts from Norway, Austria, and Sweden. In total, 577799 adults with a mean age of 44 years were followed for, on average, 12 years. Incident cancers were 22184 in men and 14744 in women, and cancer deaths were 8724 and 4525, respectively. Cox regression was used to calculate hazard ratios of cancer per 10-mmHg increments of midblood pressure, which corresponded with 0.7 SDs and, for example, an increment of systolic/diastolic blood pressure of 130/80 to 142/88 mmHg. All of the models used age as the time scale and were adjusted for possible confounders, including body mass index and smoking status. In men, midblood pressure was positively related to total incident cancer (hazard ratio per 10 mmHg increment: 1.07 [95% CI: 1.04-1.09]) and to cancer of the oropharynx, colon, rectum, lung, bladder, kidney, malignant melanoma, and nonmelanoma skin cancer. In women, midblood pressure was not related to total incident cancer but was positively related to cancer of the liver, pancreas, cervix, uterine corpus, and malignant melanoma. A positive association was also found for cancer mortality, with HRs per 10-mmHg increment of 1.12 (95% CI: 1.08-1.15) for men and 1.06 (95% CI: 1.02-1.11) for women. These results suggest a small increased cancer risk overall in men with elevated blood pressure level and a higher risk for cancer death in men and women.
PubMed ID
22353615 View in PubMed
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Cohort Profile: The Metabolic syndrome and Cancer project (Me-Can).

https://arctichealth.org/en/permalink/ahliterature151439
Source
Int J Epidemiol. 2010 Jun;39(3):660-7
Publication Type
Article
Date
Jun-2010
Author
Tanja Stocks
Wegene Borena
Susanne Strohmaier
Tone Bjørge
Jonas Manjer
Anders Engeland
Dorthe Johansen
Randi Selmer
Göran Hallmans
Kilian Rapp
Hans Concin
Håkan Jonsson
Hanno Ulmer
Pär Stattin
Author Affiliation
Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden. tanja.stocks@urologi.umu.se
Source
Int J Epidemiol. 2010 Jun;39(3):660-7
Date
Jun-2010
Language
English
Publication Type
Article
Keywords
Austria - epidemiology
Cohort Studies
Epidemiologic Research Design
Humans
Metabolic Syndrome X - epidemiology
Neoplasms - epidemiology
Norway - epidemiology
Program Development
Sweden - epidemiology
Notes
Cites: BMJ. 1993 Nov 20;307(6915):1318-228257886
Cites: Acta Oncol. 2009;48(1):27-3318767000
Cites: Scand J Prim Health Care. 1998 Sep;16(3):171-69800231
Cites: Arch Med Res. 2005 May-Jun;36(3):223-3115925012
Cites: Diabetes Care. 2005 Jul;28(7):1769-7815983333
Cites: Diabetologia. 2006 May;49(5):945-5216557372
Cites: Am J Epidemiol. 2006 Oct 15;164(8):769-7416952929
Cites: Diabetes Care. 1999 Dec;22(12):1988-9210587831
Cites: J Intern Med. 2000 Jan;247(1):19-2910672127
Cites: Diabetes Care. 2001 Apr;24(4):683-911315831
Cites: Eur Heart J. 2003 Jun;24(11):1004-1312788300
Cites: Eur J Epidemiol. 2003;18(6):479-8512908712
Cites: Acta Med Scand Suppl. 1975;588:1-381062920
Cites: Acta Med Scand Suppl. 1983;675:1-1846581684
Cites: Br Med J (Clin Res Ed). 1987 Mar 14;294(6573):671-33105680
Cites: Am J Epidemiol. 1989 Mar;129(3):458-652916539
Cites: Am J Pathol. 2006 Nov;169(5):1505-2217071576
Cites: Diabetes Care. 2007 Jan;30(1):8-1317192325
Cites: Int J Epidemiol. 2006 Dec;35(6):1570-817148467
Cites: Int J Epidemiol. 2008 Jun;37(3):481-517984119
Cites: J Intern Med. 1996 Jun;239(6):489-978656142
PubMed ID
19380371 View in PubMed
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Longitudinal study of body mass index, dyslipidemia, hyperglycemia, and hypertension in 60,000 men and women in Sweden and Austria.

https://arctichealth.org/en/permalink/ahliterature296582
Source
PLoS One. 2018; 13(6):e0197830
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Date
2018
Author
Mieke Van Hemelrijck
Hanno Ulmer
Gabriele Nagel
Raphael Simon Peter
Josef Fritz
Robin Myte
Bethany van Guelpen
Bernhard Föger
Hans Concin
Christel Häggström
Pär Stattin
Tanja Stocks
Author Affiliation
King's College London, Division of Cancer Studies, Translational Oncology & Urology Research, London, United Kingdom.
Source
PLoS One. 2018; 13(6):e0197830
Date
2018
Language
English
Publication Type
Journal Article
Research Support, Non-U.S. Gov't
Keywords
Adult
Austria - epidemiology
Body mass index
Dyslipidemias - epidemiology
Female
Humans
Hyperglycemia - epidemiology
Hypertension - epidemiology
Longitudinal Studies
Male
Middle Aged
Sweden - epidemiology
Abstract
Obesity is suggested to underlie development of other metabolic aberrations, but longitudinal relationships between metabolic factors at various ages has not been studied in detail.
Data from 27,379 men and 32,275 women with in total 122,940 health examinations in the Västerbotten Intervention Project, Sweden and the Vorarlberg Health Monitoring and Prevention Programme, Austria were used to investigate body mass index (BMI), mid-blood pressure, and fasting levels of glucose, triglycerides, and total cholesterol at baseline in relation to 10-year changes of these factors and weight. We included paired examinations performed 10±2 years apart and used them for longitudinal analysis with linear regression of changes between the ages 30 and 40, 40 and 50, or 50 and 60 years.
Higher levels of BMI were associated with increases in glucose and mid-blood pressure as well as triglycerides levels, and, to a lesser extent, decreases in cholesterol levels. For instance, per 5 kg/m2 higher BMI at age 40, glucose at age 50 increased by 0.24 mmol/l (95%CI: 0.22-0.26) and mid-blood pressure increased by 1.54 mm Hg (95%CI: 1.35-1.74). The strongest association observed was between BMI at age 30 and mid-blood pressure, which was 2.12 mm Hg (95% CI: 1.79-2.45) increase over ten years per 5 kg/m2 higher BMI level. This association was observed at an age when blood pressure levels on average remained stable. Other associations than those with BMI at baseline were much weaker. However, triglyceride levels were associated with future glucose changes among individuals with elevated BMI, particularly in the two older age groups.
BMI was most indicative of long-term changes in metabolic factors, and the strongest impact was observed for increases in blood pressure between 30 and 40 years of age. Our study supports that lifestyle interventions preventing metabolic aberrations should focus on avoiding weight increases.
PubMed ID
29897925 View in PubMed
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Metabolic factors and risk of thyroid cancer in the Metabolic syndrome and Cancer project (Me-Can).

https://arctichealth.org/en/permalink/ahliterature136429
Source
Cancer Causes Control. 2011 May;22(5):743-51
Publication Type
Article
Date
May-2011
Author
Martin Almquist
Dorthe Johansen
Tone Björge
Hanno Ulmer
Björn Lindkvist
Tanja Stocks
Göran Hallmans
Anders Engeland
Kilian Rapp
Håkan Jonsson
Randi Selmer
Guenter Diem
Christel Häggström
Steinar Tretli
Pär Stattin
Jonas Manjer
Author Affiliation
Department of Surgery, Skåne University Hospital Lund and Lund University, 221 85 Lund, Sweden. martin.almquist@med.lu.se
Source
Cancer Causes Control. 2011 May;22(5):743-51
Date
May-2011
Language
English
Publication Type
Article
Keywords
Adult
Austria - epidemiology
Blood Glucose - metabolism
Blood pressure
Body mass index
Cholesterol - blood
Cohort Studies
Female
Humans
Male
Metabolic Syndrome X - blood - epidemiology - metabolism
Middle Aged
Norway - epidemiology
Prognosis
Prospective Studies
Risk factors
Sweden - epidemiology
Thyroid Neoplasms - blood - epidemiology - metabolism
Triglycerides - blood
Abstract
To investigate metabolic factors and their possible impact on risk of thyroid cancer.
A prospective cohort study was conducted based on seven population-based cohorts in Norway, Austria, and Sweden, in the Metabolic syndrome and Cancer project (Me-Can). Altogether 578,700 men and women with a mean age of 44.0 years at baseline were followed for on average 12.0 years. Relative risk of incident thyroid cancer was assessed by levels of BMI, blood pressure, and blood levels of glucose, cholesterol, triglycerides, and by a combined metabolic syndrome (MetS) score. Risk estimates were investigated for quintiles, and a z score distribution of exposures was analyzed using Cox proportional hazards regression.
During follow-up, 255 women and 133 men were diagnosed with thyroid cancer. In women, there was an inverse association between glucose and thyroid cancer risk, with adjusted RR: 95% CI was 0.61 (0.41-0.90), p trend = 0.02 in the fifth versus the first quintile, and a positive association between BMI and thyroid cancer risk with a significant trend over quintiles. There was no association between the other metabolic factors, single or combined (Met-S), and thyroid cancer.
In women, BMI was positively, while blood glucose levels were inversely, associated with thyroid cancer.
PubMed ID
21380729 View in PubMed
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Metabolic Mediators of the Effects of Family History and Genetic Risk Score on Coronary Heart Disease-Findings From the Malmö Diet and Cancer Study.

https://arctichealth.org/en/permalink/ahliterature289811
Source
J Am Heart Assoc. 2017 Mar 20; 6(3):
Publication Type
Journal Article
Observational Study
Date
Mar-20-2017
Author
Josef Fritz
Dov Shiffman
Olle Melander
Hayato Tada
Hanno Ulmer
Author Affiliation
Department of Medical Statistics, Informatics and Health Economics, Medical University of Innsbruck, Austria.
Source
J Am Heart Assoc. 2017 Mar 20; 6(3):
Date
Mar-20-2017
Language
English
Publication Type
Journal Article
Observational Study
Keywords
Aged
Apolipoprotein A-I - genetics
Apolipoprotein B-100 - genetics
Blood pressure
Coronary Disease - epidemiology - genetics
Diabetes Mellitus - epidemiology
Female
Follow-Up Studies
Genetic Predisposition to Disease
Humans
Male
Medical History Taking
Middle Aged
Proportional Hazards Models
Prospective Studies
Risk assessment
Sweden - epidemiology
Abstract
Family history of coronary heart disease (CHD) as well as genetic predisposition to CHD assessed by a genetic risk score (GRS) are predictors of CHD risk. It is, however, uncertain to what extent these risk predictors are mediated by major metabolic pathways.
Total effects of self-reported family history and a 50-variant GRS (GRS50), as well as effects mediated by apolipoprotein B and A-I (apoB, apoA-I), blood pressure, and diabetes mellitus, on incidence of CHD were estimated in 23 595 participants of the Malmö Diet and Cancer study (a prospective, population-based study). During a median follow-up of 14.4 years, 2213 participants experienced a first CHD event. Family history of CHD and GRS50 (highest versus other quintiles) were associated with incident CHD, with hazard ratios of 1.52 (95% CI: 1.39-1.65) and 1.53 (95% CI: 1.39-1.68), respectively, after adjusting for age, sex, and smoking status. Small proportions of the family history effect were mediated by metabolic risk factors: 8.3% (95% CI: 5.8-11.7%) by the apoB pathway, 1.7% (95% CI: 0.2-3.4%) by apoA-I, 8.5% (95% CI: 5.9-12.0%) by blood pressure, and 1.5% (95% CI: -0.8% to 3.8%) by diabetes mellitus. Similarly, small proportions of GRS50 were mediated: 8.1% (95% CI: 5.5-11.8%) by apoB, 1.2% (95% CI: 0.5-3.0%) by apoA-I, 4.2% (95% CI: 1.3-7.5%) by blood pressure, and -0.9% (95% CI: -3.7% to 1.6%) by diabetes mellitus.
A fraction of the CHD risk associated with family history or with GRS50 is mediated through elevated blood lipids and hypertension, but not through diabetes mellitus. However, a major part (=80%) of the genetic effect operates independently of established metabolic risk factor pathways.
Notes
Cites: Circulation. 2001 Jul 24;104(4):393-8 PMID 11468199
Cites: Epidemiology. 2011 Jul;22(4):575-81 PMID 21552129
Cites: Circulation. 1984 Jun;69(6):1065-9 PMID 6713610
Cites: BMC Public Health. 2011 Jun 09;11:450 PMID 21658213
Cites: Circulation. 2016 Mar 22;133(12 ):1181-8 PMID 26915630
Cites: Nat Genet. 2011 Mar 06;43(4):333-8 PMID 21378990
Cites: Lancet. 2015 Jun 6;385(9984):2264-2271 PMID 25748612
Cites: J Intern Med. 1993 Jan;233(1):45-51 PMID 8429286
Cites: Int J Cardiol. 2015 Jan 20;179:409-16 PMID 25464496
Cites: JAMA. 2004 May 12;291(18):2204-11 PMID 15138242
Cites: J Clin Epidemiol. 1996 May;49(5):497-503 PMID 8636722
Cites: Stat Methods Med Res. 2007 Aug;16(4):309-30 PMID 17715159
Cites: Eur Heart J. 2016 Feb 7;37(6):561-7 PMID 26392438
Cites: Lancet. 2010 Oct 23;376(9750):1393-400 PMID 20971364
Cites: Arterioscler Thromb Vasc Biol. 2013 Sep;33(9):2267-72 PMID 23685553
Cites: Atherosclerosis. 2015 Nov;243(1):86-92 PMID 26363437
Cites: Am J Cardiol. 1991 May 1;67(11):933-8 PMID 2018010
Cites: Am J Epidemiol. 2014 Feb 15;179(4):513-8 PMID 24264291
Cites: Int J Epidemiol. 2000 Aug;29(4):722-9 PMID 10922351
Cites: Nat Genet. 2013 Jan;45(1):25-33 PMID 23202125
Cites: Am J Epidemiol. 2012 Aug 1;176(3):190-5 PMID 22781427
Cites: Eur Heart J. 2016 Feb 7;37(6):568-71 PMID 26475834
Cites: Eur J Epidemiol. 2010 Feb;25(2):95-102 PMID 19936945
Cites: Eur Heart J. 2016 Jul 1;37(25):1977-81 PMID 26908950
Cites: Circulation. 2005 Nov 29;112(22):3375-83 PMID 16316964
Cites: Cell. 2012 Mar 16;148(6):1242-57 PMID 22424232
Cites: Eur J Clin Invest. 2013 Oct;43(10):1009-15 PMID 23859101
Cites: JAMA. 2007 Aug 15;298(7):776-85 PMID 17699011
Cites: Am J Epidemiol. 1986 Jan;123(1):48-58 PMID 3940442
Cites: Eur Heart J. 2012 Feb;33(3):393-407 PMID 21804106
Cites: Eur Heart J. 2013 Apr;34(16):1198-203 PMID 23297314
Cites: Stat Methods Med Res. 2015 Aug 17;:null PMID 26282889
Cites: Arterioscler Thromb Vasc Biol. 2008 Jan;28(1):173-9 PMID 17975119
Cites: J Am Coll Cardiol. 1984 Oct;4(4):793-801 PMID 6481018
PubMed ID
28320750 View in PubMed
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Metabolic risk factors and cervical cancer in the metabolic syndrome and cancer project (Me-Can).

https://arctichealth.org/en/permalink/ahliterature127036
Source
Gynecol Oncol. 2012 May;125(2):330-5
Publication Type
Article
Date
May-2012
Author
Hanno Ulmer
Tone Bjørge
Hans Concin
Annekatrin Lukanova
Jonas Manjer
Göran Hallmans
Wegene Borena
Christel Häggström
Anders Engeland
Martin Almquist
Håkan Jonsson
Randi Selmer
Pär Stattin
Steinar Tretli
Andrea Kleiner
Tanja Stocks
Gabriele Nagel
Author Affiliation
Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Austria.
Source
Gynecol Oncol. 2012 May;125(2):330-5
Date
May-2012
Language
English
Publication Type
Article
Keywords
Adult
Aged
Austria - epidemiology
Blood Glucose - metabolism
Blood pressure
Body mass index
Cell Transformation, Neoplastic - metabolism
Cholesterol - blood
Cohort Studies
Female
Humans
Metabolic Syndrome X - epidemiology - metabolism
Middle Aged
Norway - epidemiology
Proportional Hazards Models
Risk factors
Sweden - epidemiology
Triglycerides - blood
Uterine Cervical Neoplasms - epidemiology - metabolism
Abstract
Little is known about the association between metabolic risk factors and cervical cancer carcinogenesis.
During mean follow-up of 11 years of the Me-Can cohort (N=288,834) 425 invasive cervical cancer cases were diagnosed. Hazard ratios (HRs) were estimated by the use of Cox proportional hazards regression models for quintiles and standardized z-scores (with a mean of 0 and a SD of 1) of BMI, blood pressure, glucose, cholesterol, triglycerides and MetS score. Risk estimates were corrected for random error in the measurements.
BMI (per 1SD increment) was associated with 12%, increase of cervical cancer risk, blood pressure with 25% and triglycerides with 39%, respectively. In models including all metabolic factors, the associations for blood pressure and triglycerides persisted. The metabolic syndrome (MetS) score was associated with 26% increased corrected risk of cervical cancer. Triglycerides were stronger associated with squamous cell carcinoma (HR 1.48; 95% CI, 1.20-1.83) than with adenocarcinoma (0.92, 0.54-1.56). Among older women cholesterol (50-70 years 1.34; 1.00-1.81), triglycerides (50-70 years 1.49, 1.03-2.16 and =70 years 1.54, 1.09-2.19) and glucose (= 70 years 1.87, 1.13-3.11) were associated with increased cervical cancer risk.
The presence of obesity, elevated blood pressure and triglycerides were associated with increased risk of cervical cancer.
PubMed ID
22330614 View in PubMed
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Metabolic risk factors and primary liver cancer in a prospective study of 578,700 adults.

https://arctichealth.org/en/permalink/ahliterature101343
Source
Int J Cancer. 2011 Jul 29;
Publication Type
Article
Date
Jul-29-2011
Author
Wegene Borena
Susanne Strohmaier
Annekatrin Lukanova
Tone Bjørge
Björn Lindkvist
Goran Hallmans
Michael Edlinger
Tanja Stocks
Gabriele Nagel
Jonas Manjer
Anders Engeland
Randi Selmer
Christel Häggström
Steinar Tretli
Hans Concin
Håkan Jonsson
Pär Stattin
Hanno Ulmer
Author Affiliation
Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical, University, Austria.
Source
Int J Cancer. 2011 Jul 29;
Date
Jul-29-2011
Language
English
Publication Type
Article
Abstract
Initial studies have indicated diabetes and obesity to be risk factors for hepatocellular carcinoma; but the association between other metabolic risk factors and primary liver cancer has not been investigated. The metabolic syndrome and cancer project (Me-Can) includes cohorts from Norway, Austria, and Sweden with data on 578,700 subjects. We used Cox proportional hazard models to calculate relative risks (RRs) of primary liver cancer by body mass index (BMI), blood pressure, and plasma levels of glucose, cholesterol, and triglycerides as continuous standardized variables (z-score with mean=0 and standard deviation (SD)=1) and their standardized sum of metabolic syndrome (MetS) z-score. RRs were corrected for random error in measurements. During an average follow-up of 12.0 years (SD=7.8), 266 primary liver cancers were diagnosed among cohort members. Relative risk of liver cancer per unit increment of z-score adjusted for age, smoking status and BMI and stratified by birth year, sex and sub-cohorts, was for BMI 1.39 (95% confidence interval (CI) 1.24 to 1.58), mid blood pressure 2.08 (0.95 to 4.73), blood glucose 2.13 (1.55 to 2.94) cholesterol 0.62 (0.51 to 0.76) and serum triglycerides 0.85 (0.65 to 1.10). The RR per one unit increment of the MetS z-score was 1.35 (1.12 to 1.61). BMI, glucose, and a composite metabolic syndrome score were positively and cholesterol negatively associated with risk of liver cancer.
PubMed ID
21805476 View in PubMed
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Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580,000 subjects within the Me-Can project.

https://arctichealth.org/en/permalink/ahliterature257803
Source
BMC Cancer. 2014;14:103
Publication Type
Article
Date
2014
Author
Björn Lindkvist
Dorthe Johansen
Tanja Stocks
Hans Concin
Tone Bjørge
Martin Almquist
Christel Häggström
Anders Engeland
Göran Hallmans
Gabriele Nagel
Håkan Jonsson
Randi Selmer
Hanno Ulmer
Steinar Tretli
Pär Stattin
Jonas Manjer
Author Affiliation
Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. bjorn.lindkvist@vgregion.se.
Source
BMC Cancer. 2014;14:103
Date
2014
Language
English
Publication Type
Article
Keywords
Adenocarcinoma - blood - diagnosis - epidemiology
Adult
Austria - epidemiology
Blood Glucose - metabolism
Carcinoma, Squamous Cell - blood - diagnosis - epidemiology
Cohort Studies
Esophageal Neoplasms - blood - diagnosis - epidemiology
Female
Humans
Male
Metabolic Syndrome X - blood - diagnosis - epidemiology
Middle Aged
Norway - epidemiology
Prospective Studies
Risk factors
Sweden - epidemiology
Abstract
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.
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).
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.
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.
Notes
Cites: Diabetes Care. 1999 Dec;22(12):1988-9210587831
Cites: Int J Cancer. 2010 Dec 15;127(12):2893-91721351269
Cites: World Health Organ Tech Rep Ser. 2000;894:i-xii, 1-25311234459
Cites: Cancer. 2001 Aug 1;92(3):549-5511505399
Cites: JAMA. 2003 Jul 2;290(1):66-7212837713
Cites: Eur J Epidemiol. 2003;18(6):479-8512908712
Cites: Gut. 2004 Aug;53(8):1070-415247170
Cites: Nat Rev Cancer. 2004 Aug;4(8):579-9115286738
Cites: Cancer Causes Control. 2004 Oct;15(8):837-4315456997
Cites: Lancet. 1975 May 10;1(7915):1051-648728
Cites: Acta Med Scand Suppl. 1975;588:1-381062920
Cites: N Engl J Med. 1977 May 26;296(21):1194-200854058
Cites: Am J Epidemiol. 1991 Nov 1;134(9):942-71951291
Cites: Am J Epidemiol. 1992 Nov 1;136(9):1110-41462971
Cites: J Intern Med. 1996 Jun;239(6):489-978656142
Cites: Am J Gastroenterol. 1997 Aug;92(8):1293-79260792
Cites: J Natl Cancer Inst. 1997 Sep 17;89(18):1360-59308706
Cites: Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii19327566
Cites: Eur J Cancer. 2009 May;45(7):1218-3119091545
Cites: Cancer Epidemiol Biomarkers Prev. 2009 Jul;18(7):2079-8919567501
Cites: Br J Cancer. 2009 Sep 1;101(5):855-919672254
Cites: Int J Epidemiol. 2008 Jun;37(3):481-517984119
Cites: Acta Oncol. 2009;48(1):27-3318767000
Cites: Stat Med. 2009 Mar 30;28(7):1067-9219222086
Cites: J Hypertens. 1998 Jul;16(7):933-409794733
Cites: Ann Intern Med. 1999 Jun 1;130(11):883-9010375336
Cites: Am J Epidemiol. 1999 Aug 15;150(4):341-5310453810
Cites: JAMA. 2005 Jan 12;293(2):194-20215644546
Cites: J Intern Med. 2000 Jan;247(1):19-2910672127
Cites: Cancer Causes Control. 2009 Dec;20(10):1811-2019533392
Cites: Cancer Causes Control. 2012 Feb;23(2):263-7222094992
Cites: Diabetes Care. 2012 Nov;35(11):2402-1123093685
Cites: Clin Gastroenterol Hepatol. 2013 Aug;11(8):934-4323466711
Cites: Cancer Causes Control. 2005 Apr;16(3):285-9415947880
Cites: Diabetologia. 2006 May;49(5):945-5216557372
Cites: Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):872-816702363
Cites: Am J Epidemiol. 2006 Oct 15;164(8):769-7416952929
Cites: Am J Pathol. 2006 Nov;169(5):1505-2217071576
Cites: Semin Radiat Oncol. 2007 Jan;17(1):2-917185192
Cites: Diabetes Care. 2007 Jan;30(1):8-1317192325
Cites: Int J Epidemiol. 2006 Dec;35(6):1570-817148467
Cites: J Hypertens. 2007 Sep;25(9):1751-6217762635
Cites: Gut. 2008 Feb;57(2):173-8017932103
Cites: Int J Cancer. 2008 Apr 1;122(7):1604-1018059032
Cites: Lancet. 2008 Feb 16;371(9612):569-7818280327
Cites: PLoS Med. 2009 Dec;6(12):e100020120027213
Cites: Int J Epidemiol. 2010 Jun;39(3):660-719380371
Cites: Arch Med Res. 2005 May-Jun;36(3):223-3115925012
PubMed ID
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