SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) ;srt2:(2010-2019);pers:(Manjer Jonas)"

Sökning: hsv:(MEDICIN OCH HÄLSOVETENSKAP) hsv:(Klinisk medicin) > (2010-2019) > Manjer Jonas

  • Resultat 1-10 av 193
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  • Borena, Wegene, et al. (författare)
  • A prospective study on metabolic risk factors and gallbladder cancer in the metabolic syndrome and cancer (Me-Can) collaborative study
  • 2014
  • Ingår i: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 9:2, s. e89368-
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
2.
  • Murphy, Neil, et al. (författare)
  • Consumption of Dairy Products and Colorectal Cancer in the European Prospective Investigation into Cancer and Nutrition (EPIC)
  • 2013
  • Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:9
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Prospective studies have consistently reported lower colorectal cancer risks associated with higher intakes of total dairy products, total milk and dietary calcium. However, less is known about whether the inverse associations vary for individual dairy products with differing fat contents. Materials and Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC), we investigated the associations between intakes of total milk and milk subtypes (whole-fat, semi-skimmed and skimmed), yoghurt, cheese, and dietary calcium with colorectal cancer risk amongst 477,122 men and women. Dietary questionnaires were administered at baseline. Multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models, adjusted for relevant confounding variables. Results: During the mean 11 years of follow-up, 4,513 incident cases of colorectal cancer occurred. After multivariable adjustments, total milk consumption was inversely associated with colorectal cancer risk (HR per 200 g/day 0.93, 95% CI: 0.89-0.98). Similar inverse associations were observed for whole-fat (HR per 200 g/day 0.90, 95% CI: 0.82-0.99) and skimmed milk (HR per 200 g/day 0.90, 95% CI: 0.79-1.02) in the multivariable models. Inverse associations were observed for cheese and yoghurt in the categorical models; although in the linear models, these associations were non-significant. Dietary calcium was inversely associated with colorectal cancer risk (HR per 200 mg/day 0.95, 95% CI: 0.91-0.99); this association was limited to dairy sources of calcium only (HR per 200 mg/day 0.95, 95% CI: 0.91-0.99), with no association observed for non-dairy calcium sources (HR per 200 mg/day 1.00, 95% CI: 0.81-1.24). Conclusions: Our results strengthen the evidence for a possible protective role of dairy products on colorectal cancer risk. The inverse associations we observed did not differ by the fat content of the dairy products considered.
  •  
3.
  • Beral, V., et al. (författare)
  • Ovarian Cancer and Body Size : Individual Participant Meta-Analysis Including 25,157 Women with Ovarian Cancer from 47 Epidemiological Studies
  • 2012
  • Ingår i: PLoS Medicine. - : PUBLIC LIBRARY SCIENCE. - 1549-1277 .- 1549-1676. ; 9:4
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Only about half the studies that have collected information on the relevance of women's height and body mass index to their risk of developing ovarian cancer have published their results, and findings are inconsistent. Here, we bring together the worldwide evidence, published and unpublished, and describe these relationships. Methods and Findings: Individual data on 25,157 women with ovarian cancer and 81,311 women without ovarian cancer from 47 epidemiological studies were collected, checked, and analysed centrally. Adjusted relative risks of ovarian cancer were calculated, by height and by body mass index. Ovarian cancer risk increased significantly with height and with body mass index, except in studies using hospital controls. For other study designs, the relative risk of ovarian cancer per 5 cm increase in height was 1.07 (95% confidence interval [CI], 1.05-1.09; p<0.001); this relationship did not vary significantly by women's age, year of birth, education, age at menarche, parity, menopausal status, smoking, alcohol consumption, having had a hysterectomy, having first degree relatives with ovarian or breast cancer, use of oral contraceptives, or use of menopausal hormone therapy. For body mass index, there was significant heterogeneity (p<0.001) in the findings between ever-users and never-users of menopausal hormone therapy, but not by the 11 other factors listed above. The relative risk for ovarian cancer per 5 kg/m(2) increase in body mass index was 1.10 (95% CI, 1.07-1.13; p<0.001) in never-users and 0.95 (95% CI, 0.92-0.99; p = 0.02) in ever-users of hormone therapy. Conclusions: Ovarian cancer is associated with height and, among never-users of hormone therapy, with body mass index. In high-income countries, both height and body mass index have been increasing in birth cohorts now developing the disease. If all other relevant factors had remained constant, then these increases in height and weight would be associated with a 3% increase in ovarian cancer incidence per decade.
  •  
4.
  • Wangefjord, Sakarias, et al. (författare)
  • Cyclin D1 expression in colorectal cancer is a favorable prognostic factor in men but not in women in a prospective, population-based cohort study.
  • 2011
  • Ingår i: Biology of Sex Differences. - : Springer Science and Business Media LLC. - 2042-6410. ; 2
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Although colorectal cancer (CRC) is generally not considered to be a hormone-dependent malignancy, several sex-related differences in incidence, molecular characteristics and survival have been reported. Epidemiological studies have consistently shown that increased exposure to female sex hormones is associated with a lower risk of CRC in women, and cyclin D1, an important downstream effector in estrogen-mediated signaling, is commonly activated in CRC. In this study, we analyzed the prognostic significance of cyclin D1 expression in CRC, with particular reference to sex-related differences, in tumors from a large, prospective, population-based cohort. METHODS: Using tissue microarrays and immunohistochemistry, the fraction and intensity of cyclin D1 expression was evaluated in 527 incident CRC cases from the Malmö Diet and Cancer Study. The χ2 and Spearman's rho (ρ) tests were used for comparison of cyclin D1 expression and relevant clinicopathological characteristics. Kaplan-Meier analysis and Cox proportional hazards modeling were used to assess the effect of cyclin D1 expression on cancer-specific survival (CSS) in univariate and multivariate analysis, adjusted for established prognostic factors. RESULTS: Cyclin D1 intensity was significantly lower in male compared with female CRC (P = 0.018). In the full cohort, cyclin D1 expression was associated with a significantly prolonged CSS (hazard ratio (HR) = 0.69; 95% CI 0.49 to 0.96, P = 0.026) but subgroup analysis according to gender revealed a strongly accentuated prognostic effect of cyclin D1 in male CRC (HR = 0.48; 95% CI 0.31 to 0.74, P < 0.001), which was in contrast to female CRC, where cyclin D1 was not prognostic (HR = 1.05; 95% CI 0.62 to 1.78, P = 0.864) (Pinteraction = 0.024). The prognostic value of cyclin D1 was not retained in multivariate analysis, either in the full cohort or in male CRC. CONCLUSIONS: Cyclin D1 expression is strongly associated with prolonged survival in male CRC. These findings not only support an important role for cyclin D1 in colorectal carcinogenesis, but also add further weight to the accumulating evidence that CRC is indeed a hormone-dependent malignancy, for which prognostic and treatment-predictive molecular biomarkers should be evaluated differently in women and men.
  •  
5.
  • Johansen, Dorthe, et al. (författare)
  • Pre-Diagnostic Levels of Anionic Trypsinogen, Cationic Trypsinogen, and Pancreatic Secretory Trypsin Inhibitor in Relation to Pancreatic Cancer Risk.
  • 2010
  • Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 10:2-3, s. 229-237
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/Aims: Experimental studies have suggested that trypsinogen may enhance tumor progression and that the ratio between anionic trypsinogen and cationic trypsinogen (HAT/HCT) and between the sum of trypsinogens and pancreatic secretory trypsin inhibitor (PSTI) ((HAT + HCT)/PSTI) are disturbed in patients with pancreatic cancer. The aim of this study was to investigate if pre-diagnostic levels of these parameters are associated with subsequent pancreatic cancer risk. Methods: A total of 33,346 subjects participated in a health screening programme in Malmö, Sweden. Pancreatic cancer cases (n = 84) were matched to three controls each. HAT, HCT and PSTI were analyzed in pre-diagnostic serum samples. Odds ratios for pancreatic cancer were calculated using logistic regression and were then stratified for other risk factors. Results: In the main analysis, a statistically significant association between the ratio between HAT/HCT and pancreatic cancer was observed for all, for the crude OR and for the ORs adjusted for sex, BMI or Helicobacter pylori. When stratified for sex, statistically significant associations were found for females in the crude OR and for the ORs adjusted for time to analysis, BMI, alcohol consumption or H. pylori. There was a positive association between the ratio of HAT/HCT to pancreatic cancer in the intermediate/high alcohol consumption group and subjects with a BMI <25. The sum of trypsinogens showed a similar pattern, but was only of borderline significance in the intermediate/high alcohol consumption group. Conclusion: Our hypothesis predicted an increased risk for pancreatic cancer related to an imbalance between trypsin activity and trypsin inhibition capacity. The findings concerning the ratio of HAT/HCT are in line with this. The results related to analyses stratified for other risk factors should be considered as mainly explorative. and IAP.
  •  
6.
  • Stocks, Tanja, et al. (författare)
  • Blood pressure and risk of cancer incidence and mortality in the metabolic syndrome and cancer project
  • 2012
  • Ingår i: Hypertension. - Philadelphia : Lippincott Williams & Wilkins. - 0194-911X .- 1524-4563. ; 59:4, s. 802-810
  • Tidskriftsartikel (refereegranskat)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. © 2012 American Heart Association, Inc.
  •  
7.
  • Lindkvist, Björn, et al. (författare)
  • A prospective cohort study on risk of acute pancreatitis related to serum triglycerides, cholesterol and fasting glucose
  • 2012
  • Ingår i: Pancreatology. - : Elsevier BV. - 1424-3903. ; 12:4, s. 317-324
  • Tidskriftsartikel (refereegranskat)abstract
    • Background/objectives: To investigate risk for acute pancreatitis related to moderately elevated triglycerides, cholesterol and fasting glucose. Methods: This was a prospective cohort study in Malmo, Sweden of 33 346 subjects investigated 1974 - 1992 and followed until December 31, 2006. Baseline investigation included a self-administered questionnaire and analysis of serum triglycerides, cholesterol and fasting glucose. Cases of acute pancreatitis (n = 277, median time since baseline investigation 15.6 years) were identified in diagnosis registries and validated retrospectively. Attacks were classified as obstructive or non obstructive (alcohol or non alcohol related). Cox proportional hazards analysis was used to calculate hazard ratios (HR) for acute pancreatitis related to relevant risk factors, adjusting for age, sex, smoking habits and alcohol consumption. Results: Triglycerides were associated with overall, non obstructive and non obstructive non alcohol related acute pancreatitis with adjusted HRs of 1.21 (95% confidence interval (CI), 1.07-1.36), 1.23 (95% CI, 1.06-2.43) and 1.34 (95% Cl, 1.11-1.62) per 1 mmol/l increment, respectively. Corresponding HRs for forth versus first quartile of triglycerides were 1.55 (95% Cl, 1.09-2.21), 1.60 (95% Cl, 1.60-1.01-1.35) and 2.07 (95% Cl, 1.13-3.79). Triglycerides were not associated with obstructive acute pancreatitis and there were no associations between glucose or cholesterol and the risk of acute pancreatitis. Conclusions: We found an association between prediagnostic levels of triglycerides and risk for acute pancreatitis. This association was most pronounced in the non obstructive non alcohol related group. Our findings suggest that triglycerides may be a more important risk factor for acute pancreatitis than what has previously been estimated. Copyright (c) 2012, IAP and EPC. Published by Elsevier India, a division of Reed Elsevier India Pvt. Ltd. All rights reserved.
  •  
8.
  • Lindkvist, Björn, et al. (författare)
  • Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580 000 subjects within the Me-Can project
  • 2014
  • Ingår i: BMC Cancer. - London : Springer Science and Business Media LLC. - 1471-2407. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • 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.
  •  
9.
  • Lindkvist, Björn, et al. (författare)
  • Prospective cohort study of metabolic risk factors and gastric adenocarcinoma risk in the Metabolic Syndrome and Cancer Project (Me-Can)
  • 2013
  • Ingår i: Cancer Causes and Control. - : Springer Science and Business Media LLC. - 1573-7225 .- 0957-5243. ; 24:1, s. 107-116
  • Tidskriftsartikel (refereegranskat)abstract
    • Little is known about the association between the metabolic syndrome (MetS) and the risk of gastric adenocarcinoma. The aim of this study was to investigate whether metabolic risk factors, together or combined, were associated with the risk of gastric adenocarcinoma. The Metabolic Syndrome and Cancer Project (Me-Can) is a pooling of prospective cohorts in Austria, Norway, and Sweden with information on blood pressure, lipids, glucose, and BMI available in 578,700 individuals. Cox proportional hazards analysis was used to calculate hazard ratio (HR) of gastric adenocarcinoma using metabolic risk factors categorized into quintiles and transformed into z-scores (with mean = 0 and SD = 1). The standardized sum of all z-scores created a composite MetS score. In total, 1,210 incident cases of gastric adenocarcinoma were identified. Glucose was significantly associated with the risk of gastric adenocarcinoma [calibrated HR 1.58 (1.14-2.20) per one unit increment in z-score] in women. There was a statistically significant association between triglycerides and risk of gastric adenocarcinoma per mmol increment in triglycerides [HR 1.20 (1.06-1.36) per mmol] but not for the adjusted z-score in women. There were no significant association between any metabolic factors and gastric cancer among men. The composite MetS score was associated with the risk of gastric adenocarcinoma in women [HR 1.18 (1.00-1.38) per one unit increment in z-score] but not in men. Glucose and high levels of the composite MetS score were associated with an increased risk of gastric adenocarcinoma in women but not in men.
  •  
10.
  • Wirén, Sara, et al. (författare)
  • Pooled cohort study on height and risk of cancer and cancer death
  • 2014
  • Ingår i: Cancer Causes and Control. - : Springer Berlin/Heidelberg. - 0957-5243 .- 1573-7225. ; 25:2, s. 151-159
  • Tidskriftsartikel (refereegranskat)abstract
    • PURPOSE: To assess the association between height and risk of cancer and cancer death.METHODS: The metabolic syndrome and cancer project is a prospective pooled cohort study of 585,928 participants from seven cohorts in Austria, Norway, and Sweden. Hazard ratios (HRs) and 95 % confidence intervals (CIs) for cancer incidence and death were estimated in height categories and per 5-cm increment for each cancer site using Cox proportional hazards model.RESULTS: During a mean follow-up of 12.7 years (SD = 7.2), 38,862 participants were diagnosed with cancer and 13,547 participants died of cancer. Increased height (per 5-cm increment) was associated with an increased overall cancer risk in women, HR 1.07 (95 % CI 1.06-1.09), and in men, HR 1.04 (95 % CI 1.03-1.06). The highest HR was seen for malignant melanoma in women, HR 1.17 (95 % CI 1.11-1.24), and in men HR 1.12 (95 % CI 1.08-1.19). Height was also associated with increased risk of cancer death in women, HR 1.03 (95 % CI 1.01-1.16), and in men, HR 1.03 (95 % CI 1.01-1.05). The highest HR was observed for breast cancer death in postmenopausal women (>60 years), HR 1.10 (95 % CI 1.00-1.21), and death from renal cell carcinoma in men, HR 1.18 (95 % CI 1.07-1.30). All these associations were independent of body mass index.CONCLUSION: Height was associated with risk of cancer and cancer death indicating that factors related to height such as hormonal and genetic factors stimulate both cancer development and progression.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 193
Typ av publikation
tidskriftsartikel (187)
konferensbidrag (6)
Typ av innehåll
refereegranskat (191)
övrigt vetenskapligt/konstnärligt (2)
Författare/redaktör
Overvad, Kim (46)
Trichopoulou, Antoni ... (44)
Tumino, Rosario (42)
Boeing, Heiner (40)
Khaw, Kay-Tee (39)
visa fler...
Riboli, Elio (39)
Hallmans, Göran (39)
Kaaks, Rudolf (34)
Palli, Domenico (31)
Vineis, Paolo (31)
Bueno-de-Mesquita, H ... (28)
Clavel-Chapelon, Fra ... (27)
Tjonneland, Anne (27)
Lund, Eiliv (26)
Boutron-Ruault, Mari ... (26)
Stattin, Pär (26)
Almquist, Martin (26)
Panico, Salvatore (26)
Stocks, Tanja (26)
Borgquist, Signe (25)
Nagel, Gabriele (23)
Barricarte, Aurelio (22)
Häggström, Christel (22)
Jonsson, Håkan (22)
Peeters, Petra H. M. (22)
Tretli, Steinar (22)
Sánchez, Maria-José (20)
Olsen, Anja (19)
Rodríguez, Laudina (19)
Ardanaz, Eva (18)
Jenab, Mazda (18)
Tjønneland, Anne (17)
Melander, Olle (17)
Jirström, Karin (17)
Navarro, Carmen (17)
Dorronsoro, Miren (17)
Duell, Eric J. (17)
Wareham, Nick (16)
Romieu, Isabelle (16)
Norat, Teresa (15)
Allen, Naomi E (15)
Skeie, Guri (14)
Mattiello, Amalia (14)
Riboli, E. (14)
Weiderpass, Elisabet ... (14)
Lagiou, Pagona (14)
Trichopoulos, Dimitr ... (14)
Johansson, Mattias (14)
Brennan, Paul (14)
visa färre...
Lärosäte
Lunds universitet (179)
Umeå universitet (90)
Karolinska Institutet (14)
Uppsala universitet (9)
Göteborgs universitet (6)
Kungliga Tekniska Högskolan (2)
visa fler...
Mittuniversitetet (1)
visa färre...
Språk
Engelska (193)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (193)
Lantbruksvetenskap (3)
Naturvetenskap (2)
Teknik (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy