SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Häggström Christel) "

Sökning: WFRF:(Häggström Christel)

  • Resultat 51-60 av 103
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
51.
  • Jochems, Sylvia H.J., et al. (författare)
  • Association of Blood Pressure with Prostate Cancer Risk by Disease Severity and Prostate Cancer Death
  • 2022
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research (AACR). - 1055-9965 .- 1538-7755. ; 31:7, s. 1483-1491
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The association of blood pressure (BP) with prostate cancer risk after accounting for asymptomatic prostate-specific antigen (PSA) testing, and with prostate cancer death, is unclear.METHODS: We investigated BP, measured at a mean age of 38 years among 430,472 men from five Swedish cohorts, in association with incident prostate cancer (n = 32,720) and prostate cancer death (n = 6718). HRs were calculated from multivariable Cox regression models.RESULTS: Increasing systolic and diastolic BP levels combined were associated with a slightly lower prostate cancer risk, with a HR of 0.98 (95% CI, 0.97-0.99) per standard deviation (SD) of mid-BP (average of systolic and diastolic BP). The association was restricted to the PSA era (1997 onwards, HR, 0.96; 95% CI, 0.95-0.98), to diagnoses initiated by a PSA test in asymptomatic men (HR, 0.95; 95% CI, 0.93-0.97), and to low-risk prostate cancer (HR, 0.95; 95% CI, 0.92-0.97). There was no clear association with more advanced disease at diagnosis. In cases, a slightly higher risk of prostate cancer death was observed for higher BP levels (HR, 1.05; 95% CI, 1.01-1.08) per SD of mid-BP; however, the association was restricted to distant metastatic disease (Pheterogeneity between case groups = 0.01), and there was no association for BP measured less than 10 years prior to diagnosis.CONCLUSIONS: Prediagnostic BP is unlikely an important risk factor for prostate cancer development and death. Less asymptomatic PSA testing among men with higher BP levels may explain their lower risk of prostate cancer.IMPACT: Elevated BP is unlikely to be an important risk factor for prostate cancer.
  •  
52.
  • Jochems, Sylvia H.J., et al. (författare)
  • Height, body mass index, and prostate cancer risk and mortality by way of detection and cancer risk category
  • 2020
  • Ingår i: International Journal of Cancer. - : John Wiley & Sons. - 0020-7136 .- 1097-0215. ; 147:12, s. 3328-3338
  • Tidskriftsartikel (refereegranskat)abstract
    • Obesity is a risk factor for advanced, but not localised, prostate cancer (PCa), and for poor prognosis. However, the detection of localised PCa through asymptomatic screening might influence these associations. We investigated height and body mass index (BMI) among 431 902 men in five Swedish cohorts in relation to PCa risk, according to cancer risk category and detection mode, and PCa-specific mortality using Cox regression. Statistical tests were two-sided. Height was positively associated with localised intermediate-risk PCa (HR per 5 cm, 1.03, 95% CI 1.01 to 1.05), while overweight and obesity were negatively associated with localised low- and intermediate-risk PCa (HRs per 5 kg/m2 , 0.86, 95% CI 0.81 to 0.90, and 0.92, 95% CI 0.88 to 0.97). However, these associations were partially driven by PCa's detected by asymptomatic screening and, for height, also by symptoms unrelated to PCa. The HR of localised PCa's, per 5 kg/m2 , was 0.88, 95% CI 0.83 to 0.92 for screen-detected PCa's, and 0.96, 95% CI 0.90 to 1.01 for PCa's detected through lower urinary tract symptoms. BMI was positively associated with PCa-specific mortality in the full population and in case-only analysis of each PCa risk category (HRs per 5 kg/m2 , 95% CI 1.11 to 1.22, P for heterogeneity = 0.14). More active health-seeking behaviour among tall and normal-weight men may partially explain their higher risk of localised PCa. The higher PCa-specific mortality among obese men accros all PCa risk categories in our study suggests obesity as a potential target to improve the prognosis of obese PCa patients.
  •  
53.
  • Jochems, Sylvia H.J., et al. (författare)
  • Prediagnostic markers of insulin resistance and prostate cancer risk and death : A pooled study
  • 2023
  • Ingår i: Cancer Medicine. - : John Wiley & Sons. - 2045-7634. ; 12:12, s. 13732-13744
  • Tidskriftsartikel (refereegranskat)abstract
    • BackgroundInsulin resistance has been shown to be related to a higher risk of several cancers, but the association with prostate cancer (PCa) has been inconsistent.MethodsWe investigated prediagnostic markers of insulin resistance in men in four cohorts in Sweden, in relation to PCa risk (total, non-aggressive and aggressive) and PCa death using multivariable-adjusted Cox regression. The number of men, PCa cases and PCa deaths was up to 66,668, 3940 and 473 for plasma glucose and the triglyceride-glucose (TyG) index, and up to 3898, 586 and 102 for plasma insulin, glycated haemoglobin (HbA1c) and leptin.ResultsHigher HbA1c was related to a lower risk of non-aggressive PCa but no significant associations were found for insulin resistance markers with the risk of aggressive or total PCa. In PCa cases, higher glucose and TyG index were related to a higher risk of PCa death (hazard ratio [HR] per higher standard deviation, 1.22, 95% CI 1.00–1.49 and 1.24, 95% CI 1.00–1.55), which further increased when restricting the analyses to glucose and TyG index measures taken <10 years before the PCa diagnosis (HR, 1.70, 95% CI 1.09–2.70 and 1.66, 95% CI 1.12–2.51). No associations were observed for other markers in relation to PCa death.ConclusionsThe results of this study showed no associations of insulin resistance markers with the risk of clinically relevant PCa, but higher glucose and TyG index were associated with poorer survival from PCa. The lack of association for other insulin resistance markers may be due to their smaller sample size.
  •  
54.
  • Jochems, Sylvia H J, et al. (författare)
  • Smoking and risk of prostate cancer and prostate cancer death : a pooled study
  • 2023
  • Ingår i: European Urology. - : Elsevier. - 0302-2838 .- 1873-7560. ; 83:5, s. 422-431
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Prospective and detailed investigations of smoking and prostate cancer (PCa) risk and death are lacking.Objective: To investigate prediagnosis smoking habit (status, intensity, duration, and cessation) as a risk factor, on its own and combined with body mass index (BMI), for PCa incidence and death.Design, setting, and participants: We included 351 448 men with smoking information from five Swedish cohorts. Outcome measurements and statistical analysis: We used Cox regression to calculate hazard ratios (HRs) and confidence intervals (CIs) for PCa incidence (n = 24 731) and death (n = 4322).Results and limitations: Smoking was associated with a lower risk of any PCa (HR 0.89, 95% CI 0.86–0.92), which was most pronounced for low-risk PCa (HR 0.74, 95% CI 0.69–0.79) and was restricted to PCa cases diagnosed in the prostate-specific antigen (PSA) era. Smoking was associated with a higher risk of PCa death in the full cohort (HR 1.10, 95% CI 1.02–1.18) and in case-only analysis adjusted for clinical characteristics (HR 1.20, 95% CI 1.11–1.31), which was a consistent finding across case groups (p = 0.8 for heterogeneity). Associations by smoking intensity and, to lesser degree, smoking duration and cessation, supported the associations for smoking status. Smoking in combination with obesity (BMI ≥30 kg/m2) further decreased the risk of low-risk PCa incidence (HR 0.40, 95% CI 0.30–0.53 compared to never smokers with BMI <25 kg/m2) and further increased the risk of PCa death (HR 1.49, 95% CI 1.21–1.84). A limitation of the study is that only a subgroup of men had information on smoking habit around the time of their PCa diagnosis.Conclusions: The lower PCa risk for smokers in the PSA era, particularly for low-risk PCa, can probably be attributed to low uptake of PSA testing by smokers. Poor survival for smokers, particularly obese smokers, requires further study to clarify the underlying causes and the preventive potential of smoking intervention for PCa death.Patient summary: Smokers have a higher risk of dying from prostate cancer, which further increases with obesity.
  •  
55.
  • Jochems, Sylvia, et al. (författare)
  • Waist circumference and a body shape index and prostate cancer risk and mortality
  • 2021
  • Ingår i: Cancer Medicine. - : Blackwell Publishing. - 2045-7634. ; 10:8, s. 2885-2896
  • Tidskriftsartikel (refereegranskat)abstract
    • We recently found a negative association between body mass index (BMI) and the risk of localised prostate cancer (PCa), no association with advanced PCa, and a positive association with PCa‐specific mortality. In a 15% subpopulation of that study, we here investigated the measures of abdominal adiposity including waist circumference (WC) and A Body Shape Index (ABSI) in relation to PCa risk and mortality. We used data from 58,457 men from four Swedish cohorts to assess WC and ABSI in relation to PCa risk according to cancer risk category, including localised asymptomatic and symptomatic PCa and advanced PCa, and PCa‐specific mortality. Cox regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). During, on average, 10 years of follow‐up, 3290 men were diagnosed with PCa and 387 died of PCa. WC was negatively associated with the risk of total PCa (HR per 10 cm, 0.95; 95% CI 0.92–0.99), localised PCa (HR per 10 cm, 0.93, 95% CI 0.88–0.96) and localised asymptomatic PCa cases detected through a prostate‐specific antigen (PSA) test (HR per 10 cm, 0.87, 95% CI 0.81–0.94). WC was not associated with the risk of advanced PCa (HR per 10 cm, 1.02, 95% CI 0.93–1.14) or with PCa‐specific mortality (HR per 10 cm, 1.04, 95% CI 0.92–1.19). ABSI showed no associations with the risk of PCa or PCa‐specific mortality. While the negative association between WC and the risk of localised PCa was partially driven by PSA‐detected PCa cases, no association was found between abdominal adiposity and clinically manifest PCa in our population.
  •  
56.
  • Johansen, Dorthe, et al. (författare)
  • Metabolic factors and the risk of pancreatic cancer : a prospective analysis of almost 580,000 men and women in the Metabolic Syndrome and Cancer Project
  • 2010
  • Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - : American Association for Cancer Research. - 1055-9965 .- 1538-7755. ; 19:9, s. 2307-2317
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The aim of this study was to investigate the association between factors in metabolic syndrome (MetS; single and combined) and the risk of pancreatic cancer. METHODS: The Metabolic Syndrome and Cancer Project is a pooled cohort containing data on body mass index, blood pressure, and blood levels of glucose, cholesterol, and triglycerides. During follow-up, 862 individuals were diagnosed with pancreatic cancer. Cox proportional hazards analysis was used to calculate relative risks (RR) with 95% confidence intervals using the above-mentioned factors categorized into quintiles and transformed into z-scores. All z-scores were summarized and a second z-transformation creating a composite z-score for MetS was done. All risk estimates were calibrated to correct for a regression dilution bias. RESULTS: The trend over quintiles was positively associated with the risk of pancreatic cancer for mid-blood pressure (mid-BP) and glucose in men and for body mass index, mid-BP, and glucose in women. The z-score for the adjusted mid-BP (RR, 1.10; 1.01-1.20) and the calibrated z-score for glucose (RR, 1.37; 1.14-1.34) were positively associated with pancreatic cancer in men. In women, a positive association was found for calibrated z-scores for mid-BP (RR, 1.34; 1.08-1.66), for the calibrated z-score for glucose (RR, 1.98; 1.41-2.76), and for the composite z-score for MetS (RR, 1.58; 1.34-1.87). CONCLUSION: Our study adds further evidence to a possible link between abnormal glucose metabolism and risk of pancreatic cancer. IMPACT: To our knowledge, this is the first study on MetS and pancreatic cancer using prediagnostic measurements of the examined factors.
  •  
57.
  • Johansson, Mattias, et al. (författare)
  • The influence of obesity-related factors in the etiology of renal cell carcinoma—A mendelian randomization study
  • 2019
  • Ingår i: PLoS Medicine. - : Public Library of Science (PLoS). - 1549-1277 .- 1549-1676. ; 16:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Several obesity-related factors have been associated with renal cell carcinoma (RCC), but it is unclear which individual factors directly influence risk. We addressed this question using genetic markers as proxies for putative risk factors and evaluated their relation to RCC risk in a mendelian randomization (MR) framework. This methodology limits bias due to confounding and is not affected by reverse causation.Methods and findings: Genetic markers associated with obesity measures, blood pressure, lipids, type 2 diabetes, insulin, and glucose were initially identified as instrumental variables, and their association with RCC risk was subsequently evaluated in a genome-wide association study (GWAS) of 10,784 RCC patients and 20,406 control participants in a 2-sample MR framework. The effect on RCC risk was estimated by calculating odds ratios (ORSD) for a standard deviation (SD) increment in each risk factor. The MR analysis indicated that higher body mass index increases the risk of RCC (ORSD: 1.56, 95% confidence interval [CI] 1.44–1.70), with comparable results for waist-to-hip ratio (ORSD: 1.63, 95% CI 1.40–1.90) and body fat percentage (ORSD: 1.66, 95% CI 1.44–1.90). This analysis further indicated that higher fasting insulin (ORSD: 1.82, 95% CI 1.30–2.55) and diastolic blood pressure (DBP; ORSD: 1.28, 95% CI 1.11–1.47), but not systolic blood pressure (ORSD: 0.98, 95% CI 0.84–1.14), increase the risk for RCC. No association with RCC risk was seen for lipids, overall type 2 diabetes, or fasting glucose.Conclusions: This study provides novel evidence for an etiological role of insulin in RCC, as well as confirmatory evidence that obesity and DBP influence RCC risk.
  •  
58.
  •  
59.
  •  
60.
  • Jonsson, Sarah, et al. (författare)
  • Pelvic inflammatory disease and risk of epithelial ovarian cancer : a national population-based case-control study in Sweden
  • 2023
  • Ingår i: American Journal of Obstetrics and Gynecology. - : Elsevier. - 0002-9378 .- 1097-6868. ; 230:1, s. 75.e1-75.e15
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Epithelial ovarian cancer is an insidious disease, and women are often diagnosed when the disease is beyond curative treatment. Accordingly, identifying modifiable risk factors is of paramount importance. Inflammation predisposes an individual to cancer in various organs, but whether pelvic inflammatory disease is associated with an increased risk of epithelial ovarian cancer has not been fully determined.Objective: This study aimed to investigate a possible association between clinically verified pelvic inflammatory disease and the risk of epithelial ovarian cancer.Study Design: In this national population-based case-control study, all women in Sweden diagnosed with epithelial ovarian cancer between 1999 and 2020 and 10 controls for each were identified, matched for age and residential district. Using several Swedish nationwide registers, data on previous pelvic inflammatory disease and potential confounding factors (age, parity, educational level, and previous gynecologic surgery) were retrieved. Adjusted odds ratios and 95% confidence intervals were estimated using conditional logistic regression. Histotype-specific analyses were performed for the subgroup of women diagnosed with epithelial ovarian cancer between 2015 and 2020. Moreover, hormonal contraceptives and menopausal hormone therapy were adjusted in addition to the aforementioned confounders.Results: This study included 15,072 women with epithelial ovarian cancer and 141,322 controls. Most women (9102 [60.4%]) had serous carcinoma. In a subgroup of cases diagnosed between 2015 and 2020, high-grade serous carcinoma (2319 [60.0%]) was identified. A total of 168 cases (1.1%) and 1270 controls (0.9%) were diagnosed with pelvic inflammatory disease. Previous pelvic inflammatory disease was associated with an increased risk of epithelial ovarian cancer (adjusted odds ratio, 1.39; 95% confidence interval, 1.17–1.66) and serous carcinoma (adjusted odds ratio, 1.46; 95% confidence interval, 1.18–1.80) for the entire study population. For the subgroup of women diagnosed in 2015–2020, pelvic inflammatory disease was associated with high-grade serous carcinoma (adjusted odds ratio, 1.43; 95% confidence interval, 1.01–2.04). The odds ratios of the other histotypes were as follows: endometrioid (adjusted odds ratio, 0.13; 95% confidence interval, 0.02–1.06), mucinous (adjusted odds ratio, 1.55; 95% confidence interval, 0.56–4.29), and clear cell carcinoma (adjusted odds ratio, 2.30; 95% confidence interval, 0.90–5.86). A dose-response relationship was observed between the number of pelvic inflammatory disease episodes and the risk of epithelial ovarian cancer (Ptrend<.001).Conclusion: A history of pelvic inflammatory disease is associated with an increased risk of epithelial ovarian cancer and a dose-response relationship is evident. Histotype-specific analyses show an association with increased risk of serous epithelial ovarian cancer and high-grade serous carcinoma and potentially also with clear cell carcinoma, but there is no significant association with other histotypes. Infection and inflammation of the upper reproductive tract might have serious long-term consequences, including epithelial ovarian cancer.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 51-60 av 103
Typ av publikation
tidskriftsartikel (94)
annan publikation (4)
forskningsöversikt (3)
doktorsavhandling (2)
Typ av innehåll
refereegranskat (96)
övrigt vetenskapligt/konstnärligt (7)
Författare/redaktör
Häggström, Christel (99)
Stattin, Pär (52)
Stocks, Tanja (42)
Manjer, Jonas (28)
Holmberg, Lars (28)
Nagel, Gabriele (27)
visa fler...
Ulmer, Hanno (27)
Jonsson, Håkan (26)
Engeland, Anders (26)
Liedberg, Fredrik (22)
Tretli, Steinar (21)
Hallmans, Göran (20)
Concin, Hans (20)
Ströck, Viveka (19)
Jahnson, Staffan (19)
Björge, Tone (19)
Selmer, Randi (18)
Sherif, Amir (17)
Hagberg, Oskar (16)
Van Hemelrijck, Miek ... (16)
Jerlström, Tomas, 19 ... (15)
Malmström, Per-Uno (14)
Aljabery, Firas (11)
Garmo, Hans (11)
Almquist, Martin (10)
Gårdmark, Truls (9)
Gardmark, T. (9)
Söderkvist, Karin (9)
Abdul-Sattar Aljaber ... (8)
Hosseini, Abolfazl (8)
Lindkvist, Björn (8)
Johansen, Dorthe (8)
Hosseini, A. (7)
Russell, Beth (7)
Overvad, Kim (6)
van Guelpen, Bethany (6)
Hallmans, Göran, 194 ... (6)
Ullen, A (6)
Bessa, Agustina (6)
Borena, Wegene (6)
Lilja, Hans (5)
Trichopoulou, Antoni ... (5)
Tumino, Rosario (5)
Weiderpass, Elisabet ... (5)
Harlid, Sophia, 1978 ... (5)
Tsilidis, Konstantin ... (5)
Lang, Alois (5)
Enting, Deborah (5)
Amery, Suzanne (5)
Chatterton, Kathryn (5)
visa färre...
Lärosäte
Umeå universitet (83)
Uppsala universitet (39)
Lunds universitet (38)
Göteborgs universitet (15)
Örebro universitet (15)
Karolinska Institutet (2)
visa fler...
Linköpings universitet (1)
Sveriges Lantbruksuniversitet (1)
visa färre...
Språk
Engelska (103)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (103)
Lantbruksvetenskap (2)

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