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  • 1.
    Arthur, Rhonda
    et al.
    Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, New York, NY 10461 USA;Kings Coll London, Translat Oncol & Urol Res, London, England;Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, 1300 Morris Pk, Bronx, NY 10461 USA.
    Møller, Henrik
    Kings Coll London, Translat Oncol & Urol Res, London, England.
    Garmo, Hans
    Kings Coll London, Translat Oncol & Urol Res, London, England;Uppsala Univ Hosp, Dept Surg Sci, Uppsala, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Holmberg, Lars
    Kings Coll London, Translat Oncol & Urol Res, London, England.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Malmström, Håkan
    Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden;Swedish Orphan Biovitrum Sobi, Biostat Data Management & Med Writing, Res & Dev, Stockholm, Sweden.
    Lambe, Mats
    Uppsala Univ Hosp, Reg Canc Ctr, Uppsala, Sweden.
    Hammar, Niklas
    AstraZeneca, Med Evidence & Observat Res, Global Med Dev, Molndal, Sweden.
    Walldius, Göran
    Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden.
    Robinson, David
    Ryhov Hosp, Dept Urol, Jonkoping, Sweden.
    Jungner, Ingmar
    Karolinska Inst, Dept Clin Epidemiol, Stockholm, Sweden;CALAB Res, Stockholm, Sweden.
    Van Hemelrijck, Mieke
    Kings Coll London, Translat Oncol & Urol Res, London, England.
    Serum glucose, triglycerides, and cholesterol in relation to prostate cancer death in the Swedish AMORIS study2019Ingår i: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, nr 2, s. 195-206Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: Lifestyle-related conditions such as obesity are associated with prostate cancer progression, but the associations with hyperglycemia and dyslipidemia are unclear. This study, therefore, aims to examine the association of glucose, triglycerides, and total cholesterol with prostate cancer death

    Methods: From the Swedish AMORIS cohort, we selected 14,150 men diagnosed with prostate cancer between 1996 and 2011 who had prediagnostic measurements of serum glucose, triglycerides, and total cholesterol. Multivariable Cox proportional hazards regressionmodels were used to determine the hazard ratios for death in relation to the aforementioned metabolic markers.

    Results: Using clinical cut-off points, a non-significant positive association was observed between glucose and prostate cancer death. When compared to those with glucose in the lowest quartile, those in the highest quartile had greater risk of prostate cancer death (HR 1.19; 95% CI 1.02-1.39). However, neither total cholesterol nor triglycerides were associated with prostate cancer death. Glucose and triglycerides were positively associated with overall, cardiovascular, and other deaths. Hypercholesterolemia was only associated with risk of CVD death.

    Conclusion: Our results suggest that glucose levels may influence prostate cancer survival, but further studies using repeated measurements are needed to further elucidate how glucose levels may influence prostate cancer progression.

  • 2.
    Beckmann, Kerri
    et al.
    Univ South Australia, UniSA Canc Res Inst, Adelaide, SA, Australia;Kings Coll London, Sch Canc & Pharmaceut Studies Translat Oncol, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Russell, Beth
    Kings Coll London, Sch Canc & Pharmaceut Studies Translat Oncol, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Josephs, Debra
    Kings Coll London, Sch Canc & Pharmaceut Studies Translat Oncol, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Garmo, Hans
    Kings Coll London, Sch Canc & Pharmaceut Studies Translat Oncol, Sch Canc & Pharmaceut Studies, TOUR, London, England;Uppsala Univ Hosp, Reg Canc Ctr Uppsala, Uppsala, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Kings Coll London, Sch Canc & Pharmaceut Studies Translat Oncol, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Van Hemelrijck, Mieke
    Kings Coll London, Sch Canc & Pharmaceut Studies Translat Oncol, Sch Canc & Pharmaceut Studies, TOUR, London, England;Karolinska Inst, Inst Environm Med, Unit Epidemiol, Stockholm, Sweden.
    Adolfsson, Jan
    Karolinska Inst, CLINTEC Dept, Stockholm, Sweden.
    Chronic inflammatory diseases, anti-inflammatory medications and risk of prostate cancer: a population-based case-control study2019Ingår i: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 19, artikel-id 612Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Whether chronic inflammation increases prostate cancer risk remains unclear. This study investigated whether chronic inflammatory diseases (CID) or anti-inflammatory medication use (AIM) were associated with prostate cancer risk.

    Methods: Fifty-five thousand nine hundred thirty-seven cases (all prostate cancer, 2007-2012) and 279,618 age-matched controls were selected from the Prostate Cancer Database Sweden. CIDs and AIMs was determined from national patient and drug registers. Associations were investigated using conditional logistic regression, including for disease/drug subtypes and exposure length/dose.

    Results: Men with a history of any CID had slightly increased risk of any prostate cancer diagnosis (OR: 1.08; 95%CI: 1.04-1.12) but not unfavourable' (high-risk or advanced) prostate cancer. Generally, risk of prostate cancer was highest for shorter exposure times. However, a positive association was observed for asthma >5years before prostate cancer diagnosis (OR: 1.21; 95%CI: 1.05-1.40). Risk of prostate cancer was increased with prior use of any AIMs (OR: 1.26; 95%CI: 1.24-1.29). A positive trend with increasing cumulative dose was only observed for inhaled glucocorticoids (p<0.011).

    Conclusion: Detection bias most likely explains the elevated risk of prostate cancer with prior history of CIDs or use of AIMs, given the higher risk immediately after first CID event and lack of dose response. However, findings for length of time with asthma and dose of inhaled glucocorticoids suggest that asthma may increase risk of prostate cancer through other pathways.

  • 3.
    Bessa, Agustina
    et al.
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Maclennan, Steven
    Univ Aberdeen, Acad Urol Unit, Aberdeen, Scotland.
    Enting, Deborah
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England;Guys & St Thomas NHS Fdn Trust, Dept Med Oncol, London, England.
    Bryan, Richard
    Univ Birmingham, Inst Canc & Genom Sci, Birmingham, W Midlands, England.
    Josephs, Debra
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England;Guys & St Thomas NHS Fdn Trust, Dept Med Oncol, London, England.
    Hughes, Simon
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England;Guys & St Thomas NHS Fdn Trust, Dept Clin Oncol, London, England.
    Amery, Suzanne
    Guys & St Thomas NHS Fdn Trust, Dept Urol, London, England.
    Khan, Muhammad Shamim
    Guys & St Thomas NHS Fdn Trust, Dept Urol, London, England.
    Malde, Sachin
    Guys & St Thomas NHS Fdn Trust, Dept Urol, London, England.
    Nair, Rajesh
    Guys & St Thomas NHS Fdn Trust, Dept Urol, London, England.
    Cahill, Fidelma
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Wylie, Harriet
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Thurairaja, Ramesh
    Guys & St Thomas NHS Fdn Trust, Dept Urol, London, England.
    Chatterton, Kathryn
    Guys & St Thomas NHS Fdn Trust, Dept Urol, London, England.
    Kinsella, Netty
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England;Royal Marsden NHS Fdn Trust, London, England.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Van Hemelrijck, Mieke
    Kings Coll London, Sch Canc & Pharmaceut Studies, TOUR, London, England.
    Consensus in Bladder Cancer Research Priorities Between Patients and Healthcare Professionals Using a Four-stage Modified Delphi Method2019Ingår i: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 76, nr 2, s. 258-259Artikel i tidskrift (Övrigt vetenskapligt)
  • 4. Borena, Wegene
    et al.
    Edlinger, Michael
    Bjørge, Tone
    Häggström, Christel
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden.
    Lindkvist, Björn
    Nagel, Gabriele
    Engeland, Anders
    Stocks, Tanja
    Strohmaier, Susanne
    Manjer, Jonas
    Selmer, Randi
    Tretli, Steinar
    Concin, Hans
    Hallmans, Goran
    Jonsson, Håkan
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Ulmer, Hanno
    A prospective study on metabolic risk factors and gallbladder cancer in the metabolic syndrome and cancer (Me-Can) collaborative study2014Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 9, nr 2, s. e89368-Artikel i tidskrift (Refereegranskat)
    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.

  • 5.
    Crawley, Danielle
    et al.
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England..
    Garmo, Hans
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England..
    Rudman, Sarah
    Guys & St Thomas NHS Fdn Trust, London, England.;Kings Coll Londons Comprehens, Biomed Res Ctr, London, England..
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden.;Umea Univ, Dept Biobank Res, Umea, Sweden..
    Zethelius, Björn
    Karolinska Inst, Dept Clin Sci Intervent & Technol, Stockholm, Sweden..
    Holmberg, Lars
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England..
    Adolfsson, Jan
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Van Hemelrijck, Mieke
    Kings Coll London, Div Canc Studies, Canc Epidemiol Grp, London, England..
    Association between duration and type of androgen deprivation therapy and risk of diabetes in men with prostate cancer2016Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 139, nr 12, s. 2698-2704Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Androgen deprivation therapy (ADT) for prostate cancer (PCa) increases risk of type 2 diabetes (T2DM); however the association between types and duration of ADT has not been fully elucidated. We examined how type and duration of ADT affects risk of T2DM. Using data from Prostate Cancer database Sweden (PCBaSe) we investigated risk of T2DM in a cohort of 34,031 men with PCa on ADT; i.e., anti-androgens (AA), orchiectomy, or gonadotropin-releasing hormone (GnRH) agonists compared to an age-matched, PCa-free comparison cohort (n=167,205) using multivariate Cox proportional hazard regression. T2DM was defined as a newly filled prescription for metformin, sulphonylurea, or insulin in the Prescribed Drug Register. A total of 21,874 men with PCa received GnRH agonists, 9,143 AA and 3,014 underwent orchiectomy. Risk of T2DM was increased in men in the GnRH agonists/orchiectomy group during the first 3 years of ADT [i.e., 121.5 years HR: 1.61 (95% CI: 1.36-1.91)], compared to PCa-free men. The risk decreased thereafter (e.g., 324 years HR: 1.17 (95% CI: 0.98-1.40)). Conversely, no increased risk was seen in men on AA (HR: 0.74 (95% CI: 0.65-0.84). The incidence of T2DM per 1,000 person-years was 10 for PCa-free men, 8 for men on AA, and 13 for men on GnRH agonists/orchiectomy. Duration of ADT has a significant impact on risk of T2DM. With the peak after three years of treatment, our data indicates that men on ADT, even for a limited period of time, such as adjuvant to radiotherapy, are at increased risk of T2DM.

  • 6.
    Häggström, Christel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Garmo, Hans
    Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England;Reg Canc Ctr Uppsala Orebro, Uppsala, Sweden.
    de Luna, Xavier
    Umea Univ, Dept Stat, USBE, Umea, Sweden.
    Van Hemelrijck, Mieke
    Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England;Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Söderkvist, Karin
    Umea Univ, Dept Radiat Sci, Oncol, Umea, Sweden.
    Aljabery, Firas
    Linkoping Univ, Div Urol, Dept Clin & Expt Med, Linkoping, Sweden.
    Ströck, Viveka
    Sahlgrens Univ Hosp, Dept Urol, Gothenburg, Sweden.
    Hosseini, Abolfazl
    Karolinska Univ Hosp, Dept Urol, Stockholm, Sweden.
    Gårdmark, Truls
    Danderyd Hosp, Dept Clin Sci, Karolinska Inst, Stockholm, Sweden.
    Malmström, Per-Uno
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Jahnson, Staffan
    Linkoping Univ, Div Urol, Dept Clin & Expt Med, Linkoping, Sweden.
    Liedberg, Fredrik
    Skane Univ Hosp, Dept Urol, Malmo, Sweden;Lund Univ, Dept Translat Med, Malmo, Sweden.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Survival after radiotherapy versus radical cystectomy for primary muscle-invasive bladder cancer: A Swedish nationwide population-based cohort study2019Ingår i: Cancer Medicine, ISSN 2045-7634, E-ISSN 2045-7634, Vol. 8, nr 5, s. 2196-2204Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Studies of survival comparing radical cystectomy (RC) and radiotherapy for muscle-invasive bladder cancer have provided inconsistent results and have methodological limitations. The aim of the study was to investigate risk of death after radiotherapy as compared to RC.

    Methods: We selected patients with muscle-invasive urothelial carcinoma without distant metastases, treated with radiotherapy or RC from 1997 to 2014 in the Bladder Cancer Data Base Sweden (BladderBaSe) and estimated absolute and relative risk of bladder cancer death and all-cause death. In a group of patients, theoretically eligible for a trial comparing radiotherapy and RC, we calculated risk difference in an instrumental variable analysis. We have not investigated chemoradiotherapy as this treatment was not used in the study time period.

    Results: The study included 3 309 patients, of those 17% were treated with radiotherapy and 83% with RC. Patients treated with radiotherapy were older, had more advanced comorbidity, and had a higher risk of death as compared to patients treated with RC (relative risks of 1.5-1.6). In the "trial population," all-cause death risk difference was 6 per 100 patients lower after radiotherapy at 5 years of follow-up, 95% confidence interval -41 to 29.

    Conclusion(s): Patient selection between the treatments make it difficult to evaluate results from conventionally adjusted and propensity-score matched survival analysis. When taking into account unmeasured confounding by instrumental variable analysis, no differences in survival was found between the treatments for a selected group of patients. Further clinical studies are needed to characterize this group of patients, which can serve as a basis for future comparison studies for treatment recommendations.

  • 7.
    Häggström, Christel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, S-90185 Umea, Sweden;Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden.
    Jonsson, Håkan
    Umea Univ, Dept Radiat Sci, Umea, Sweden.
    Björge, Tone
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway;Canc Registry Norway, Oslo, Norway.
    Nagel, Gabriele
    Ulm Univ, Inst Epidemiol & Med Biometry, Ulm, Germany;Agcy Prevent & Social Med, Vorarlberg Canc Registry, Bregenz, Aks, Austria.
    Manjer, Jonas
    Lund Univ, Skane Univ Hosp, Dept Surg, Malmo, Sweden.
    Ulmer, Hanno
    Innsbruck Med Univ, Dept Med Stat Informat & Hlth Econ, Innsbruck, Austria.
    Drake, Isabel
    Lund Univ, Dept Clin Sci Malmo, Lund, Sweden.
    Ghaderi, Sara
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway.
    Lang, Alois
    Agcy Prevent & Social Med, Vorarlberg Canc Registry, Bregenz, Aks, Austria.
    Engeland, Anders
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway;Norwegian Inst Publ Hlth, Bergen, Norway.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Stocks, Tanja
    Lund Univ, Dept Clin Sci Lund, Lund, Sweden.
    Linear age-course effects on the associations between body mass index, triglycerides, and female breast and male liver cancer risk: An internal replication study of 800,000 individuals2020Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 146, nr 1, s. 58-67Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Apart from the consistently observed differential association between obesity and breast cancer risk by menopausal status, the associations between obesity and other metabolic imbalances with risks of cancers have not been systematically investigated across the age-course. We created two random 50-50% cohorts from six European cohorts comprising 813,927 individuals. In the "discovery cohort", we used Cox regression with attained age as time-scale and tested interactions between body mass index (BMI), blood pressure, plasma glucose, triglycerides and cholesterol, and attained age in relation to cancer risk. Results with a p-value below 0.05 were additionally tested in the "replication cohort" where a replicated result was considered evidence of a linear interaction with attained age. These findings were investigated by flexible parametric survival models for any age-plateaus in their shape of associations with cancer risk across age. Consistent with other studies, BMI was negatively related to breast cancer risk (n cases = 11,723) among younger (premenopausal) women. However, the association remained negative for several years after menopause and, although gradually weakening over age, the association became positive only at 62 years of age. This linear and positive age-interaction was also found for triglycerides and breast cancer, and for BMI and triglycerides in relation to liver cancer among men (n cases = 444). These findings are unlikely to be due to chance owing to the replication. The linear age-interactions in breast cancer may suggest an influence by other age-related factors than menopause; however, further investigation of age-related effect modifiers in both breast and liver cancer is needed.

  • 8.
    Häggström, Christel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umeå University, Department of Biobank Research.
    Liedberg, Fredrik
    Skåne University Hospital, Department of Urology; Lund University, Department of Translational Medicine.
    Hagberg, Oskar
    Regional Cancer Centre South, Lund.
    Aljabery, Firas
    Linköping University, Division of Urology, Department of Clinical and Experimental Medicine.
    Ströck, Viveka
    Sahlgrenska University Hospital, Department of Urology.
    Hosseini, Abolfazl
    Karolinska University Hospital, Department of Urology.
    Gårdmark, Truls
    Karolinska Institute, Danderyd Hospital, Department of Clinical Sciences.
    Sherif, Amir
    Umeå University, Department of Surgical and Perioperative Sciences, Urology and Andrology.
    Malmström, Per-Uno
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Garmo, Hans
    King’s College London, Faculty of Life Sciences and Medicine, Division of Cancer Studies; Regional Cancer Centre Uppsala/Örebro.
    Jahnson, Staffan
    Linköping University, Division of Urology, Department of Clinical and Experimental Medicine.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. King’s College London, Faculty of Life Sciences and Medicine, Division of Cancer Studies.
    Cohort profile: The Swedish National Register of Urinary Bladder Cancer (SNRUBC) and the Bladder Cancer Data Base Sweden (BladderBaSe)2017Ingår i: BMJ Open, ISSN 2044-6055, E-ISSN 2044-6055, Vol. 7, nr 9, artikel-id e016606Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: To monitor the quality of bladder cancer care, the Swedish National Register of Urinary Bladder Cancer (SNRUBC) was initiated in 1997. During 2015, in order to study trends in incidence, effects of treatment and survival of men and women with bladder cancer, we linked the SNRUBC to other national healthcare and demographic registers and constructed the Bladder Cancer Data Base Sweden (BladderBaSe).

    Participants: The SNRUBC is a nationwide register with detailed information on 97% of bladder cancer cases in Sweden as compared with the Swedish Cancer Register. Participants in the SNRUBC have registered data on tumour characteristics at diagnosis, and for 98% of these treatment data have been captured. From 2009, the SNRUBC holds data on 88% of eligible participants for follow-up 5 years after diagnosis of non-muscle invasive bladder cancer, and from 2011, data on surgery details and complications for 85% of participants treated with radical cystectomy. The BladderBaSe includes all data in the SNRUBC from 1997 to 2014, and additional covariates and follow-up data from linked national register sources on comorbidity, socioeconomic factors, detailed information on readmissions and treatment side effects, and causes of death.

    Findings to date: Studies based on data in the SNRUBC have shown inequalities in survival and treatment indication by gender, regions and hospital volume. The BladderBaSe includes 38 658 participants registered in SNRUBC with bladder cancer diagnosed from 1 January 1997 to 31 December 2014. The BladderBaSe initiators are currently in collaboration with researchers from the SNRUBC investigating different aspects of bladder cancer survival.

    Future plans: The SNRUBC and the BladderBaSe project are open for collaborations with national and international research teams. Collaborators can submit proposals for studies and study files can be uploaded to servers for remote access and analysis. For more information, please contact the corresponding author.

  • 9.
    Häggström, Christel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Umea Univ, Dept Surg & Perioperat Sci, Urol & Androl, Umea, Sweden.;Umea Univ, Dept Biobank Res, S-90185 Umea, Sweden..
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi. Umea Univ, Dept Surg & Perioperat Sci, Urol & Androl, Umea, Sweden..
    Stocks, Tanja
    Umea Univ, Dept Surg & Perioperat Sci, Urol & Androl, Umea, Sweden.;Lund Univ, Dept Clin Sci Diabet & Cardiovasc Dis, Genet Epidemiol, Lund, Sweden..
    Garmo, Hans
    Reg Canc Ctr Uppsala Orebro, Uppsala, Sweden.;Kings Coll London, Fac Life Sci & Med, Div Canc Studies, London, England..
    Holmberg, Lars
    Reg Canc Ctr Uppsala Orebro, Uppsala, Sweden.;Kings Coll London, Fac Life Sci & Med, Div Canc Studies, London, England..
    Van Hemelrijck, Mieke
    Kings Coll London, Fac Life Sci & Med, Div Canc Studies, London, England.;Karolinska Inst, Inst Environm Med, Stockholm, Sweden..
    Interpretation of conventional survival analysis and competing-risk analysis: an example of hypertension and prostate cancer2016Ingår i: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 118, nr 6, s. 850-852Artikel i tidskrift (Övrigt vetenskapligt)
  • 10.
    Häggström, Christel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, S-90185 Umea, Sweden;Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Van Hemelrijck, Mieke
    Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England;Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Garmo, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR). Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Robinson, David
    Ryhov Hosp, Dept Urol, Jonkoping, Sweden.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Rowley, Mark
    Kings Coll London, Inst Math & Mol Biomed, London, England;Saddle Point Sci, London, England.
    Coolen, Anthony C. C.
    Kings Coll London, Inst Math & Mol Biomed, London, England.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Heterogeneity in risk of prostate cancer: A Swedish population-based cohort study of competing risks and Type 2 diabetes mellitus2018Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 143, nr 8, s. 1868-1875Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Most previous studies of prostate cancer have not taken into account that men in the studied populations are also at risk of competing event, and that these men may have different susceptibility to prostate cancer risk. The aim of our study was to investigate heterogeneity in risk of prostate cancer, using a recently developed latent class regression method for competing risks. We further aimed to elucidate the association between Type 2 diabetes mellitus (T2DM) and prostate cancer risk, and to compare the results with conventional methods for survival analysis. We analysed the risk of prostate cancer in 126,482 men from the comparison cohort of the Prostate Cancer Data base Sweden (PCBaSe) 3.0. During a mean follow-up of 6years 6,036 men were diagnosed with prostate cancer and 22,393 men died. We detected heterogeneity in risk of prostate cancer with two distinct latent classes in the study population. The smaller class included 9% of the study population in which men had a higher risk of prostate cancer and the risk was stronger associated with class membership than any of the covariates included in the study. Moreover, we found no association between T2DM and risk of prostate cancer after removal of the effect of informative censoring due to competing risks. The recently developed latent class for competing risks method could be used to provide new insights in precision medicine with the target to classify individuals regarding different susceptibility to a particular disease, reaction to a risk factor or response to treatment.

  • 11.
    Häggström, Christel
    et al.
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden.; Umea Univ, Dept Biobank Res, S-90185 Umea, Sweden..
    Van Hemelrijck, Mieke
    Kings Coll London, Div Canc Studies, Fac Life Sci & Med, London, England.;Karolinska Inst, Inst Environm Med, Stockholm, Sweden..
    Zethelius, Björn
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för folkhälso- och vårdvetenskap, Geriatrik. Med Prod Agcy, Dept Sci Support, Uppsala, Sweden..
    Robinson, David
    Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden..
    Grundmark, Birgitta
    Med Prod Agcy, Dept Sci Support, Uppsala, Sweden.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Kings Coll London, Div Canc Studies, Fac Life Sci & Med, London, England.
    Gudbjörnsdottir, Soffia
    Gothenburg Univ, Sahlgrenska Univ Hosp, Dept Med, Gothenburg, Sweden..
    Garmo, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Kings Coll London, Div Canc Studies, Fac Life Sci & Med, London, England.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi. Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden.
    Prospective study of Type 2 diabetes mellitus, anti-diabetic drugs and risk of prostate cancer2017Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 140, nr 3, s. 611-617Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Type 2 diabetes mellitus (T2DM) has consistently been associated with decreased risk of prostate cancer; however, if this decrease is related to the use of anti-diabetic drugs is unknown. We prospectively studied men in the comparison cohort in the Prostate Cancer data Base Sweden 3.0, with data on T2DM, use of metformin, sulfonylurea and insulin retrieved from national health care registers and demographic databases. Cox proportional hazards regression models were used to compute hazard ratios (HR) and 95% confidence intervals (CI) of prostate cancer, adjusted for confounders. The study consisted of 612,846 men, mean age 72 years (standard deviation; SD=9 years), out of whom 25,882 men were diagnosed with prostate cancer during follow up, mean time of 5 years (SD=3 years). Men with more than 1 year's duration of T2DM had a decreased risk of prostate cancer compared to men without T2DM (HR=0.85, 95% CI=0.82-0.88) but among men with T2DM, those on metformin had no decrease (HR=0.96, 95% CI=0.77-1.19), whereas men on insulin (89%) or sulfonylurea (11%) had a decreased risk (HR=0.73, 95% CI=0.55-0.98), compared to men with T2DM not on anti-diabetic drugs. Men with less than 1 year's duration of T2DM had no decrease in prostate cancer risk (HR=1.11, 95% CI=0.95-1.31). Our results gave no support to the hypothesis that metformin protects against prostate cancer as recently proposed. However, our data gave some support to an inverse association between T2DM severity and prostate cancer risk.

    What's new? Although Type 2 diabetes mellitus (T2DM) increases the risk of several cancers, multiple studies point toward a significantly inverse relationship between T2DM and prostate cancer risk in men. Use of the anti-diabetic drug metformin is suspected of underlying the association. In this prospective study in Sweden, however, metformin failed to decrease the risk of prostate cancer. By comparison, risk was decreased in association with the use of insulin or sulfonylurea. These findings add some support to an inverse association between T2DM severity and prostate cancer risk.

  • 12.
    Jahnson, Staffan
    et al.
    Linkoping Univ, Dept Clin & Expt Med, Div Urol, Linkoping, Sweden.
    Gårdmark, Truls
    Karolinska Inst, Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden.
    Hosseini, Abolfazl
    Karolinska Univ Hosp, Dept Urol, Stockholm, Sweden.
    Jedström, Tomas
    Orebro Univ Hosp, Dept Urol, Orebro, Sweden.
    Liedberg, Fredrik
    Skane Univ Hosp, Dept Urol, Malmo, Sweden;Lund Univ, Inst Translat Med, Malmo, Sweden.
    Malmström, Per-Uno
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Rosell, Johan
    Linkoping Univ, Reg Canc Ctr Southeast Sweden, Linkoping, Sweden;Linkoping Univ, Dept Clin & Expt Med, Linkoping, Sweden.
    Sherif, Amir
    Umea Univ Hosp, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden.
    Ströck, Viveka
    Sahlgrens Univ Hosp, Dept Urol, Gothenburg, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Kings Coll London, Sch Med, London, England.
    Aljabery, Firas
    Linkoping Univ, Dept Clin & Expt Med, Div Urol, Linkoping, Sweden.
    Management and outcome of TaG3 tumours of the urinary bladder in the nationwide, population-based bladder cancer database Sweden (BladderBaSe)2019Ingår i: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 53, nr 4, s. 200-205Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Purpose: To investigate the management of TaG3 tumours of the urinary bladder using nationwide population-based data in relation to the prevailing guidelines, patients' characteristics, and outcome. Materials and methods: The Bladder Cancer Data Base Sweden (BladderBaSe), including data from the Swedish National Register for Urinary Bladder Cancer (SNRUBC), was used to study all patients with TaG3 bladder cancer diagnosed from 2008 to 2014. Patients were divided into the following management groups: (1) transurethral resection (TUR) only, (2) TUR and intravesical instillation therapy (IVIT), (3) TUR and second-look resection (SLR), and (4) TUR with both SLR and IVIT. Patient and tumour characteristics and outcome were studied. Results: There were 831 patients (83% males) with a median age of 74 years. SLR was performed more often on younger patients, on men, and less often in the Western and Uppsala/orebro Healthcare regions. IVIT was performed more often with younger patients, with men, in the Western Healthcare region, and less often in the Uppsala/orebro Healthcare region. Death from bladder cancer occurred in 6% of cases within a median of 29 months (0-84 months) and was lower in the TUR/IVIT and TUR/SLR/IVIT groups compared to the other two groups. Conclusion: In the present study, there was, according to the prevailing treatment guidelines, an under-treatment with SLR for older patients, women, and in some healthcare regions and, similarly, there was an under-treatment with IVIT for older patients. Cancer-specific survival and relative survival were lower in the TUR only group compared to the TUR/IVIT and TUR/SLR/IVIT groups.

  • 13.
    Johansson, Mattias
    et al.
    IARC, Lyon, France.
    Carreras-Torres, Robert
    IARC, Lyon, France.
    Scelo, Ghislaine
    IARC, Lyon, France.
    Purdue, Mark P.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Mariosa, Daniela
    IARC, Lyon, France.
    Muller, David C.
    Imperial Coll, London, England.
    Timpson, Nicolas J.
    Univ Bristol, MRC Integrat Epidemiol Unit, Bristol, Avon, England.
    Haycock, Philip C.
    Univ Bristol, MRC Integrat Epidemiol Unit, Bristol, Avon, England.
    Brown, Kevin M.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Wang, Zhaoming
    St Jude Childrens Res Hosp, Memphis, TN USA.
    Ye, Yuanqing
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Div Canc Prevent & Populat Sci, Houston, TX USA.
    Hofmann, Jonathan N.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Foll, Matthieu
    IARC, Lyon, France.
    Gaborieau, Valerie
    IARC, Lyon, France.
    Machiela, Mitchell J.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Colli, Leandro M.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Li, Peng
    IARC, Lyon, France;Max Planck Inst Demog Res, Rostock, Germany.
    Garnier, Jean-Guillaume
    Ctr Energie Atom & Energies Alternat, Inst Genom, Ctr Natl Genotypage, Evry, France; Ctr Etud Polymorphisme Humain, Fdn Jean Dausset, Paris, France.
    Blanche, Helene
    Ctr Energie Atom & Energies Alternat, Inst Genom, Ctr Natl Genotypage, Evry, France.
    Boland, Anne
    Ctr Energie Atom & Energies Alternat, Inst Genom, Ctr Natl Genotypage, Evry, France.
    Burdette, Laurie
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Prokhortchouk, Egor
    Russian Acad Sci, Fed Res Ctr Fundamentals Biotechnol, Moscow, Russia.
    Skryabin, Konstantin G.
    Russian Acad Sci, Fed Res Ctr Fundamentals Biotechnol, Moscow, Russia; Kurchatov Sci Ctr, Moscow, Russia.
    Yeager, Meredith
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Radojevic-Skodric, Sanja
    Univ Belgrade Sch Med, Inst Pathol, Belgrade, Serbia; Clin Ctr Serbia, Clin Urol, Belgrade, Serbia.
    Ognjanovic, Simona
    Mayo Clin, Grad Sch Biomed Sci, Rochester, MN USA; IOCPR, Belgrade, Serbia.
    Foretova, Lenka
    Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
    Holcatova, Ivana
    Charles Univ Prague, Fac Med 2, Inst Publ Hlth & Prevent Med, Prague, Czech Republic.
    Janout, Vladimir
    Palacky Univ, Fac Med, Dept Prevent Med, Olomouc, Czech Republic.
    Mates, Dana
    Natl Inst Publ Hlth, Bucharest, Romania.
    Mukeriya, Anush
    Russian NN Blokhin Canc Res Ctr, Moscow, Russia.
    Rascu, Stefan
    Carol Davila Univ Med & Pharm, Th Burghele Hosp, Bucharest, Romania.
    Zaridze, David
    Russian NN Blokhin Canc Res Ctr, Moscow, Russia.
    Bencko, Vladimir
    Charles Univ Prague, Fac Med 1, Inst Hyg & Epidemiol, Prague, Czech Republic.
    Cybulski, Cezary
    Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
    Fabianova, Eleonora
    Reg Author Publ Hlth Banska Bystr, Banska Bystrica, Slovakia.
    Jinga, Viorel
    Carol Davila Univ Med & Pharm, Th Burghele Hosp, Bucharest, Romania.
    Lissowska, Jolanta
    M Sklodowska Curie Canc Ctr, Warsaw, Poland; Inst Oncol, Warsaw, Poland.
    Lubinski, Jan
    Pomeranian Med Univ, Dept Genet & Pathol, Int Hereditary Canc Ctr, Szczecin, Poland.
    Navratilova, Marie
    Masaryk Mem Canc Inst, Dept Canc Epidemiol & Genet, Brno, Czech Republic.
    Rudnai, Peter
    Natl Publ Hlth Ctr, Natl Directorate Environm Hlth, Budapest, Hungary.
    Benhamou, Simone
    INSERM, U946, Paris, France; CNRS, Inst Gustave Roussy, UMR 8200, Villejuif, France.
    Cancel-Tassin, Geraldine
    CeRePP, Paris, France; UPMC Univ Paris 06, Inst Univ Cancerol, GRC 5, Paris, France.
    Cussenot, Olivier
    CeRePP, Paris, France; UPMC Univ Paris 06, Inst Univ Cancerol, GRC 5, Paris, France; Hopitaux Univ Est Parisien Tenon, AP HP, Dept Urol, Paris, France.
    Weiderpass, Elisabete
    Canc Registry Norway, Inst Population Based Canc Res, Dept Res, Oslo, Norway; Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden; Folkhalsan Res Ctr, Genet Epidemiol Grp, Helsinki, Finland; Arctic Univ Norway, Univ Tromso, Dept Community Med, Tromso, Norway.
    Ljungberg, Borje
    Umeå Univ, Dept Surg & Perioperat Sci Urol & Androl, Umeå, Sweden.
    Sitaram, Raviprakash Tumkur
    Umeå Univ, Dept Surg & Perioperat Sci Urol & Androl, Umeå, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umeå Univ, Dept Biobank Res, Umeå, Sweden.
    Bruinsma, Fiona
    Canc Council Victoria, Canc Epidemiol Ctr, Melbourne, Vic, Australia.
    Jordan, Susan J.
    QIMR Berghofer Med Res Inst, Herston, Qld, Australia; Univ Queensland, Sch Publ Hlth, Brisbane, Qld, Australia.
    Severi, Gianluca
    Univ Paris Saclay, Univ Paris Sud, Hlth Generat Team, CESP,INSERM,Fac Med,UVSQ,Gustave Roussy, Villejuif, France; Human Genet Fdn HuGeF, Turin, Italy.
    Winship, Ingrid
    Univ Melbourne, Royal Melbourne Hosp, Dept Med, Melbourne, Vic, Australia.
    Hveem, Kristian
    Norwegian Univ Sci & Technol, Dept Publ Hlth, KG Jebsen Ctr Genet Epidemiol, Trondheim, Norway.
    Vatten, Lars J.
    Norwegian Univ Sci & Technol, Fac Med, Dept Publ Hlth & Gen Practice, Trondheim, Norway.
    Fletcher, Tony
    Univ London, London Sch Hyg & Trop Med, London, England.
    Larsson, Susanna C.
    Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Wolk, Alicja
    Karolinska Inst, Inst Environm Med, Stockholm, Sweden.
    Banks, Rosamonde E.
    Univ Leeds, St Jamess Univ Hosp, Leeds Inst Canc & Pathol, Leeds, W Yorkshire, England.
    Selby, Peter J.
    Imperial Coll London, St Marys Hosp, Div Surg, Natl Inst Hlth Res Diagnost Evidence Cooperat, London, England.
    Easton, Douglas F.
    Univ Cambridge, Dept Oncol, Cambridge, England; Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge, England.
    Andreotti, Gabriella
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD USA.
    Freeman, Laura E. Beane
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Koutros, Stella
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Mannisto, Satu
    Natl Inst Hlth & Welf, Helsinki, Finland.
    Weinstein, Stephanie
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Clark, Peter E.
    Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
    Edwards, Todd L.
    Vanderbilt Genet Inst, Vanderbilt Ingram Canc Ctr, Div Epidemiol, Dept Med, Nashville, TN USA.
    Lipworth, Loren
    Vanderbilt Ingram Canc Ctr, Nashville, TN USA.
    Gapstur, Susan M.
    Amer Canc Soc, Atlanta, GA 30329 USA.
    Stevens, Victoria L.
    Amer Canc Soc, Atlanta, GA 30329 USA.
    Carol, Hallie
    Dana Farber Canc Inst, Boston, MA 02115 USA.
    Freedman, Matthew L.
    Dana Farber Canc Inst, Boston, MA 02115 USA.
    Pomerantz, Mark M.
    Dana Farber Canc Inst, Boston, MA 02115 USA.
    Cho, Eunyoung
    Brown Univ, Providence, RI 02912 USA.
    Wilson, Kathryn M.
    Harvard TH Chan Sch Publ Hlth, Boston, MA USA.
    Gaziano, J. Michael
    Harvard Med Sch, Brigham & Womens Hosp, Boston, MA USA.
    Sesso, Howard D.
    Harvard TH Chan Sch Publ Hlth, Boston, MA USA; Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
    Freedman, Neal D.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Parker, Alexander S.
    Mayo Clin, Dept Hlth Sci Res, Jacksonville, FL 32224 USA.
    Eckel-Passow, Jeanette E.
    Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN USA.
    Huang, Wen-Yi
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Kahnoski, Richard J.
    Spectrum Hlth, Div Urol, Grand Rapids, MI USA.
    Lane, Brian R.
    Spectrum Hlth, Div Urol, Grand Rapids, MI USA; Michigan State Univ, Coll Human Med, Grand Rapids, MI USA.
    Noyes, Sabrina L.
    Van Andel Res Inst, Ctr Canc Genom & Quantitat Biol, Grand Rapids, MI USA; Spectrum Hlth, Grand Rapids, MI USA.
    Petillo, David
    Van Andel Res Inst, Ctr Canc Genom & Quantitat Biol, Grand Rapids, MI USA; Ferris State Univ, Diagnost Program, Grand Rapids, MI USA.
    Teh, Bin Tean
    Van Andel Res Inst, Ctr Canc Genom & Quantitat Biol, Grand Rapids, MI USA; Natl Univ Singapore, Med Sch, Program Canc & Stem Cell Biol, Duke Natl, Singapore, Singapore; ASTAR, Inst Mol & Cell Biol, Singapore, Singapore; Natl Canc Ctr Singapore, Div Med Sci, Lab Canc Epigenome, Singapore, Singapore; Natl Univ Singapore, Canc Sci Inst Singapore, Singapore, Singapore.
    Peters, Ulrike
    Fred Hutchinson Canc Res Ctr, Canc Prevent Program, 1124 Columbia St, Seattle, WA 98104 USA.
    White, Emily
    Fred Hutchinson Canc Res Ctr, Canc Prevent Program, 1124 Columbia St, Seattle, WA 98104 USA.
    Anderson, Garnet L.
    Fred Hutchinson Canc Res Ctr, WHI Clin Coordinating Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Johnson, Lisa
    Fred Hutchinson Canc Res Ctr, 1124 Columbia St, Seattle, WA 98104 USA.
    Luo, Juhua
    Indiana Univ, Sch Publ Hlth, Dept Epidemiol & Biostat, Bloomington, IN USA.
    Buring, Julie
    Harvard Med Sch, Brigham & Womens Hosp, Boston, MA USA; Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
    Lee, I-Min
    Harvard Med Sch, Brigham & Womens Hosp, Boston, MA USA; Brigham & Womens Hosp, Dept Med, 75 Francis St, Boston, MA 02115 USA.
    Chow, Wong-Ho
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Div Canc Prevent & Populat Sci, Houston, TX 77030 USA.
    Moore, Lee E.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Eisen, Timothy
    Univ Cambridge, Cambridge, England.
    Henrion, Marc
    Inst Canc Res, London, England; Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Larkin, James
    Royal Marsden NHS Fdn Trust, London, England.
    Barman, Poulami
    Mayo Clin, Dept Hlth Sci Res, Div Biomed Stat & Informat, Rochester, MN USA.
    Leibovich, Bradley C.
    Mayo Clin, Dept Urol, Rochester, MN USA.
    Choueiri, Toni K.
    Dana Farber Canc Inst, Boston, MA 02115 USA.
    Lathrop, G. Mark
    McGill Univ, Montreal, PQ, Canada;Genome Quebec Innovat Ctr, Montreal, PQ, Canada.
    Deleuze, Jean-Francois
    Ctr Energie Atom & Energies Alternat, Inst Genom, Ctr Natl Genotypage, Evry, France; Ctr Etud Polymorphisme Humain, Fdn Jean Dausset, Paris, France.
    Gunter, Marc
    IARC, Lyon, France.
    McKay, James D.
    IARC, Lyon, France.
    Wu, Xifeng
    Univ Texas MD Anderson Canc Ctr, Dept Epidemiol, Div Canc Prevent & Populat Sci, Houston, TX 77030 USA.
    Houlston, Richard S.
    Inst Canc Res, London, England.
    Chanock, Stephen J.
    NCI, Div Canc Epidemiol & Genet, Dept Hlth & Human Serv, NIH, Bethesda, MD 20892 USA.
    Relton, Caroline
    Univ Bristol, MRC Integrat Epidemiol Unit, Bristol, Avon, England; Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
    Richards, J. Brent
    McGill Univ, Jewish Gen Hosp, Dept Med, Montreal, PQ, Canada;McGill Univ, Jewish Gen Hosp, Dept Human Genet, Montreal, PQ, Canada;McGill Univ, Jewish Gen Hosp, Dept Epidemiol & Biostat, Montreal, PQ, Canada.
    Martin, Richard M.
    Univ Bristol, MRC Integrat Epidemiol Unit, Bristol, Avon, England; Univ Bristol, Sch Social & Community Med, Bristol, Avon, England; Univ Bristol, Univ Hosp Bristol NHS Fdn Trust, Natl Inst Hlth Res, Bristol Nutr Biomed Res Unit, Bristol, Avon, England.
    Smith, George Davey
    Univ Bristol, MRC Integrat Epidemiol Unit, Bristol, Avon, England; Univ Bristol, Sch Social & Community Med, Bristol, Avon, England.
    Brennan, Paul
    IARC, Lyon, France.
    The influence of obesity-related factors in the etiology of renal cell carcinoma—A mendelian randomization study2019Ingår i: PLoS Medicine, ISSN 1549-1277, E-ISSN 1549-1676, Vol. 16, nr 1, artikel-id e1002724Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    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.

  • 14.
    Li, Weiqiang
    et al.
    Icahn Sch Med Mt Sinai, Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Middha, Mridu
    Icahn Sch Med Mt Sinai, Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Bicak, Mesude
    Icahn Sch Med Mt Sinai, Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Sjoberg, Daniel D.
    Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10065 USA.
    Vertosick, Emily
    Mem Sloan Kettering Canc Ctr, Dept Epidemiol & Biostat, New York, NY 10065 USA.
    Dahlin, Anders
    Lund Univ, Dept Clin Sci, Malmo, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umeå Univ, Dept Biobank Res, Umeå, Sweden.
    Hallmans, Goran
    Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden.
    Ronn, Ann-Charlotte
    Karolinska Univ Hosp, Clin Res Ctr, Huddinge, Sweden.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Melander, Olle
    Lund Univ, Dept Clin Sci, Malmo, Sweden.
    Ulmert, David
    Sloan Kettering Inst, Mol Pharmacol Program, New York, NY USA.
    Lilja, Hans
    Mem Sloan Kettering Canc Ctr, Dept Lab Med, New York, NY 10065 USA;Mem Sloan Kettering Canc Ctr, Dept Surg, New York, NY 10065 USA;Mem Sloan Kettering Canc Ctr, Dept Med, New York, NY 10065 USA;Univ Oxford, Nuffield Dept Surg Sci, Oxford, England;Lund Univ, Dept Translat Med, Malmo, Sweden.
    Klein, Robert J.
    Icahn Sch Med Mt Sinai, Icahn Inst Genom & Multiscale Biol, New York, NY 10029 USA;Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, New York, NY 10029 USA.
    Genome-wide Scan Identifies Role for AOX1 in Prostate Cancer Survival2018Ingår i: European Urology, ISSN 0302-2838, E-ISSN 1873-7560, Vol. 74, nr 6, s. 710-719Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: Most men diagnosed with prostate cancer have low-risk cancers. How to predict prostate cancer progression at the time of diagnosis remains challenging. Objective: To identify single nucleotide polymorphisms (SNPs) associated with death from prostate cancer. Design, setting, and participants: Blood samples from 11 506 men in Sweden were collected during 1991-1996. Of these, 1053 men were diagnosed with prostate cancer and 245 died from the disease. Stage and grade at diagnosis and outcome information were obtained, and DNA from all cases was genotyped. Outcome measurements and statistical analysis: A total of 6 126 633 SNPs were tested for association with prostate-cancer-specific survival time using a Cox proportional hazard model, adjusted for age, stage, and grade at diagnosis. A value of 1 x 10(-6) was used as suggestive significance threshold. Positive candidate SNPs were tested for association with gene expression using expression quantitative trait locus analysis. Results and limitations: We found 12 SNPs at seven independent loci associated with prostate-cancerspecific survival time. One of 6 126 633 SNPs tested reached genome-wide significance (p < 5 x 10(-8)) and replicated in an independent cohort: rs73055188 (p = 5.27 x 10(-9), per-allele hazard ratio [HR] = 2.27, 95% confidence interval [CI] 1.72-2.98) in the AOX1 gene. A second SNP reached a suggestive level of significance (p <1 x 10(-6)) and replicated in an independent cohort: rs2702185 (p = 7.1 x 10(-7), per-allele HR = 2.55, 95% CI = 1.76-3.69) in the SMG7 gene. The SNP rs73055188 is correlated with AOX1 expression levels, which is associated with biochemical recurrence of prostate cancer in independent cohorts. This association is yet to be validated in other ethnic groups. Conclusions: The SNP rs73055188 at the AOX1 locus is associated with prostate-cancer-specific survival time, and AOX1 gene expression level is correlated with biochemical recurrence of prostate cancer. Patient summary: We identify two genetic markers that are associated with prostate-cancer-specific survival time.

  • 15.
    Liedberg, Fredrik
    et al.
    Skane Univ Hosp, Dept Urol, Jan Waldenstroms Gata 7, SE-20502 Malmo, Sweden;Lund Univ, Inst Translat Med, Jan Waldenstroms Gata 7, SE-20502 Malmo, Sweden.
    Hagberg, Oskar
    Reg Canc Ctr South, Lund, Sweden.
    Aljabery, Firas
    Linkoping Univ, Dept Clin & Expt Med, Div Urol, Linkoping, Sweden.
    Gardmark, Truls
    Karolinska Inst, Danderyd Hosp, Dept Clin Sci, Stockholm, Sweden.
    Hosseini, Abolfazl
    Karolinska Univ Hosp, Dept Urol, Stockholm, Sweden.
    Jahnson, Staffan
    Linkoping Univ, Dept Clin & Expt Med, Div Urol, Linkoping, Sweden.
    Jancke, Georg
    Skane Univ Hosp, Dept Urol, Jan Waldenstroms Gata 7, SE-20502 Malmo, Sweden;Lund Univ, Inst Translat Med, Jan Waldenstroms Gata 7, SE-20502 Malmo, Sweden.
    Jerlstrom, Tomas
    Orebro Univ, Sch Hlth & Med Sci, Dept Urol, Orebro, Sweden.
    Malmström, Per-Uno
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Sherif, Amir
    Umea Univ, Dept Surg & Perioperat Sci Urol & Androl, Umea, Sweden.
    Strock, Viveka
    Sahlgrens Univ Hosp, Dept Urol, Gothenburg, Sweden;Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Gothenburg, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Kings Coll London, Sch Med, London, England.
    Period-specific mean annual hospital volume of radical cystectomy is associated with outcome and perioperative quality of care: a nationwide population-based study2019Ingår i: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 124, nr 3, s. 449-456Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective

    To investigate the association between hospital volume and overall survival (OS), cancer‐specific survival (CSS), and quality of care of patients with bladder cancer who undergo radical cystectomy (RC), defined as the use of extended lymphadenectomy (eLND), continent reconstruction, neoadjuvant chemotherapy (NAC), and treatment delay of <3 months.

    Patients and Methods

    We used the Bladder Cancer Data Base Sweden (BladderBaSe) to study survival and indicators of perioperative quality of care in all 3172 patients who underwent RC for primary invasive bladder cancer stage T1–T3 in Sweden between 1997 and 2014. The period‐specific mean annual hospital volume (PSMAV) during the 3 years preceding surgery was applied as an exposure and analysed using univariate and multivariate mixed models, adjusting for tumour and nodal stage, age, gender, comorbidity, educational level, and NAC. PSMAV was either categorised in tertiles, dichotomised (at ≥25 RCs annually), or used as a continuous variable for every increase of 10 RCs annually.

    Results

    PSMAV in the highest tertile (≥25 RCs annually) was associated with improved OS (hazard ratio [HR] 0.87, 95% confidence interval [CI] 0.75–1.0), whereas the corresponding HR for CSS was 0.87 (95% CI 0.73–1.04). With PSMAV as a continuous variable, OS was improved for every increase of 10 RCs annually (HR 0.95, 95% CI 0.90–0.99). Moreover, higher PSMAV was associated with increased use of eLND, continent reconstruction and NAC, but also more frequently with a treatment delay of >3 months after diagnosis.

    Conclusions

    The current study supports centralisation of RC for bladder cancer, but also underpins the need for monitoring treatment delays associated with referral.

  • 16. Lindkvist, Björn
    et al.
    Johansen, Dorthe
    Stocks, Tanja
    Concin, Hans
    Bjørge, Tone
    Almquist, Martin
    Häggström, Christel
    Department of Surgical and Perioperative Sciences, Urology and Andrology, Umeå University, Umeå, Sweden .
    Engeland, Anders
    Hallmans, Göran
    Nagel, Gabriele
    Jonsson, Håkan
    Selmer, Randi
    Ulmer, Hanno
    Tretli, Steinar
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Manjer, Jonas
    Metabolic risk factors for esophageal squamous cell carcinoma and adenocarcinoma: a prospective study of 580,000 subjects within the Me-Can project2014Ingår i: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 14, s. 103-Artikel i tidskrift (Refereegranskat)
    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.

  • 17. Melvin, Jennifer C
    et al.
    Garmo, Hans
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Daniel, Rhian
    Shanmugalingam, Thurkaa
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper.
    Rudman, Sarah
    Holmberg, Lars
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper. Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska och farmaceutiska vetenskapsområdet, centrumbildningar mm, Uppsala kliniska forskningscentrum (UCR).
    Van Hemelrijck, Mieke
    An investigation into the relationship between Statins and Cancer using population-based data2015Ingår i: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 116, nr 5, s. 681-683Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Results to date for the association between use of statins and prostate cancer (PCa) death in observational studies are inconsistent. We investigated the application of causal inference methods, which aim to address observational data as if they were from a randomised clinical trial (RCT).

    MATERIAL AND METHODS: We examined the association between statins and PCa-death in 14,926 men in PCBaSe Sweden. We used inverse probability weighted (IPW) estimation of marginal structural models (MSM), as well incorporating truncated IPW in the presence of time-dependent confounders (TDC) (e.g., disease severity), affected by the exposure.

    RESULTS: The baseline adjusted odds ratio (OR) was 0.62 (95%CI: 0.51-0.75), which compared risk of PCa-death between men on statins and men not on statins. The calculated IPW for the MSM were highly variable, with the smallest weight at 0.0019 and the largest at 13,574, resulting in an OR of 0.89 (95%CI: 0.69-1.14). Truncating the weights improved variability, reducing the largest weight to 13.16. The truncated MSM OR was 0.86 (95%CI: 0.81-0.91).

    CONCLUSION: An association of statins and risk of PCa-death could not be reliably discerned, due to lack of data on essential confounders, namely serum cholesterol levels and disease severity. No observational studies on statin-use to date present information on serum cholesterol levels and disease severity in one setting, highlighting the need for careful interpretation of investigations into drugs in relation to diseases other than their intended purpose in observational settings.

  • 18.
    Myte, Robin
    et al.
    Umea Univ, Dept Radiat Sci, Oncol, SE-90187 Umea, Sweden.
    Gylling, Bjorn
    Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden.
    Haggstrom, Jenny
    Umea Univ, Umea Sch Business & Econ, Dept Stat, Umea, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden.
    Zingmark, Carl
    Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden.
    Burstrom, Anna Lofgren
    Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden.
    Palmqvist, Richard
    Umea Univ, Dept Med Biosci, Pathol, Umea, Sweden.
    Van Guelpen, Bethany
    Umea Univ, Dept Radiat Sci, Oncol, SE-90187 Umea, Sweden;Umea Univ, Wallenberg Ctr Mol Med, Umea, Sweden.
    Metabolic factors and the risk of colorectal cancer by KRAS and BRAF mutation status2019Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 145, nr 2, s. 327-337Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Factors related to energy metabolism and the metabolic syndrome, such as higher body mass index (BMI), blood glucose, or blood lipids, and blood pressure, are associated with an increased risk of colorectal cancer (CRC). However, CRC is a heterogeneous disease, developing through distinct pathways with differences in molecular characteristics and prognosis, and possibly also in risk factors. For subtypes defined by KRAS and BRAF mutation status, BMI is the only metabolic factor previously studied, with inconsistent findings. We investigated whether associations between BMI, blood glucose, blood lipids, and blood pressure and CRC risk differed by tumor KRAS and BRAF mutation status in 117,687 participants from two population-based cohorts within the Northern Sweden Health and Disease Study (NSHDS). Hazard ratios (HRs) for overall CRC and CRC subtypes by metabolic factors were estimated with Cox proportional hazards regression, using multiple imputation to handle missing exposure and tumor data. During a median follow-up of 15.6 years, we acquired 1,250 prospective CRC cases, of which 766 cases had complete baseline and molecular tumor data. Consistent with previous evidence, higher BMI, total cholesterol, triglyceride levels, and blood pressure were associated with an increased risk of overall CRC (HRs per 1 standard deviation increase: 1.07 to 1.12). These associations were similar regardless of CRC subtype by KRAS and BRAF mutation status (all p(heterogeneity) > 0.05). The same was true for subtypes based on microsatellite instability status. Poor metabolic health may therefore be a universal mechanism for colorectal cancer, acting across multiple developmental pathways.

  • 19.
    Russell, Beth
    et al.
    Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Sherif, Amir
    Umea Univ, Dept Surg & Perioperat Sci, Urol & Androl, Umea, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi.
    Josephs, Debra
    Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Kumar, Pardeep
    Royal Marsden NHS Fdn Trust, London, England.
    Malmström, Per-Uno
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Van Hemelrijck, Mieke
    Kings Coll London, Sch Canc & Pharmaceut Sci, TOUR, London, England.
    Neoadjuvant chemotherapy for muscle invasive bladder cancer: a nationwide investigation on survival2019Ingår i: Scandinavian journal of urology, ISSN 2168-1805, E-ISSN 2168-1813, Vol. 53, nr 4, s. 206-212Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objectives: Randomised controlled trials (RCTs) have investigated the use of neoadjuvant chemotherapy (NAC) and its effect on survival patients with non-metastatic muscle-invasive bladder cancer (MIBC). However, these RCTs have limited external validity and generalisability and, therefore, the current study aims to use real world evidence in the form of observational data to identify the effect that NAC may have on survival, compared to the use of radical cystectomy (RC) alone. Materials and methods: The study cohort (consisting of 944 patients) was selected as a target trial from the Bladder Cancer Data Base Sweden (BladderBaSe). This study calculated 5-year survival and risk of bladder cancer (BC)-specific and overall death by Cox proportional hazard models for the study cohort and a propensity score (PS) matched cohort. Results: Those who had received NAC had higher 5-year survival proportions and decreased risk of both overall and BC specific death (HR = 0.71, 95% CI = 0.52-0.97 and HR = 0.67, 95% CI = 0.48-0.94), respectively, as compared to patients who did not receive NAC. The PS matched cohort showed similar estimates, but with larger statistical uncertainty (Overall death: HR = 0.76, 95% CI = 0.53-1.09 and BC-specific death: HR = 0.73, 95% CI = 0.50-1.07). Conclusion: Results from the current observational study found similar point estimates for 5-year survival and of relative risks as previous studies. However, the results based on real world evidence had larger statistical variability, resulting in a non-statistically significant effect of NAC on survival. Future studies with detailed validated data can be used to further investigate the effect of NAC in narrower patient groups.

  • 20.
    Teleka, Stanley
    et al.
    Lund Univ, Dept Clin Sci Malmo, Lund, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden;Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden.
    Nagel, Gabriele
    Univ Ulm, Inst Epidemiol & Med Biometry, Ulm, Germany;Vorarlberg Canc Registry, Agcy Prevent & Social Med, Bregenz, Aks, Austria.
    Bjorge, Tone
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway;Canc Registry Norway, Oslo, Norway.
    Manjer, Jonas
    Lund Univ, Skane Univ Hosp, Dept Surg, Malmo, Sweden.
    Ulmer, Hanno
    Innsbruck Med Univ, Dept Med Stat Informat & Hlth Econ, Innsbruck, Austria.
    Liedberg, Fredrik
    Lund Univ, Inst Translat Med, Div Urol Res, Malmo, Sweden.
    Ghaderi, Sara
    Univ Bergen, Dept Global Publ Hlth & Primary Care, Bergen, Norway.
    Lang, Alois
    Vorarlberg Canc Registry, Agcy Prevent & Social Med, Bregenz, Aks, Austria.
    Jonsson, Hakan
    Umea Univ, Dept Radiat Sci, Umea, Sweden.
    Jahnson, Staffan
    Linkoping Univ, Dept Urol, Linkoping, Sweden;Linkoping Univ, IKE, Linkoping, Sweden.
    Orho-Melander, Marju
    Lund Univ, Dept Clin Sci Malmo, Lund, Sweden.
    Tretli, Steinar
    Canc Registry Norway, Oslo, Norway.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Stocks, Tanja
    Lund Univ, Dept Clin Sci Malmo, Lund, Sweden.
    Risk of bladder cancer by disease severity in relation to metabolic factors and smoking: A prospective pooled cohort study of 800,000 men and women2018Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 143, nr 12, s. 3071-3082Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Previous studies on metabolic factors and bladder cancer (BC) risk have shown inconsistent results and have commonly not investigated associations separately by sex, smoking, and tumor invasiveness. Among 811,633 participants in six European cohorts, we investigated sex-specific associations between body mass index (BMI), mid-blood pressure (BP, [systolic + diastolic]/2), plasma glucose, triglycerides, total cholesterol and risk of BC overall, non-muscle invasive BC (NMIBC) and muscle invasive BC (MIBC). Among men, we additionally assessed additive interactions between metabolic factors and smoking on BC risk. During follow-up, 2,983 men and 754 women were diagnosed with BC. Among men, triglycerides and BP were positively associated with BC risk overall (hazard ratio [HR] per standard deviation [SD]: 1.17 [95% confidence interval (CI) 1.06-1.27] and 1.09 [1.02-1.17], respectively), and among women, BMI was inversely associated with risk (HR: 0.90 [0.82-0.99]). The associations for BMI and BP differed between men and women (p(interaction) <= 0.005). Among men, BMI, cholesterol and triglycerides were positively associated with risk for NMIBC (HRs: 1.09 [95% CI 1.01-1.18], 1.14 [1.02-1.25], and 1.30 [1.12-1.48] respectively), and BP was positively associated with MIBC (HR: 1.23 [1.02-1.49]). Among women, glucose was positively associated with MIBC (HR: 1.99 [1.04-3.81]). Apart from cholesterol, HRs for metabolic factors did not significantly differ between MIBC and NMIBC, and there were no interactions between smoking and metabolic factors on BC. Our study supports an involvement of metabolic aberrations in BC risk. Whilst some associations were significant only in certain sub-groups, there were generally no significant differences in associations by smoking or tumor invasiveness.

  • 21.
    Tomic, Katarina
    et al.
    Umeå Univ, Dept Surg & Perioperat Sci, Urol & Androl, Umeå, Sweden.
    Ventimiglia, Eugenio
    URI, Unit Urol, Div Expt Oncol, Milan, Italy; IRCCS, Osped San Raffaele, Milan, Italy.
    Robinson, David
    Ryhov Hosp, Dept Urol, Jönköpinh, Sweden.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umeå Univ, Dept Biobank Res, Umeå, Sweden.
    Lambe, Mats
    Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden; Uppsala Univ Hosp, Reg Canc Ctr Uppsala Örebro, Uppsala, Sweden.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Socioeconomic status and diagnosis, treatment, and mortality in men with prostate cancer. Nationwide population-based study2018Ingår i: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 142, nr 12, s. 2478-2484Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Patients with high socioeconomic status (SES) have better cancer outcomes than patients with low SES. This has also been shown in Sweden, a country with tax‐financed health care aiming to provide care on equal terms to all residents. The association between income and educational level and diagnostics and treatment as outlined in national guidelines and prostate cancer (Pca) and all‐cause mortality was assessed in 74,643 men by use of data in the National Prostate Cancer Register of Sweden and a number of other health care registers and demographic databases. In multivariable logistic regression analysis, men with high income had higher probability of Pca detected in a health‐check‐up, top versus bottom income quartile, odds ratio (OR) 1.60 (95% CI 1.45–1.77) and lower probability of waiting more than 3 months for prostatectomy, OR 0.77 (0.69–0.86). Men with the highest incomes also had higher probability of curative treatment for intermediate and high‐risk cancer, OR 1.77 (1.61–1.95) and lower risk of positive margins, (incomplete resection) at prostatectomy, OR 0.80 (0.71–0.90). Similar, but weaker associations were observed for educational level. At 6 years of follow‐up, Pca mortality was modestly lower for men with high income, which was statistically significant for localized high‐risk and metastatic Pca in men with no comorbidities. All‐cause mortality was less than half in top versus bottom quartile of income (12% vs. 30%, p < 0.001) among men above age 65. Our findings underscore the importance of adherence to guidelines to ensure optimal and equal care for all patients diagnosed with cancer.

  • 22.
    Van Hemelrijck, Mieke
    et al.
    Kings Coll London, Div Canc Studies Translat Oncol & Urol Res, London, England.
    Ulmer, Hanno
    Med Univ Innsbruck, Dept Med Stat Informat & Hlth Econ, Innsbruck, Austria.
    Nagel, Gabriele
    Ulm Univ, Inst Epidemiol & Med Biometry, Ulm, Germany;Agcy Prevent & Social Med, Bregenz, Austria.
    Peter, Raphael Simon
    Ulm Univ, Inst Epidemiol & Med Biometry, Ulm, Germany.
    Fritz, Josef
    Med Univ Innsbruck, Dept Med Stat Informat & Hlth Econ, Innsbruck, Austria.
    Myte, Robin
    Umea Univ, Dept Radiat Sci, Umea, Sweden.
    Van Guelpen, Bethany
    Umea Univ, Dept Radiat Sci, Umea, Sweden.
    Föger, Bernhard
    Agcy Prevent & Social Med, Bregenz, Austria.
    Concin, Hans
    Agcy Prevent & Social Med, Bregenz, Austria.
    Häggström, Christel
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Endokrinkirurgi. Umea Univ, Dept Biobank Res, Umea, Sweden;Umea Univ, Dept Publ Hlth & Clin Med, Nutr Res, Umea, Sweden.
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Stocks, Tanja
    Lund Univ, Dept Clin Sci Malmo, Malmo, Sweden.
    Longitudinal study of body mass index, dyslipidemia, hyperglycemia, and hypertension in 60,000 men and women in Sweden and Austria2018Ingår i: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, nr 6, artikel-id e0197830Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: 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.

    Methods: Data from 27,379 men and 32,275 women with in total 122,940 health examinations in the Vasterbotten 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.

    Results: 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/m(2) higher BMI at age 40, glucose at age 50 increased by 0.24 mmol/l (95%Cl:0.22-0.26) and mid-blood pressure increased by 1.54 mm Hg (95%Cl: 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/m(2) 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.

    Conclusion: 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.

  • 23. Wirén, Sara
    et al.
    Häggström, Christel
    Department of Surgery and Perioperative Sciences, Urology and Andrology, Umeå, Sweden.
    Ulmer, Hanno
    Manjer, Jonas
    Bjørge, Tone
    Nagel, Gabriele
    Johansen, Dorthe
    Hallmans, Göran
    Engeland, Anders
    Concin, Hans
    Jonsson, Håkan
    Selmer, Randi
    Tretli, Steinar
    Stocks, Tanja
    Stattin, Pär
    Uppsala universitet, Medicinska och farmaceutiska vetenskapsområdet, Medicinska fakulteten, Institutionen för kirurgiska vetenskaper, Urologkirurgi.
    Pooled cohort study on height and risk of cancer and cancer death2014Ingår i: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 25, nr 2, s. 151-159Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    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.

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