| 21. |
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| 22. |
- da Silva, M., et al.
(author)
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Excess body weight, weight gain and obesity-related cancer risk in women in Norway: the Norwegian Women and Cancer study
- 2018
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In: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 119:5, s. 646-656
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Journal article (peer-reviewed)abstract
- BACKGROUND: Excess body weight and weight gain have been reported to independently increase the risk of several cancers. There are few published studies in nationally representative populations of women on specific, 'obesity-related' cancers in relation to prior weight change and relevant confounders. METHODS: Based on self-reported anthropometry, we prospectively assessed body mass index (BMI), weight change over 6 years and subsequent obesity-related cancer risk in the Norwegian Women and Cancer study. We used Cox proportional hazard models to calculate hazard ratios and restricted cubic splines to model potential non-linear dose-response relationships. RESULTS: Excess body weight increased the risk of overall obesity-related cancer, postmenopausal breast, colorectal, colon, endometrial and kidney cancer, with endometrial cancer showing a threefold elevated risk. High weight gain (>= 10 kg) increased the risk of overall obesity-related cancer, postmenopausal breast, endometrial and pancreatic cancer. The association between high weight gain and pancreatic cancer was strong, with 91% increased risk. CONCLUSIONS: Maintaining stable weight in middle adulthood, irrespective of BMI category at baseline, and avoiding excess body weight are both important in the prevention of several obesity-related cancers in women. Our finding of increased risk of pancreatic cancer in women with moderate and high weight gain is novel.
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| 23. |
- Defferrari, R., et al.
(author)
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Influence of segmental chromosome abnormalities on survival in children over the age of 12 months with unresectable localised peripheral neuroblastic tumours without MYCN amplification
- 2015
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In: British Journal of Cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 112:2, s. 290-295
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Journal article (peer-reviewed)abstract
- Background: The prognostic impact of segmental chromosome alterations (SCAs) in children older than 1 year, diagnosed with localised unresectable neuroblastoma (NB) without MYCN amplification enrolled in the European Unresectable Neuroblastoma (EUNB) protocol is still to be clarified, while, for other group of patients, the presence of SCAs is associated with poor prognosis. Methods: To understand the role of SCAs we performed multilocus/pangenomic analysis of 98 tumour samples from patients enrolled in the EUNB protocol. Results: Age at diagnosis was categorised into two groups using 18 months as the age cutoff. Significant difference in the presence of SCAs was seen in tumours of patients between 12 and 18 months and over 18 months of age at diagnosis, respectively (P = 0.04). A significant correlation (P = 0.03) was observed between number of SCAs per tumour and age. Event-free (EFS) and overall survival (OS) were calculated in both age groups, according to both the presence and number of SCAs. In older patients, a poorer survival was associated with the presence of SCAs (EFS = 46% vs 75%, P = 0.023; OS = 66.8% vs 100%, P = 0.003). Moreover, OS of older patients inversely correlated with number of SCAs (P = 0.002). Finally, SCAs provided additional prognostic information beyond histoprognosis, as their presence was associated with poorer OS in patients over 18 months with unfavourable International Neuroblastoma Pathology Classification (INPC) histopathology (P = 0.018). Conclusions: The presence of SCAs is a negative prognostic marker that impairs outcome of patients over the age of 18 months with localised unresectable NB without MYCN amplification, especially when more than one SCA is present. Moreover, in older patients with unfavourable INPC tumour histoprognosis, the presence of SCAs significantly affects OS.
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| 24. |
- Disney-Hogg, Linden, et al.
(author)
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Influence of obesity-related risk factors in the aetiology of glioma
- 2018
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In: British Journal of Cancer. - : Nature Publishing Group. - 0007-0920 .- 1532-1827. ; 118:7, s. 1020-1027
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Journal article (peer-reviewed)abstract
- BACKGROUND: Obesity and related factors have been implicated as possible aetiological factors for the development of glioma in epidemiological observation studies. We used genetic markers in a Mendelian randomisation framework to examine whether obesity-related traits influence glioma risk. This methodology reduces bias from confounding and is not affected by reverse causation. METHODS: Genetic instruments were identified for 10 key obesity-related risk factors, and their association with glioma risk was evaluated using data from a genome-wide association study of 12,488 glioma patients and 18,169 controls. The estimated odds ratio of glioma associated with each of the genetically defined obesity-related traits was used to infer evidence for a causal relationship. RESULTS: No convincing association with glioma risk was seen for genetic instruments for body mass index, waist-to-hip ratio, lipids, type-2 diabetes, hyperglycaemia or insulin resistance. Similarly, we found no evidence to support a relationship between obesity-related traits with subtypes of glioma-glioblastoma (GBM) or non-GBM tumours. CONCLUSIONS: This study provides no evidence to implicate obesity-related factors as causes of glioma.
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| 25. |
- Donat-Vargas, Carolina, et al.
(author)
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Dietary exposure to polychlorinated biphenyls and risk of breast, endometrial and ovarian cancer in a prospective cohort
- 2016
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In: British Journal of Cancer. - : NATURE PUBLISHING GROUP. - 0007-0920 .- 1532-1827. ; 115:9, s. 1113-1121
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Journal article (peer-reviewed)abstract
- Background: Observational studies on polychlorinated biphenyl (PCB) exposure and hormone-related cancer risk are either inconsistent or lacking. We aimed to assess associations of dietary PCB exposure with breast, endometrial and ovarian cancer risk in middle-aged and elderly women. Methods: We included 36 777 cancer-free women at baseline in 1997 from the prospective population-based Swedish Mammography Cohort. Validated estimates of dietary PCB exposure were obtained via a food frequency questionnaire. Incident cancer cases were ascertained through register linkage. Results: During 14 years of follow-up, we ascertained 1593, 437 and 195 incident cases of breast, endometrial and ovarian cancer. We found no overall association between dietary PCB exposure and any of these cancer forms. The multivariable-adjusted relative risks comparing women in the highest and lowest tertile of PCB exposure were 0.96 (95% confidence interval (CI): 0.75, 1.24), 1.21 (95% CI: 0.73, 2.01) and 0.90 (95% CI: 0.45, 1.79) for breast, endometrial and ovarian cancer. In analyses stratified by factors influencing oestrogen exposure, possibly masking associations with PCBs, indications of higher risks were observed for endometrial cancer. Conclusions: This study suggests that dietary exposure to PCBs play no critical role in the development of breast, endometrial or ovarian cancer during middle-age and old ages.
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| 26. |
- Elander, N. O., et al.
(author)
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Expression of dihydropyrimidine dehydrogenase (DPD) and hENT1 predicts survival in pancreatic cancer
- 2018
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In: British Journal of Cancer. - : Springer Nature. - 0007-0920 .- 1532-1827. ; 118:7, s. 947-954
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Journal article (peer-reviewed)abstract
- Background: Dihydropyrimidine dehydrogenase (DPD) tumour expression may provide added value to human equilibrative nucleoside transporter-1 (hENT1) tumour expression in predicting survival following pyrimidine-based adjuvant chemotherapy.Methods: DPD and hENT1 immunohistochemistry and scoring was completed on tumour cores from 238 patients with pancreatic cancer in the ESPAC-3(v2) trial, randomised to either postoperative gemcitabine or 5-fluorouracil/folinic acid (5FU/FA).Results: DPD tumour expression was associated with reduced overall survival (hazard ratio, HR = 1.73 [95% confidence interval, CI = 1.21-2.49], p = 0.003). This was significant in the 5FU/FA arm (HR = 2.07 [95% CI = 1.22-3.53], p = 0.007), but not in the gemcitabine arm (HR = 1.47 [0.91-3.37], p = 0.119). High hENT1 tumour expression was associated with increased survival in gemcitabine treated (HR = 0.56 [0.38-0.82], p = 0.003) but not in 5FU/FA treated patients (HR = 1.19 [0.80-1.78], p = 0.390). In patients with low hENT1 tumour expression, high DPD tumour expression was associated with a worse median [95% CI] survival in the 5FU/FA arm (9.7 [5.3-30.4] vs 29.2 [19.5-41.9] months, p = 0.002) but not in the gemcitabine arm (14.0 [9.1-15.7] vs. 18.0 [7.6-15.3] months, p = 1.000). The interaction of treatment arm and DPD expression was not significant (p = 0.303), but the interaction of treatment arm and hENT1 expression was (p = 0.009).Conclusion: DPD tumour expression was a negative prognostic biomarker. Together with tumour expression of hENT1, DPD tumour expression defined patient subgroups that might benefit from either postoperative 5FU/FA or gemcitabine.
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| 27. |
- Elander, N. O., et al.
(author)
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Intratumoural expression of deoxycytidylate deaminase or ribonuceotide reductase subunit M1 expression are not related to survival in patients with resected pancreatic cancer given adjuvant chemotherapy
- 2018
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In: British Journal of Cancer. - : NATURE PUBLISHING GROUP. - 0007-0920 .- 1532-1827. ; 118:8, s. 1084-1088
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Journal article (peer-reviewed)abstract
- BACKGROUND: Deoxycytidylate deaminase (DCTD) and ribonucleotide reductase subunit M1 (RRM1) are potential prognostic and predictive biomarkers for pyrimidine-based chemotherapy in pancreatic adenocarcinoma.METHODS: Immunohistochemical staining of DCTD and RRM1 was performed on tissue microarrays representing tumour samples from 303 patients in European Study Group for Pancreatic Cancer (ESPAC)-randomised adjuvant trials following pancreatic resection, 272 of whom had received gemcitabine or 5-fluorouracil with folinic acid in ESPAC-3(v2), and 31 patients from the combined ESPAC-3(v1) and ESPAC-1 post-operative pure observational groups.RESULTS: Neither log-rank testing on dichotomised strata or Cox proportional hazard regression showed any relationship of DCTD or RRM1 expression levels to survival overall or by treatment group.CONCLUSIONS: Expression of either DCTD or RRM1 was not prognostic or predictive in patients with pancreatic adenocarcinoma who had had post-operative chemotherapy with either gemcitabine or 5-fluorouracil with folinic acid.
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| 28. |
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| 29. |
- Fisher, O M, et al.
(author)
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MIC-1/GDF15 in Barrett's oesophagus and oesophageal adenocarcinoma.
- 2015
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In: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 112:8, s. 1384-1391
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Journal article (peer-reviewed)abstract
- Biomarkers are needed to improve current diagnosis and surveillance strategies for patients with Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC). Macrophage inhibitory cytokine 1/growth differentiation factor 15 (MIC-1/GDF15) tissue and plasma levels have been shown to predict disease progression in other cancer types and was therefore evaluated in BO/OAC.
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| 30. |
- Fortner, Renée T., et al.
(author)
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Anti-Mullerian hormone and endometrial cancer : a multi-cohort study
- 2017
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In: British Journal of Cancer. - : Nature Publishing Group. - 0007-0920 .- 1532-1827. ; 117:9, s. 1412-1418
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Journal article (peer-reviewed)abstract
- Background: The Mullerian ducts are the embryological precursors of the female reproductive tract, including the uterus; anti-Mullerian hormone (AMH) has a key role in the regulation of foetal sexual differentiation. Anti-Mullerian hormone inhibits endometrial tumour growth in experimental models by stimulating apoptosis and cell cycle arrest. To date, there are no prospective epidemiologic data on circulating AMH and endometrial cancer risk. Methods: We investigated this association among women premenopausal at blood collection in a multicohort study including participants from eight studies located in the United States, Europe, and China. We identified 329 endometrial cancer cases and 339 matched controls. AntiMullerian hormone concentrations in blood were quantified using an enzyme-linked immunosorbent assay. Conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) across tertiles and for a doubling of AMH concentrations (ORlog2). Subgroup analyses were performed by ages at blood donation and diagnosis, oral contraceptive use, and tumour characteristics. Results: Anti-Mullerian hormone was not associated with the risk of endometrial cancer overall (ORlog(2): 1.07 (0.99-1.17)), or with any of the examined subgroups. Conclusions: Although experimental models implicate AMH in endometrial cancer growth inhibition, our findings do not support a role for circulating AMH in the aetiology of endometrial cancer.
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