Methodological issues in a prospective study on plasma concentrations of persistent organic pollutants and pancreatic cancer risk within the EPIC cohort

Gasull, Magda; Pumarega, José; Kiviranta, Hannu; Rantakokko, Panu; Raaschou-Nielsen, Ole; Bergdahl, Ingvar A.; Sandanger, Torkjel M.; Goñi, Fernando; Cirera, Lluís; Donat‐Vargas, Carolina; Alguacil, Juan; Iglesias, Mar; Tjønneland, Anne; Overvad, Kim; Mancini, Francesca Romana; Boutron-Ruault, Marie Christine; Severi, Gianluca; Johnson, Theron; Kühn, Tilman; Trichopoulou, Antonia; Karakatsani, Anna; Peppa, Eleni; Palli, Domenico; Pala, Valeria; Tumino, Rosario; Naccarati, Alessio; Panico, Salvatore; Verschuren, Monique; Vermeulen, Roel; Rylander, Charlotta; Nøst, Therese Haugdahl; Rodríguez‐Barranco, Miguel; Molinuevo, Amaia; Chirlaque, María Dolores; Ardanaz, Eva; Sund, Malin; Key, Tim; Ye, Weimin; Jenab, Mazda; Michaud, Dominique S.; Matullo, Giuseppe; Canzian, Federico; Kaaks, Rudolf; Nieters, Alexandra; Nöthlings, Ute; Jeurnink, Suzanne M.; Chajès, Véronique; Matejcic, Marco; Gunter, Marc J.; Aune, Dagfinn; Riboli, Elio; Agudo, Antoni; González, Carlos; Weiderpass, Elisabete; Bueno‐de‐Mesquita, Bas; Duell, Eric J.; Víneis, Paolo; Porta, Miquel

doi:10.1016/j.envres.2018.11.027

Cited by 21 publications

(44 citation statements)

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“…Disease progression bias (Porta et al 2014 ) may occur when the biological samples where the exposure biomarkers will be analyzed are collected just before or after the diagnosis of the disease, and when disease-related conditions experienced during the development of the disease and around its diagnosis cause a change in the biomarkers. One type of such conditions are the disease-induced pathophysiological processes that we already mentioned in the Introduction and in previous papers (Porta et al 2007 , 2008 , 2009 , 2014 , 2005 , 2021 ; Porta 2001 ; Gasull et al 2019 ). Related but different are the metabolic requirements of the tumor (He 2011 ; Gutiérrez-González et al 2019 ; Salcedo-Bellido et al 2021 ; Signes-Pastor et al 2020 ; Longnecker et al 1993 ; Garland et al 1993 ; Hunter et al 1990 ; Hopps 1977 ; Sukumar 2006 ).…”

Section: Discussionmentioning

confidence: 96%

“…As expected (Porta et al 2009 ; Porta 2001 ), a substantial number of clinical and epidemiological studies continue to be based on diagnosed cases; hence, they collect post-diagnostic biological samples from cases, rather than collecting the samples from the entire cohort at baseline and conducting nested case–control studies after cases are ascertained during follow-up (Gasull et al 2019 ; Porta et al 2021 ). Among other strengths, the latter approach has considerable advantages with regard to timing of the biological sample collection; notably, avoidance of disease progression bias.…”

Section: Discussionmentioning

confidence: 98%

“…Disease progression bias is thus a form of reverse causation. It results in a lack of etiologic significance of the disease-altered exposure biomarkers (Porta et al 2007 ; Porta et al 2008 ; Porta et al 2009 ; Porta et al 2014 ; Porta et al 2005 ; Porta et al 2021 ; Porta 2001 ; Gasull et al 2019 ). This conceptual and empirical framework provides the rationale to hypothesize that pancreatic cancer progression might also modify concentrations of trace elements in toenails (Gómez-Tomás et al 2019 ; Camargo et al 2019 ; Amaral et al 2012 ; Crous-Bou 2009 ).…”

Section: Introductionmentioning

confidence: 99%

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Timing of Toenail Collection and Concentrations of Metals in Pancreatic Cancer. Evidence Against Disease Progression Bias

et al. 2021

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Trace elements such as cadmium, arsenic, zinc or selenium increase or decrease risk of a wide range of human diseases. Their levels in toenails may provide a measure of mid-term intake of trace elements for studies in humans. However, in biologically and clinically aggressive diseases as pancreatic cancer, the progression of the disease could modify such concentrations and produce reverse causation bias. The aim was to analyze the influence of specific time intervals between several clinical events and the collection of toenails upon concentrations of trace elements in patients with pancreatic cancer. Subjects were 118 incident cases of pancreatic adenocarcinoma prospectively recruited in eastern Spain. Toenails were collected at cancer diagnosis, and soon thereafter interviews were conducted. Information on cancer signs and symptoms was obtained from medical records and patient interviews. Levels of 12 trace elements were determined in toenail samples by inductively coupled plasma mass spectrometry. General linear models adjusting for potential confounders were applied to analyze relations between log concentrations of trace elements and the time intervals, including the interval from first symptom of cancer to toenail collection (iST). Toenail concentrations of the 12 trace elements were weakly or not influenced by the progression of the disease or the diagnostic procedures. Concentrations of aluminum were slightly higher in subjects with a longer iST (age, sex and stage adjusted geometric means: 11.44 vs. 7.75 µg/g for iST > 120 days vs. ≤ 40 days). There was a weak inverse relation of iST with concentrations of zinc and selenium (maximum differences of about 20 and 0.08 µg/g, respectively). Conclusions: concentrations of the trace elements were weakly or not influenced by the development of the disease before toenail collection. Only concentrations of aluminum increased slightly with increasing iST, whereas levels of zinc and selenium decreased weakly. Even in an aggressive disease as pancreatic cancer, toenail concentrations of trace elements may provide a valid measure of mid-term intake of trace elements, unaffected by clinical events and disease progression. Supplementary Information The online version contains supplementary material available at 10.1007/s12403-021-00436-2.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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Timing of Toenail Collection and Concentrations of Metals in Pancreatic Cancer. Evidence Against Disease Progression Bias

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“…35 However, the association between persistent organic pollutants and pancreatic cancer has not been well studied and remains unclear. 57 Nevertheless, the potential link between cumulative breastfeeding duration and pancreatic cancer incidence should be further explored in both experimental and epidemiological studies.…”

Section: Discussionmentioning

confidence: 99%

Reproductive Factors, Use of Exogenous Hormones, and Pancreatic Cancer Incidence: The Norwegian Women and Cancer Study

Alvarez¹,

Borch²,

Rylander³

2021

CLEP

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Introduction The incidence of pancreatic cancer is increasing worldwide and characterized by a particularly low survival rate. Studies have reported weak and inconsistent evidence for associations among reproductive factors, use of exogenous hormones, and pancreatic cancer incidence in women. Purpose To investigate relationships between reproductive factors, exogenous hormones, and the rate of pancreatic cancer incidence in a large population-based prospective cohort of women in Norway. Methods We used data from the Norwegian Women and Cancer study on 588 incident cases of pancreatic cancer diagnosed among 165,419 women, with mean follow-up of 18.7 years. Cox proportional-hazard models were used to estimate HRs and 95% CIs for associations of interest. Results Cumulative breastfeeding duration >24 months was associated with 63% decreased incidence of pancreatic cancer compared to no breastfeeding. We observed an inverse linear dose–response trend between cumulative breastfeeding duration and pancreatic cancer incidence, which was confirmed in parous women and ever-smokers. Higher age at first birth and menopause were inversely associated with pancreatic cancer incidence, though with less precise effect estimates. Current use of oral contraceptives was associated with a doubling of pancreatic cancer incidence, but the analysis was hampered by a small number of cases. There was no evidence of any associations between age at menarche, parity or use of menopausal hormone therapy, and incidence of pancreatic cancer. Conclusion Our results suggest a potential protective effect of breastfeeding duration against pancreatic cancer incidence. Inconsistent results for the other reproductive factors suggested no important role of estrogens in pancreatic cancer etiology.

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“…The discovery set (n=454) was nested in the EPIC cross-sectional study [17, 18]. The first replication set included control subjects from two EPIC nested case-control studies of hepatocellular carcinoma (HCC; n=129) and pancreatic cancer (n=152) with untargeted metabolomics data [19-21]. Non-metastatic incident HCC (n=129) and pancreatic cancer (n=152) cases, were matched 1:1 with cancer-free controls on study center, sex, age at blood collection (□±□1 year), date (□±□6 months) and time of the day (□±□2□h) of blood collection, fasting status, and, for women, exogenous hormone use.…”

Section: Methodsmentioning

confidence: 99%

Novel biomarkers of habitual alcohol intake and associations with risk of pancreatic and liver cancers and liver disease mortality

Loftfield

Stępień

Viallon

et al. 2021

Preprint

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Background: Alcohol is an established risk factor for several cancers, but modest alcohol-cancer associations may be missed due to measurement error in self-reported assessments. The identification of biomarkers of habitual alcohol intake may enhance evidence on the role of alcohol in cancer onset. Methods: Untargeted metabolomics was used to identify metabolites correlated with habitual alcohol intake in a discovery dataset from the European Prospective Investigation into Cancer and Nutrition (EPIC; n=454). Significant correlations were replicated in independent datasets of controls from case-control studies nested within EPIC (n=281) and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC; n=438) study. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals for associations of alcohol-associated metabolites and self-reported alcohol intake with risk of pancreatic cancer, hepatocellular carcinoma (HCC), liver cancer, and liver disease mortality in the contributing studies. Results: Two metabolites displayed a dose-response association with alcohol intake: 2-hydroxy-3-methylbutyric acid and an unidentified compound (m/z(+):231.0839). A 1-SD increase in log2-transformed levels of 2-hydroxy-3-methylbutyric acid was associated with risk of HCC (OR=2.14; 1.39-3.31) and pancreatic cancer (OR=1.65; 1.17-2.32) in EPIC and liver cancer (OR=2.00; 1.44-2.77) and liver disease mortality (OR=2.16; 1.63-2.86) in ATBC. Conversely, a 1-SD increase in log2-transformed questionnaire-derived alcohol intake was not associated with HCC or pancreatic cancer in EPIC or liver cancer in ATBC but was associated with liver disease mortality (OR=2.19; 1.60-2.98) in ATBC. Conclusions: 2-Hydroxy-3-methylbutyric acid is a candidate biomarker of habitual alcohol intake that may advance the study of alcohol and cancer risk in population-based studies.

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Methodological issues in a prospective study on plasma concentrations of persistent organic pollutants and pancreatic cancer risk within the EPIC cohort

Cited by 21 publications

References 42 publications

Timing of Toenail Collection and Concentrations of Metals in Pancreatic Cancer. Evidence Against Disease Progression Bias

Timing of Toenail Collection and Concentrations of Metals in Pancreatic Cancer. Evidence Against Disease Progression Bias

Reproductive Factors, Use of Exogenous Hormones, and Pancreatic Cancer Incidence: The Norwegian Women and Cancer Study

Novel biomarkers of habitual alcohol intake and associations with risk of pancreatic and liver cancers and liver disease mortality

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