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Article ; Online: Opioid medications: an emerging cancer risk factor?

Sheikh, Mahdi / Brennan, Paul / Mariosa, Daniela / Robbins, Hilary A

2023 Volume 130, Issue 3, Page(s) e401–e403

MeSH term(s)	Humans ; Analgesics, Opioid/adverse effects ; Opioid-Related Disorders/epidemiology ; Opioid-Related Disorders/drug therapy ; Risk Factors ; Neoplasms/drug therapy
Chemical Substances	Analgesics, Opioid
Language	English
Publishing date	2023-01-20
Publishing country	England
Document type	Letter
ZDB-ID	80074-0
ISSN	1471-6771 ; 0007-0912
ISSN (online)	1471-6771
ISSN	0007-0912
DOI	10.1016/j.bja.2022.12.007
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Article ; Online: Genetically proxied impaired GIPR signaling and risk of 6 cancers.

Rogers, Miranda / Gill, Dipender / Ahlqvist, Emma / Robinson, Tim / Mariosa, Daniela / Johansson, Mattias / Cortez Cardoso Penha, Ricardo / Dossus, Laure / Gunter, Marc J / Moreno, Victor / Davey Smith, George / Martin, Richard M / Yarmolinsky, James

iScience

2023 Volume 26, Issue 6, Page(s) 106848

Abstract: Preclinical and genetic studies suggest that impaired glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling worsens glycemic control. The relationship between GIPR signaling and the risk of cancers influenced by impaired glucose ... ...

Abstract	Preclinical and genetic studies suggest that impaired glucose-dependent insulinotropic polypeptide receptor (GIPR) signaling worsens glycemic control. The relationship between GIPR signaling and the risk of cancers influenced by impaired glucose homeostasis is unclear. We examined the association of a variant in
Language	English
Publishing date	2023-05-09
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106848
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Article ; Online: The role of genomics in global cancer prevention.

Ginsburg, Ophira / Ashton-Prolla, Patricia / Cantor, Anna / Mariosa, Daniela / Brennan, Paul

Nature reviews. Clinical oncology

2020 Volume 18, Issue 2, Page(s) 116–128

Abstract: Despite improvements in the understanding of cancer causation, much remains unknown regarding the mechanisms by which genomic and non-genomic factors initiate carcinogenesis, drive cell invasion and metastasis, and enable cancer to develop. Technological ...

Abstract	Despite improvements in the understanding of cancer causation, much remains unknown regarding the mechanisms by which genomic and non-genomic factors initiate carcinogenesis, drive cell invasion and metastasis, and enable cancer to develop. Technological advances have enabled the analysis of whole genomes, comprising thousands of tumours across populations worldwide, with the aim of identifying mutation signatures associated with particular tumour types. Large collaborative efforts have resulted in the identification and improved understanding of causal factors, and have shed light on new opportunities to prevent cancer. In this new era in cancer genomics, discoveries from studies conducted on an international scale can inform evidence-based strategies in cancer control along the cancer care continuum, from prevention to treatment. In this Review, we present the relevant history and emerging frontiers of cancer genetics and genomics from the perspective of global cancer prevention. We highlight the importance of local context in the adoption of new technologies and emergent evidence, with illustrative examples from worldwide. We emphasize the challenges in implementing important genomic findings in clinical settings with disparate resource availability and present a conceptual framework for the translation of such findings into clinical practice, and evidence-based policies in order to maximize the utility for a population.
MeSH term(s)	Brazil ; Cost-Benefit Analysis ; Founder Effect ; Genetic Predisposition to Disease ; Genomics/economics ; Genomics/methods ; Germ-Line Mutation ; Humans ; Mendelian Randomization Analysis ; Mutation ; Neoplasms/epidemiology ; Neoplasms/genetics ; Neoplasms/prevention & control ; United States
Language	English
Publishing date	2020-09-24
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2491410-1
ISSN	1759-4782 ; 1759-4774
ISSN (online)	1759-4782
ISSN	1759-4774
DOI	10.1038/s41571-020-0428-5
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Zs.A 6029: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Lipids, Apolipoproteins, and the Risk of Parkinson Disease.

Fang, Fang / Zhan, Yiqiang / Hammar, Niklas / Shen, Xia / Wirdefeldt, Karin / Walldius, Göran / Mariosa, Daniela

Circulation research

2019 Volume 125, Issue 6, Page(s) 643–652

Abstract: Rationale: A complete picture of the associations of the most common lipid fractions, including total cholesterol (TC), LDL-C (low-density lipoprotein cholesterol), HDL-C (high-density lipoprotein cholesterol), triglycerides, and apolipoproteins, with ... ...

Abstract	Rationale: A complete picture of the associations of the most common lipid fractions, including total cholesterol (TC), LDL-C (low-density lipoprotein cholesterol), HDL-C (high-density lipoprotein cholesterol), triglycerides, and apolipoproteins, with the risk of Parkinson disease (PD), is lacking. Objective: To assess the associations of lipids and apolipoproteins with the future risk of PD. Methods and results: In the AMORIS (Apolipoprotein-Related Mortality Risk) Study, we enrolled ≈600 000 participants during 1985 to 1996 in Stockholm, Sweden, with repeated measurements of TC, LDL-C, HDL-C, triglycerides, ApoB (apolipoprotein B), and ApoA-I (apolipoprotein A-I). The cohort was followed until the end of 2011, and incident cases of PD were identified through the Swedish Patient Register. We first used Cox models to estimate the associations of these biomarkers with later risk of PD. We further applied a Mendelian randomization analysis for TC, LDL-C, and triglycerides using the GWAS (Genome-wide association study) summary statistics from the public PD GWAS data and 23andMe PD cohorts with >800 000 individuals. One SD increase of TC was associated with a lower hazard of PD (hazard ratio, 0.90; 95% CI, 0.87-0.94). Similar associations were observed for LDL-C (hazard ratio, 0.93; 95% CI, 0.88-0.98), triglycerides (hazard ratio, 0.94; 95% CI, 0.90-0.97), and ApoB (hazard ratio, 0.91; 95% CI, 0.85-0.97). A clear dose-response relation was also noted when using these biomarkers as categorical variables. A causal inverse association of TC, LDL-C, and triglycerides with PD risk was further suggested by the Mendelian randomization analysis. Conclusions: Our findings reinforce that higher levels of TC, LDL-C, and triglycerides are associated with a lower future risk of PD and further suggest that these associations may be causal. The findings for ApoB in relation to PD risk are novel, and whether such association is causal needs to be examined.
MeSH term(s)	Adult ; Apolipoproteins/blood ; Apolipoproteins/genetics ; Case-Control Studies ; Cohort Studies ; Female ; Humans ; Lipids/blood ; Lipids/genetics ; Male ; Mendelian Randomization Analysis/methods ; Middle Aged ; Parkinson Disease/blood ; Parkinson Disease/epidemiology ; Parkinson Disease/genetics ; Prospective Studies ; Risk Factors ; Sweden/epidemiology
Chemical Substances	Apolipoproteins ; Lipids
Language	English
Publishing date	2019-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80100-8
ISSN	1524-4571 ; 0009-7330 ; 0931-6876
ISSN (online)	1524-4571
ISSN	0009-7330 ; 0931-6876
DOI	10.1161/CIRCRESAHA.119.314929
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Article ; Online: Commentary: What can Mendelian randomization tell us about causes of cancer?

Mariosa, Daniela / Carreras-Torres, Robert / Martin, Richard M / Johansson, Mattias / Brennan, Paul

International journal of epidemiology

2019 Volume 48, Issue 3, Page(s) 816–821

MeSH term(s)	Biological Specimen Banks ; Causality ; Humans ; Mendelian Randomization Analysis ; Neoplasms/epidemiology ; Obesity/epidemiology ; Overweight/epidemiology ; United Kingdom/epidemiology
Language	English
Publishing date	2019-09-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	187909-1
ISSN	1464-3685 ; 0300-5771
ISSN (online)	1464-3685
ISSN	0300-5771
DOI	10.1093/ije/dyz151
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Article ; Online: Peripheral immune biomarkers and neurodegenerative diseases: A prospective cohort study with 20 years of follow-up.

Yazdani, Solmaz / Mariosa, Daniela / Hammar, Niklas / Andersson, John / Ingre, Caroline / Walldius, Göran / Fang, Fang

Annals of neurology

2019 Volume 86, Issue 6, Page(s) 913–926

Abstract: Objective: To assess the associations of several blood immune biomarkers with the future risks of amyotrophic lateral sclerosis and Parkinson disease in a prospective cohort study with 20 years of follow-up.: Methods: The Swedish Apolipoprotein- ... ...

Abstract	Objective: To assess the associations of several blood immune biomarkers with the future risks of amyotrophic lateral sclerosis and Parkinson disease in a prospective cohort study with 20 years of follow-up. Methods: The Swedish Apolipoprotein-Related Mortality Risk study is a longitudinal cohort study including 812,073 participants with repeated blood biomarker measurements between 1985 and 1996 and a follow-up until 2011. Using a Cox model, we first estimated hazard ratios of amyotrophic lateral sclerosis and Parkinson disease in relation to leukocytes, immunoglobulin G, haptoglobin, and uric acid. We further described the temporal changes of these biomarkers during the 20 years prior to the diagnosis of these diseases. Results: A total of 585 incident cases of amyotrophic lateral sclerosis and 3,769 incident cases of Parkinson disease were identified during the follow-up. Increasing concentrations of leukocytes, haptoglobin, and uric acid were associated with a lower risk of Parkinson disease. No statistically significant association was, however, noted between the studied biomarkers and amyotrophic lateral sclerosis. Parkinson disease patients appeared to have lower levels of leukocytes and haptoglobin between 20 and 10 years before diagnosis and lower levels of uric acid during the 20 years before diagnosis, compared to controls, although statistically significant differences were only noted during parts of the respective time intervals after multivariable adjustment. No clear differences were noted between patients with amyotrophic lateral sclerosis and controls. Interpretation: If verified in studies of independent populations, our findings may suggest a different role of systemic inflammation on the risk of Parkinson disease compared to amyotrophic lateral sclerosis. ANN NEUROL 2019;86:913-926.
MeSH term(s)	Aged ; Amyotrophic Lateral Sclerosis/blood ; Amyotrophic Lateral Sclerosis/epidemiology ; Amyotrophic Lateral Sclerosis/immunology ; Biomarkers/blood ; Cohort Studies ; Female ; Follow-Up Studies ; Humans ; Immunity, Cellular/immunology ; Longitudinal Studies ; Male ; Middle Aged ; Neurodegenerative Diseases/blood ; Neurodegenerative Diseases/epidemiology ; Neurodegenerative Diseases/immunology ; Parkinson Disease/blood ; Parkinson Disease/epidemiology ; Parkinson Disease/immunology ; Prospective Studies ; Sweden/epidemiology ; Time Factors
Chemical Substances	Biomarkers
Language	English
Publishing date	2019-10-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.25614
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Zs.A 1370: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article: Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomisation analysis.

Cornish, Naomi / Haycock, Philip / Brenner, Hermann / Figueiredo, Jane C / Galesloot, Tessel / Grant, Robert C / Johansson, Mattias / Mariosa, Daniela / McKay, James / Pai, Rish / Pellatt, Andrew J / Samadder, N Jewel / Shi, Jianxin / Thibord, Florian / Trégouët, David-Alexandre / Voegele, Catherine / Thirlwell, Chrissie / Mumford, Andrew / Langdon, Ryan

medRxiv : the preprint server for health sciences

2023

Abstract: Background: People with cancer experience high rates of venous thromboembolism (VTE). Additionally, risk of subsequent cancer is increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely ... ...

Abstract	Background: People with cancer experience high rates of venous thromboembolism (VTE). Additionally, risk of subsequent cancer is increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, and it is unknown whether VTE is itself a risk factor for cancer. Methods: We used data from large genome-wide association study meta-analyses to perform bi-directional Mendelian randomisation analyses to estimate causal associations between genetically-proxied lifetime risk of VTE and risk of 18 different cancers. Results: We found no conclusive evidence that genetically-proxied lifetime risk of VTE was causally associated with an increased incidence of cancer, or vice-versa. We observed an association between VTE and pancreatic cancer risk (odds ratio for pancreatic cancer 1.23 (95% confidence interval 1.08 - 1.40) per log-odds increase in risk of VTE, Conclusions: These findings do not support the hypothesis that genetically-proxied lifetime risk of VTE is a cause of cancer. Existing observational epidemiological associations between VTE and cancer are therefore more likely to be driven by pathophysiological changes which occur in the setting of active cancer and anti-cancer treatments. Further work is required to explore and synthesise evidence for these mechanisms.
Language	English
Publishing date	2023-05-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.16.23289792
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Article ; Online: Causal relationships between risk of venous thromboembolism and 18 cancers: a bidirectional Mendelian randomization analysis.

Cornish, Naomi / Haycock, Philip / Brenner, Hermann / Figueiredo, Jane C / Galesloot, Tessel E / Grant, Robert C / Johansson, Mattias / Mariosa, Daniela / McKay, James / Pai, Rish / Pellatt, Andrew J / Samadder, N Jewel / Shi, Jianxin / Thibord, Florian / Trégouët, David-Alexandre / Voegele, Catherine / Thirlwell, Chrissie / Mumford, Andrew / Langdon, Ryan

International journal of epidemiology

2023 Volume 53, Issue 1

Abstract: Background: People with cancer experience high rates of venous thromboembolism (VTE). Risk of subsequent cancer is also increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, ... ...

Abstract	Background: People with cancer experience high rates of venous thromboembolism (VTE). Risk of subsequent cancer is also increased in people experiencing their first VTE. The causal mechanisms underlying this association are not completely understood, and it is unknown whether VTE is itself a risk factor for cancer. Methods: We used data from large genome-wide association study meta-analyses to perform bidirectional Mendelian randomization analyses to estimate causal associations between genetic liability to VTE and risk of 18 different cancers. Results: We found no conclusive evidence that genetic liability to VTE was causally associated with an increased incidence of cancer, or vice versa. We observed an association between liability to VTE and pancreatic cancer risk [odds ratio for pancreatic cancer: 1.23 (95% confidence interval: 1.08-1.40) per log-odds increase in VTE risk, P = 0.002]. However, sensitivity analyses revealed this association was predominantly driven by a variant proxying non-O blood group, with inadequate evidence to suggest a causal relationship. Conclusions: These findings do not support the hypothesis that genetic liability to VTE is a cause of cancer. Existing observational epidemiological associations between VTE and cancer are therefore more likely to be driven by pathophysiological changes which occur in the setting of active cancer and anti-cancer treatments. Further work is required to explore and synthesize evidence for these mechanisms.
MeSH term(s)	Humans ; Venous Thromboembolism/epidemiology ; Venous Thromboembolism/genetics ; Mendelian Randomization Analysis ; Genome-Wide Association Study ; Risk Factors ; Pancreatic Neoplasms/epidemiology ; Pancreatic Neoplasms/genetics
Language	English
Publishing date	2023-12-20
Publishing country	England
Document type	Journal Article
ZDB-ID	187909-1
ISSN	1464-3685 ; 0300-5771
ISSN (online)	1464-3685
ISSN	0300-5771
DOI	10.1093/ije/dyad170
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Article ; Online: Genetically Raised Circulating Bilirubin Levels and Risk of Ten Cancers: A Mendelian Randomization Study.

Seyed Khoei, Nazlisadat / Carreras-Torres, Robert / Murphy, Neil / Gunter, Marc J / Brennan, Paul / Smith-Byrne, Karl / Mariosa, Daniela / Mckay, James / O'Mara, Tracy A / Jarrett, Ruth / Hjalgrim, Henrik / Smedby, Karin E / Cozen, Wendy / Onel, Kenan / Diepstra, Arjan / Wagner, Karl-Heinz / Freisling, Heinz

Cells

2021 Volume 10, Issue 2

Abstract: Bilirubin, an endogenous antioxidant, may play a protective role in cancer development. We applied two-sample Mendelian randomization to investigate whether genetically raised bilirubin levels are causally associated with the risk of ten cancers ( ... ...

Abstract	Bilirubin, an endogenous antioxidant, may play a protective role in cancer development. We applied two-sample Mendelian randomization to investigate whether genetically raised bilirubin levels are causally associated with the risk of ten cancers (pancreas, kidney, endometrium, ovary, breast, prostate, lung, Hodgkin's lymphoma, melanoma, and neuroblastoma). The number of cases and their matched controls of European descent ranged from 122,977 and 105,974 for breast cancer to 1200 and 6417 for Hodgkin's lymphoma, respectively. A total of 115 single-nucleotide polymorphisms (SNPs) associated (
MeSH term(s)	Bilirubin/genetics ; Biomarkers/analysis ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; Genome-Wide Association Study ; Humans ; Mendelian Randomization Analysis/methods ; Polymorphism, Single Nucleotide/genetics ; Risk Factors
Chemical Substances	Biomarkers ; Bilirubin (RFM9X3LJ49)
Language	English
Publishing date	2021-02-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10020394
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Article ; Online: Neurodegenerative and psychiatric diseases among families with amyotrophic lateral sclerosis.

Longinetti, Elisa / Mariosa, Daniela / Larsson, Henrik / Ye, Weimin / Ingre, Caroline / Almqvist, Catarina / Lichtenstein, Paul / Piehl, Fredrik / Fang, Fang

Neurology

2017 Volume 89, Issue 6, Page(s) 578–585

Abstract: Objective: To estimate risks of neurodegenerative and psychiatric diseases among patients with amyotrophic lateral sclerosis (ALS) and their families.: Methods: We conducted a register-based nested case-control study during 1990-2013 in Sweden to ... ...

Abstract	Objective: To estimate risks of neurodegenerative and psychiatric diseases among patients with amyotrophic lateral sclerosis (ALS) and their families. Methods: We conducted a register-based nested case-control study during 1990-2013 in Sweden to assess whether patients with ALS had higher risks of other neurodegenerative and psychiatric diseases before diagnosis. We included 3,648 patients with ALS and 36,480 age-, sex-, and county of birth-matched population controls. We further conducted a follow-up study of the cases and controls to assess the risks of other neurodegenerative and psychiatric diseases after ALS diagnosis. To assess the potential contribution of familial factors, we conducted similar studies for the relatives of patients with ALS and their controls. Results: Individuals with previous neurodegenerative or psychiatric diseases had a 49% increased risk of ALS (odds ratio 1.49, 95% confidence interval 1.35-1.66) compared to individuals without these diseases. After diagnosis, patients with ALS had increased risks of other neurodegenerative or psychiatric diseases (hazard ratio 2.90, 95% confidence interval 2.46-3.43) compared to individuals without ALS. The strongest associations were noted for frontotemporal dementia, Parkinson disease, other dementia, Alzheimer disease, neurotic disorders, depression, stress-related disorders, and drug abuse/dependence. First-degree relatives of patients with ALS had higher risk of neurodegenerative diseases, whereas only children of patients with ALS had higher risk of psychiatric disorders, compared to relatives of the controls. Conclusions: Familial aggregation of ALS and other neurodegenerative diseases implies a shared etiopathogenesis among all neurodegenerative diseases. The increased risk of psychiatric disorders among patients with ALS and their children might be attributable to nonmotor symptoms of ALS and severe stress response toward the diagnosis.
MeSH term(s)	Aged ; Amyotrophic Lateral Sclerosis/epidemiology ; Amyotrophic Lateral Sclerosis/genetics ; Case-Control Studies ; Family ; Female ; Follow-Up Studies ; Genetic Predisposition to Disease ; Humans ; Male ; Mental Disorders/epidemiology ; Mental Disorders/genetics ; Middle Aged ; Odds Ratio ; Prospective Studies ; Registries ; Sweden/epidemiology
Language	English
Publishing date	2017-07-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000004179
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