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Melin, Beatrice S.
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Publications (10 of 195) Show all publications
Dahlin, A. M., Wibom, C., Andersson, U., Bybjerg-Grauholm, J., Deltour, I., Hougaard, D. M., . . . Melin, B. S. (2020). A genome-wide association study on medulloblastoma. Journal of Neuro-Oncology
Open this publication in new window or tab >>A genome-wide association study on medulloblastoma
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2020 (English)In: Journal of Neuro-Oncology, ISSN 0167-594X, E-ISSN 1573-7373Article in journal (Refereed) Epub ahead of print
Abstract [en]

Introduction: Medulloblastoma is a malignant embryonal tumor of the cerebellum that occurs predominantly in children. To find germline genetic variants associated with medulloblastoma risk, we conducted a genome-wide association study (GWAS) including 244 medulloblastoma cases and 247 control subjects from Sweden and Denmark.

Methods: Genotyping was performed using Illumina BeadChips, and untyped variants were imputed using IMPUTE2.

Results: Fifty-nine variants in 11 loci were associated with increased medulloblastoma risk (p < 1 × 10–5), but none were statistically significant after adjusting for multiple testing (p < 5 × 10–8). Thirteen of these variants were genotyped, whereas 46 were imputed. Genotyped variants were further investigated in a validation study comprising 249 medulloblastoma cases and 629 control subjects. In the validation study, rs78021424 (18p11.23, PTPRM) was associated with medulloblastoma risk with OR in the same direction as in the discovery cohort (ORT = 1.59, pvalidation = 0.02). We also selected seven medulloblastoma predisposition genes for investigation using a candidate gene approach: APCBRCA2PALB2PTCH1SUFUTP53, and GPR161. The strongest evidence for association was found for rs201458864 (PALB2, ORT = 3.76, p = 3.2 × 10–4) and rs79036813 (PTCH1, ORA = 0.42, p = 2.6 × 10–3).

Conclusion: The results of this study, including a novel potential medulloblastoma risk loci at 18p11.23, are suggestive but need further validation in independent cohorts.

Place, publisher, year, edition, pages
Springer, 2020
Keywords
Pediatric cancers, CNS cancers, Adolescents and young adults (AYA), Epidemiology, Genetics of risk, outcome, and prevention
National Category
Cancer and Oncology Neurology
Identifiers
urn:nbn:se:umu:diva-168914 (URN)10.1007/s11060-020-03424-9 (DOI)000516094000001 ()32056145 (PubMedID)
Funder
Swedish Childhood Cancer Foundation, NCS2009-0001Swedish Childhood Cancer Foundation, PR2017-0157Swedish Childhood Cancer Foundation, NC2011-0004Swedish Childhood Cancer Foundation, TJ2015-0044Swedish Cancer Society, CAN 2018/390Swedish Research Council, 2016-01159_ 3NIH (National Institute of Health), P30ES007033NIH (National Institute of Health), R01CA116724NIH (National Institute of Health), R03CA106011Novo Nordisk
Available from: 2020-03-17 Created: 2020-03-17 Last updated: 2020-03-17
Saunders, C. N., Cornish, A. J., Kinnersley, B., Law, P. J., Claus, E. B., Il'yasova, D., . . . Houlston, R. S. (2020). Lack of association between modifiable exposures and glioma risk: a Mendelian randomization analysis. Neuro-Oncology, 22(2), 207-215
Open this publication in new window or tab >>Lack of association between modifiable exposures and glioma risk: a Mendelian randomization analysis
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2020 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 22, no 2, p. 207-215Article, review/survey (Refereed) Published
Abstract [en]

Background. The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian randomization (MR) framework to examine if lifestyle, cardiometabolic, and inflammatory factors influence the risk of glioma. This methodology reduces bias from confounding and is not affected by reverse causation. Methods. We identified genetic instruments for 37 potentially modifiable risk factors and evaluated their association with glioma risk using data from a genome-wide association study of 12488 glioma patients and 18169 controls. We used the estimated odds ratio of glioma associated with each of the genetically defined traits to infer evidence for a causal relationship with the following exposures: Lifestyle and dietary factors-height, plasma insulin-like growth factor 1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamins (A1, B12, B6, E, and 25-hydroxyvitamin D), fatty acid levels (monounsaturated, omega-3, and omega-6) and circulating fetuin-A; Cardiometabolic factors-birth weight, high density lipoprotein cholesterol, low density lipoprotein cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, glycated hemoglobin levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio; and Inflammatory factors- C-reactive protein, plasma interleukin-6 receptor subunit alpha and serum immunoglobulin E. Results. After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism, no significant association with glioma risk was observed (ie, P-Corrected > 0.05). Conclusions. This study did not provide evidence supporting any of the 37 factors examined as having a significant influence on glioma risk.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS INC, 2020
Keywords
cancer, glioma, Mendelian randomization, risk
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-169385 (URN)10.1093/neuonc/noz209 (DOI)000518531900008 ()31665421 (PubMedID)
Available from: 2020-04-03 Created: 2020-04-03 Last updated: 2020-04-03Bibliographically approved
Rentoft, M., Svensson, D., Sjödin, A., Olason, P. I., Sjöström, O., Nylander, C., . . . Johansson, E. (2019). A geographically matched control population efficiently limits the number of candidate disease-causing variants in an unbiased whole-genome analysis. PLoS ONE, 14(3), Article ID e0213350.
Open this publication in new window or tab >>A geographically matched control population efficiently limits the number of candidate disease-causing variants in an unbiased whole-genome analysis
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2019 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 14, no 3, article id e0213350Article in journal (Refereed) Published
Abstract [en]

Whole-genome sequencing is a promising approach for human autosomal dominant disease studies. However, the vast number of genetic variants observed by this method constitutes a challenge when trying to identify the causal variants. This is often handled by restricting disease studies to the most damaging variants, e.g. those found in coding regions, and overlooking the remaining genetic variation. Such a biased approach explains in part why the genetic causes of many families with dominantly inherited diseases, in spite of being included in whole-genome sequencing studies, are left unsolved today. Here we explore the use of a geographically matched control population to minimize the number of candidate disease-causing variants without excluding variants based on assumptions on genomic position or functional predictions. To exemplify the benefit of the geographically matched control population we apply a typical disease variant filtering strategy in a family with an autosomal dominant form of colorectal cancer. With the use of the geographically matched control population we end up with 26 candidate variants genome wide. This is in contrast to the tens of thousands of candidates left when only making use of available public variant datasets. The effect of the local control population is dual, it (1) reduces the total number of candidate variants shared between affected individuals, and more importantly (2) increases the rate by which the number of candidate variants are reduced as additional affected family members are included in the filtering strategy. We demonstrate that the application of a geographically matched control population effectively limits the number of candidate disease-causing variants and may provide the means by which variants suitable for functional studies are identified genome wide.

Place, publisher, year, edition, pages
Public Library of Science, 2019
National Category
Medical Genetics
Identifiers
urn:nbn:se:umu:diva-158021 (URN)10.1371/journal.pone.0213350 (DOI)000462465800028 ()30917156 (PubMedID)
Funder
Knut and Alice Wallenberg Foundation, 2011.0042
Available from: 2019-04-10 Created: 2019-04-10 Last updated: 2019-04-12Bibliographically approved
Amirian, E. S., Ostrom, Q. T., Armstrong, G. N., Lai, R. K., Gu, X., Jacobs, D. I., . . . Bondy, M. L. (2019). Aspirin, NSAIDs, and Glioma Risk: Original Data from the Glioma International Case-Control Study and a Meta-analysis. Cancer Epidemiology, Biomarkers and Prevention, 28(3), 555-562
Open this publication in new window or tab >>Aspirin, NSAIDs, and Glioma Risk: Original Data from the Glioma International Case-Control Study and a Meta-analysis
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2019 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 28, no 3, p. 555-562Article in journal (Refereed) Published
Abstract [en]

Background: There have been few studies of sufficient size to address the relationship between glioma risk and the use of aspirin or NSAIDs, and results have been conflicting. The purpose of this study was to examine the associations between glioma and aspirin/NSAID use, and to aggregate these findings with prior published studies using meta-analysis.

Methods: The Glioma International Case-Control Study (GICC) consists of 4,533 glioma cases and 4,171 controls recruited from 2010 to 2013. Interviews were conducted using a standardized questionnaire to obtain information on aspirin/NSAID use. We examined history of regular use for ≥6 months and duration-response. Restricted maximum likelihood meta-regression models were used to aggregate site-specific estimates, and to combine GICC estimates with previously published studies.

Results: A history of daily aspirin use for ≥6 months was associated with a 38% lower glioma risk, compared with not having a history of daily use [adjusted meta-OR = 0.62; 95% confidence interval (CI), 0.54–0.70]. There was a significant duration-response trend (P = 1.67 × 10−17), with lower ORs for increasing duration of aspirin use. Duration-response trends were not observed for NSAID use. In the meta-analysis aggregating GICC data with five previous studies, there was a marginally significant association between use of aspirin and glioma (mOR = 0.84; 95% CI, 0.70–1.02), but no association for NSAID use.

Conclusions: Our study suggests that aspirin may be associated with a reduced risk of glioma.

Impact: These results imply that aspirin use may be associated with decreased glioma risk. Further research examining the association between aspirin use and glioma risk is warranted.

Place, publisher, year, edition, pages
American Association for Cancer Research (AACR), 2019
National Category
Occupational Health and Environmental Health Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-158972 (URN)10.1158/1055-9965.EPI-18-0702 (DOI)000465326400017 ()30482874 (PubMedID)
Funder
NIH (National Institute of Health), R01CA207972NIH (National Institute of Health), R01CA139020NIH (National Institute of Health), R01CA52689NIH (National Institute of Health), P50CA097257NIH (National Institute of Health), P30CA008748NIH (National Institute of Health), P30CA125123
Available from: 2019-05-27 Created: 2019-05-27 Last updated: 2020-03-24Bibliographically approved
Dahlin, A. M., Wibom, C., Andersson, U., Hougaard, D. M., Bybjerg-Grauholm, J., Deltour, I., . . . Melin, B. S. (2019). Genetic Variants in the 9p21.3 Locus Associated with Glioma Risk in Children, Adolescents, and Young Adults: A Case-Control Study. Cancer Epidemiology, Biomarkers and Prevention, 28(7), 1252-1258
Open this publication in new window or tab >>Genetic Variants in the 9p21.3 Locus Associated with Glioma Risk in Children, Adolescents, and Young Adults: A Case-Control Study
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2019 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 28, no 7, p. 1252-1258Article in journal (Refereed) Published
Abstract [en]

Background: Genome-wide association studies have identified germline genetic variants in 25 genetic loci that increase the risk of developing glioma in adulthood. It is not known if these variants increase the risk of developing glioma in children and adolescents and young adults (AYA). To date, no studies have performed genome-wide analyses to find novel genetic variants associated with glioma risk in children and AYA.

Methods: We investigated the association between 8,831,628 genetic variants and risk of glioma in 854 patients diagnosed up to the age of 29 years and 3,689 controls from Sweden and Denmark. Recruitment of patients and controls was population based. Genotyping was performed using Illumina BeadChips, and untyped variants were imputed with IMPUTE2. We selected 41 established adult glioma risk variants for detailed investigation.

Results: Three adult glioma risk variants, rs634537, rs2157719, and rs145929329, all mapping to the 9p21.3 (CDKN2B-AS1) locus, were associated with glioma risk in children and AYA. The strongest association was seen for rs634537 (odds ratioG = 1.21; 95% confidence interval = 1.09–1.35; P = 5.8 × 10−4). In genome-wide analysis, an association with risk was suggested for 129 genetic variants (P <1 × 10−5).

Conclusions: Carriers of risk alleles in the 9p21.3 locus have an increased risk of glioma throughout life. The results from genome-wide association analyses require validation in independent cohorts.

Impact: Our findings line up with existing evidence that some, although not all, established adult glioma risk variants are associated with risk of glioma in children and AYA. Validation of results from genome-wide analyses may reveal novel susceptibility loci for glioma in children and AYA.

Place, publisher, year, edition, pages
American Association for Cancer Research, 2019
National Category
Cancer and Oncology Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-162886 (URN)10.1158/1055-9965.EPI-18-1026 (DOI)000481682500019 ()31040135 (PubMedID)
Available from: 2019-09-04 Created: 2019-09-04 Last updated: 2019-09-04Bibliographically approved
Späth, F., Wibom, C., Krop, E., Izarra Santamaria, A., Johansson, A. S., Bergdahl, I., . . . Melin, B. S. (2019). Immune marker changes and risk of multiple myeloma: a nested case-control study using repeated prediagnostic blood samples. Haematologica, 104(12), 2456-2464
Open this publication in new window or tab >>Immune marker changes and risk of multiple myeloma: a nested case-control study using repeated prediagnostic blood samples
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2019 (English)In: Haematologica, ISSN 0390-6078, E-ISSN 1592-8721, Vol. 104, no 12, p. 2456-2464Article in journal (Refereed) Published
Abstract [en]

Biomarkers reliably predicting progression to multiple myeloma (MM) are lacking. Myeloma risk has been associated with low blood levels of monocyte chemotactic protein-3 (MCP-3), macrophage inflammatory protein-1 alpha (MIP-1 alpha), vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), fractalkine, and transforming growth factor-alpha (TGF-alpha). In this study, we aimed to replicate these findings and study the individual dynamics of each marker in a prospective longitudinal cohort, thereby examining their potential as markers of myeloma progression. For this purpose, we identified 65 myeloma cases and 65 matched cancer-free controls each with two donated blood samples within the Northern Sweden Health and Disease Study. The first and repeated samples from myeloma cases were donated at a median 13 and 4 years, respectively, before the myeloma was diagnosed. Known risk factors for progression were determined by protein-, and immunofixation electrophoresis, and free light chain assays. We observed lower levels of MCP-3, VEGF, FGF-2, and TGF-alpha in myeloma patients than in controls, consistent with previous data. We also observed that these markers decreased among future myeloma patients while remaining stable in controls. Decreasing trajectories were noted for TGF-alpha (P=2.5 x 10(-4)) indicating progression to MM. Investigating this, we found that low levels of TGF-alpha assessed at the time of the repeated sample were independently associated with risk of progression in a multivariable model (hazard ratio = 3.5; P=0.003). TGF-alpha can potentially improve early detection of MM.

Place, publisher, year, edition, pages
Ferrata Storti Foundation, 2019
Keywords
prospective longitudinal study, multiple myeloma risk, progression, marker trajectories
National Category
Clinical Medicine
Research subject
Oncology; Cancer Epidemiology
Identifiers
urn:nbn:se:umu:diva-156420 (URN)10.3324/haematol.2019.216895 (DOI)000499687600030 ()30948485 (PubMedID)2-s2.0-85075958352 (Scopus ID)
Funder
Swedish Research CouncilSwedish Cancer Society
Note

Originally included in thesis in manuscript form

Available from: 2019-02-14 Created: 2019-02-14 Last updated: 2020-01-07Bibliographically approved
Walker, E. V., Davis, F. G., Shaw, A., Louchini, R., Shack, L., Woods, R., . . . Bryant, H. (2019). Malignant primary brain and other central nervous system tumors diagnosed in Canada from 2009 to 2013. Neuro-Oncology, 21(3), 360-369
Open this publication in new window or tab >>Malignant primary brain and other central nervous system tumors diagnosed in Canada from 2009 to 2013
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2019 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 21, no 3, p. 360-369Article in journal (Refereed) Published
Abstract [en]

Background: We present a national surveillance report on malignant primary brain and other central nervous system (CNS) tumors diagnosed in the Canadian population in 2009–2013.

Methods: Patients were identified through the Canadian Cancer Registry, an administrative dataset that includes cancer incidence data from all provinces/territories in Canada. Tumor types were classified by site and histology using the definitions from the Central Brain Tumor Registry of the United States (CBTRUS). Incidence rates (IRs) and 95% confidence intervals (CIs) were calculated per 100000 person-years (py) and age-standardized to the 2011 Canadian population for comparisons within Canada and to the 2000 United States population for comparisons with the US.

Results: Overall, 12515 malignant brain and other CNS tumors were diagnosed in the Canadian population in 2009–2013 (IR: 8.71/100000 py; 95% CI: 8.56, 8.86); 7085 were among males (IR: 10.06/100000 py; 95% CI: 9.82, 10.29) and 5430 among females (IR: 7.41/100000 py; 95% CI: 7.22, 7.61). Of these, 12115 were classifiable according to histological subgroups defined by CBTRUS. The most common histology was glioblastoma (IR: 4.06/100000 py; 95% CI: 3.95, 4.16). Among those aged 0–19 years, 1130 malignant brain and CNS tumors were diagnosed in 2009–2013 (IR: 3.36/100000 py; 95% CI: 3.16, 3.56). The most common histology among the pediatric population was embryonal tumor (IR: 0.74/100000 py; 95% CI: 0.65, 0.84).

Conclusions: These data represent an initial detailed report on the frequency and distribution of primary malignant brain and other CNS tumors diagnosed in the Canadian population in 2009–2013. The reported distributions of tumor diagnoses by sex and age reflected expected patterns based on the literature from similar populations. A report incorporating data on nonmalignant primary brain tumors is forthcoming.

Place, publisher, year, edition, pages
Oxford University Press, 2019
Keywords
malignant brain neoplasms, malignant central nervous system neoplasms, neuro-oncology, Canadian rveillance report, epidemiology
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-157966 (URN)10.1093/neuonc/noy195 (DOI)000462164400009 ()30649461 (PubMedID)
Available from: 2019-04-16 Created: 2019-04-16 Last updated: 2019-04-16Bibliographically approved
Ostrom, Q. T., Armstrong, G., Amos, C. I., Bernstein, J. L., Claus, E. B., Eckel-Passow, J. E., . . . Bondy, M. L. (2019). Previously identified common glioma risk SNPs are associated with familial glioma. Paper presented at Annual Meeting of the American-Association-for-Cancer-Research (AACR), MAR 29-APR 03, 2019, Atlanta, GA. Cancer Research, 79(13), Article ID 4173.
Open this publication in new window or tab >>Previously identified common glioma risk SNPs are associated with familial glioma
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2019 (English)In: Cancer Research, ISSN 0008-5472, E-ISSN 1538-7445, Vol. 79, no 13, article id 4173Article in journal, Meeting abstract (Other academic) Published
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-165707 (URN)10.1158/1538-7445.AM2019-4173 (DOI)000488279404064 ()
Conference
Annual Meeting of the American-Association-for-Cancer-Research (AACR), MAR 29-APR 03, 2019, Atlanta, GA
Available from: 2019-12-06 Created: 2019-12-06 Last updated: 2019-12-06Bibliographically approved
Costas, L., Lujan-Barroso, L., Benavente, Y., Allen, N. E., Amiano, P., Ardanaz, E., . . . Casabonne, D. (2019). Reproductive Factors, Exogenous Hormone Use, and Risk of B-Cell Non-Hodgkin Lymphoma in a Cohort of Women From the European Prospective Investigation Into Cancer and Nutrition. American Journal of Epidemiology, 188(2), 274-281
Open this publication in new window or tab >>Reproductive Factors, Exogenous Hormone Use, and Risk of B-Cell Non-Hodgkin Lymphoma in a Cohort of Women From the European Prospective Investigation Into Cancer and Nutrition
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2019 (English)In: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 188, no 2, p. 274-281Article in journal (Refereed) Published
Abstract [en]

The role of hormonal factors in the etiology of lymphoid neoplasms remains unclear. Previous studies have yielded conflicting results, have lacked sufficient statistical power to assess many lymphoma subtypes, or have lacked detailed information on relevant exposures. Within the European Prospective Investigation Into Cancer and Nutrition cohort, we analyzed comprehensive data on reproductive factors and exogenous hormone use collected at baseline (1992-2000) among 343,458 women, including data on 1,427 incident cases of B-cell non-Hodgkin lymphoma (NHL) and its major subtypes identified after a mean follow-up period of 14 years (through 2015). We estimated hazard ratios and 95% confidence intervals using multivariable proportional hazards modeling. Overall, we observed no statistically significant associations between parity, age at first birth, breastfeeding, oral contraceptive use, or ever use of postmenopausal hormone therapy and risk of B-cell NHL or its subtypes. Women who had undergone surgical menopause had a 51% higher risk of B-cell NHL (based on 67 cases) than women with natural menopause (hazard ratio = 1.51, 95% confidence interval: 1.17, 1.94). Given that this result may have been due to chance, our results provide little support for the hypothesis that sex hormones play a role in lymphomagenesis.

Place, publisher, year, edition, pages
OXFORD UNIV PRESS INC, 2019
Keywords
cohort studies, hormone therapy, hysterectomy, lymphoma, menopause, menstrual factors, phorectomy, parity
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-157536 (URN)10.1093/aje/kwy259 (DOI)000460620100002 ()30481275 (PubMedID)
Available from: 2019-04-01 Created: 2019-04-01 Last updated: 2019-04-01Bibliographically approved
Sjöberg, R. L., Wu, W.-Y. Y., Dahlin, A. M., Tsavachidis, S., Bondy, M. L. & Melin, B. S. (2019). Role of monoamine-oxidase-A-gene variation in the development of glioblastoma in males: a case control study. Journal of Neuro-Oncology, 145(2), 287-294
Open this publication in new window or tab >>Role of monoamine-oxidase-A-gene variation in the development of glioblastoma in males: a case control study
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2019 (English)In: Journal of Neuro-Oncology, ISSN 0167-594X, E-ISSN 1573-7373, Vol. 145, no 2, p. 287-294Article in journal (Refereed) Published
Abstract [en]

Background: The Mono-amine oxidase-A (MAO-A) enzyme is involved in the degradation and regulation of catecholamines such as serotonin, dopamine, epinephrine and nor-epinephrine. Preclinical studies suggest that this enzyme may contribute to an environment favorable for growth of malignant glioma. The MAO-A gene is located on the X-chromosome and has at least one functional genetic polymorphism. The aim of the present study was to explore possible effects of MAO-A genotype on development of glioblastoma in males.

Methods: Genotypes for 437 glioma cases and 876 population-based controls from the Swedish Glioma International Case–Control study (GICC) were compared. We analyzed the germline DNA using the Illumina Oncoarray. We selected seven single nucleotide polymorphisms (SNPs) located in the MAO-A gene, and imputed genotypes based on data from the 1000 genomes project. We used 1579 male glioblastoma cases and 1875 controls comprising the whole GICC cohort for subsequent validation of findings.

Results: The rs144551722 SNP was a significant predictor of development of glioblastoma in males (p-value = 0.0056) but not in females even after correction for multiple testing. We conducted haplotype analysis to confirm an association between MAO-A gene and risk of glioblastoma (p-value = 0.016). We found similar results in the validation sample.

Conclusions: These results suggest the possibility of a role for the MAO-A enzyme and the MAO-A gene in the development of glioblastoma in males.

Place, publisher, year, edition, pages
Springer, 2019
Keywords
MAOA genetics glioblastoma males
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-166478 (URN)10.1007/s11060-019-03294-w (DOI)000496571900010 ()31556016 (PubMedID)
Funder
NIH (National Institute of Health), R01CA139020NIH (National Institute of Health), R01 CA139020
Available from: 2020-01-02 Created: 2020-01-02 Last updated: 2020-01-02Bibliographically approved
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