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Melin, Beatrice S.
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Publications (10 of 191) Show all publications
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 gliomarisk. Further research examining the association between aspirin use and glioma risk is warranted.

Place, publisher, year, edition, pages
AMER ASSOC CANCER RESEARCH, 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)
Available from: 2019-05-27 Created: 2019-05-27 Last updated: 2019-05-27Bibliographically 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. J., 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, Article ID haematol.2019.216895.
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, article id haematol.2019.216895Article in journal (Refereed) Epub ahead of print
Abstract [en]

Biomarkers reliably predicting progression to multiple myeloma are lacking. Myeloma risk has been associated with low blood levels of monocyte chemotactic protein 3, macrophage inflammatory protein 1 alpha, vascular endothelial growth factor, fibroblast growth factor 2, fractalkine, and transforming growth factor 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. Samples from myeloma cases were donated in median 13 and 4 years before myeloma diagnosis. Known risk factors of progression were determined by protein-, and immunofixation electrophoresis, and free light chain assays. We observed lower levels of monocyte chemotactic protein 3, vascular endothelial growth factor, fibroblast growth factor 2, fractalkine, and transforming growth factor alpha in myeloma patients than controls, consistent with previous data. We also observed that these markers decreased among future myeloma patients while remaining stable in controls. Decreasing trajectories were marked for transforming growth factor alpha (P = 2.5 x 10-4) indicating progression to multiple myeloma. Investigating this, we found that low levels of transforming growth factor alpha assessed at time of the repeated sample were independently associated with risk of progression in a multivariable model (hazard ratio = 3.5; P = 0.003). Transforming growth factor alpha can potentially improve early detection of multiple myeloma. .

Keywords
Immune marker change, Monoclonal Gammopathy of Undetermined Significance, Multiple Myeloma, Progression, prospective longitudinal study
Identifiers
urn:nbn:se:umu:diva-158803 (URN)10.3324/haematol.2019.216895 (DOI)30948485 (PubMedID)
Available from: 2019-05-09 Created: 2019-05-09 Last updated: 2019-05-10
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
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
Ostrom, Q. T., Coleman, W., Huang, W., Rubin, J. B., Lathia, J. D., Berens, M. E., . . . Buring, J. (2019). Sex-specific gene and pathway modeling of inherited glioma risk. Neuro-Oncology, 21(1), 71-82
Open this publication in new window or tab >>Sex-specific gene and pathway modeling of inherited glioma risk
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2019 (English)In: Neuro-Oncology, ISSN 1522-8517, E-ISSN 1523-5866, Vol. 21, no 1, p. 71-82Article in journal (Refereed) Published
Abstract [en]

Background To date, genome-wide association studies (GWAS) have identified 25 risk variants for glioma, explaining 30% of heritable risk. Most histologies occur with significantly higher incidence in males, and this difference is not explained by currently known risk factors. A previous GWAS identified sex-specific glioma risk variants, and this analysis aims to further elucidate risk variation by sex using gene- and pathway-based approaches. Methods Results from the Glioma International Case-Control Study were used as a testing set, and results from 3 GWAS were combined via meta-analysis and used as a validation set. Using summary statistics for nominally significant autosomal SNPs (P < 0.01 in a previous meta-analysis) and nominally significant X-chromosome SNPs (P < 0.01), 3 algorithms (Pascal, BimBam, and GATES) were used to generate gene scores, and Pascal was used to generate pathway scores. Results were considered statistically significant in the discovery set when P < 3.3 x 10(-6) and in the validation set when P < 0.001 in 2 of 3 algorithms. Results Twenty-five genes within 5 regions and 19 genes within 6 regions reached statistical significance in at least 2 of 3 algorithms in males and females, respectively. EGFR was significantly associated with all glioma and glioblastoma in males only and a female-specific association in TERT, all of which remained nominally significant after conditioning on known risk loci. There were nominal associations with the BioCarta telomeres pathway in both males and females. Conclusions These results provide additional evidence that there may be differences by sex in genetic risk for glioma. Additional analyses may further elucidate the biological processes through which this risk is conferred.

Place, publisher, year, edition, pages
Oxford University Press, 2019
National Category
Cancer and Oncology Medical Genetics
Identifiers
urn:nbn:se:umu:diva-158124 (URN)10.1093/neuonc/noy135 (DOI)000462586300009 ()30124908 (PubMedID)
Funder
Swedish Research CouncilSwedish Cancer SocietyNIH (National Institute of Health), R01CA139020NIH (National Institute of Health), R01CA52689NIH (National Institute of Health), P50CA097257NIH (National Institute of Health), R01CA126831
Available from: 2019-04-12 Created: 2019-04-12 Last updated: 2019-04-12Bibliographically approved
Papworth, K. E., Arroyo, V. M., Styring, E., Zaikova, O., Melin, B. S. & Lupo, P. J. (2019). Soft-tissue sarcoma in adolescents and young adults compared with older adults: a report among 5000 patients from the Scandinavian Sarcoma Group Central Register. Cancer
Open this publication in new window or tab >>Soft-tissue sarcoma in adolescents and young adults compared with older adults: a report among 5000 patients from the Scandinavian Sarcoma Group Central Register
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2019 (English)In: Cancer, ISSN 0008-543X, E-ISSN 1097-0142Article in journal (Refereed) Epub ahead of print
Abstract [en]

Background: In recent years, there has been growing awareness of the distinct characteristics of adolescents and young adults (AYA) diagnosed with cancer. Soft-tissue sarcoma (STS) accounts for approximately 1% of all cancers diagnosed in adults and 8% of cancers diagnosed in AYA. To the best of our knowledge, only a few sarcoma registers include data regarding histological subtype, age at diagnosis, and detailed clinical information. Therefore, little is known regarding clinical presentation and outcomes in AYA diagnosed with STS.

Methods: Using the Scandinavian Sarcoma Group Central Register, data were obtained regarding 4977 patients who were diagnosed with STS for the period between 1986 and 2011. AYA (those aged 18-39 years) were compared with older adults (OA; those aged 40-80 years) with respect to clinical presentation, treatment, and outcome.

Results: There were 868 AYA and 4109 OA. Overall and by STS subtype, there were significant differences noted between AYA and OA with regard to presentation, treatment, and survival. The distribution of STS subtypes was different between OA and AYA (eg, OA were more likely to be diagnosed with malignant fibrous histiocytoma compared with AYA [34% vs 16%; P < .001]). OA also were more likely to have tumors measuring >= 5 cm (68% vs 56%; P < .001) and a higher malignancy grade (75% vs 67%; P < .001). In the majority of STS subtypes AYA had significantly better overall survival and less disease recurrence compared with OA, but this finding was not true for those with malignant peripheral nerve sheath tumors.

Conclusions: There are several differences between AYA and OA with STS with regard to presentation, treatment, and survival, and such differences must be taken into consideration when designing clinical trials. Additional work also is needed to characterize the potential biological mechanisms underlying these differences.

Keywords
adolescents and young adults, clinical presentation, older adults, soft-tissue sarcoma, survival
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-162678 (URN)10.1002/cncr.32367 (DOI)000479645900001 ()31287163 (PubMedID)
Available from: 2019-09-02 Created: 2019-09-02 Last updated: 2019-09-02
Olsson, A., Bouaoun, L., Auvinen, A., Feychting, M., Johansen, C., Mathiesen, T., . . . Schüz, J. (2019). Survival of glioma patients in relation to mobile phone use in Denmark, Finland and Sweden. Journal of Neuro-Oncology, 141(1), 139-149
Open this publication in new window or tab >>Survival of glioma patients in relation to mobile phone use in Denmark, Finland and Sweden
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2019 (English)In: Journal of Neuro-Oncology, ISSN 0167-594X, E-ISSN 1573-7373, Vol. 141, no 1, p. 139-149Article in journal (Refereed) Published
Abstract [en]

Purpose: Gliomas are the most common cancer of the brain, with a poor prognosis in particular for glioblastoma. In 2014, a study suggested reduced survival in relation to latency of mobile phone use among glioblastoma patients. A joint epidemiological/experimental project to study effects of RF-EMF on tumor development and progression was established. The current analysis relates to the epidemiological part and addresses whether pre-diagnostic mobile phone use was associated with survival among glioma patients.

Methods: Glioma cases (n = 806) previously enrolled in a collaborative population-based case–control study in Denmark, Finland and Sweden were followed up for survival. Vital status, date of death, date of emigration, or date last known to be alive was obtained based on registry linkages with a unique personal ID in each country. Cox regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CI) stratified by country. Covariates investigated were sex, age, education, histology, treatment, anatomic location and marital status.

Results: No indication of reduced survival among glioblastoma patients was observed for various measures of mobile phone use (ever regular use, time since start of regular use, cumulative call time overall or in the last 12 months) relative to no or non-regular use. All significant associations suggested better survival for mobile phone users. Results were similar for high-grade and low-grade gliomas.

Conclusions: We found no evidence of reduced survival among glioma patients in relation to previous mobile phone use.

Place, publisher, year, edition, pages
Springer, 2019
Keywords
Glioma, Radiofrequency electromagnetic fields, Survival, Case-control studies, Mobile phones
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-156613 (URN)10.1007/s11060-018-03019-5 (DOI)000456968600014 ()30421160 (PubMedID)
Funder
Swedish Research CouncilSwedish Cancer Society
Available from: 2019-02-20 Created: 2019-02-20 Last updated: 2019-02-20Bibliographically approved
Andersson, U., Degerman, S., Dahlin, A. M., Wibom, C., Johansson, G., Bondy, M. L. & Melin, B. S. (2019). The association between longer relative leukocyte telomere length and risk of glioma is independent of the potentially confounding factors allergy, BMI, and smoking. Cancer Causes and Control, 30(2), 177-185
Open this publication in new window or tab >>The association between longer relative leukocyte telomere length and risk of glioma is independent of the potentially confounding factors allergy, BMI, and smoking
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2019 (English)In: Cancer Causes and Control, ISSN 0957-5243, E-ISSN 1573-7225, Vol. 30, no 2, p. 177-185Article in journal (Refereed) Published
Abstract [en]

Purpose: Previous studies have suggested an association between relative leukocyte telomere length (rLTL) and glioma risk. This association may be influenced by several factors, including allergies, BMI, and smoking. Previous studies have shown that individuals with asthma and allergy have shortened relative telomere length, and decreased risk of glioma. Though, the details and the interplay between rLTL, asthma and allergies, and glioma molecular phenotype is largely unknown. Methods: rLTL was measured by qPCR in a Swedish population-based glioma case–control cohort (421 cases and 671 controls). rLTL was related to glioma risk and health parameters associated with asthma and allergy, as well as molecular events in glioma including IDH1 mutation, 1p/19q co-deletion, and EGFR amplification. Results: Longer rLTL was associated with increased risk of glioma (OR = 1.16; 95% CI 1.02–1.31). Similar to previous reports, there was an inverse association between allergy and glioma risk. Specific, allergy symptoms including watery eyes was most strongly associated with glioma risk. High body mass index (BMI) a year prior diagnosis was significantly protective against glioma in our population. Adjusting for allergy, asthma, BMI, and smoking did not markedly change the association between longer rLTL and glioma risk. rLTL among cases was not associated with IDH1 mutation, 1p/19q co-deletion, or EGFR amplification, after adjusting for age at diagnosis and sex. Conclusions: In this Swedish glioma case–control cohort, we identified that long rLTL increases the risk of glioma, an association not confounded by allergy, BMI, or smoking. This highlights the complex interplay of the immune system, rLTL and cancer risk.

Place, publisher, year, edition, pages
Springer, 2019
Keywords
Glioma, Relative leukocyte telomere length (rLTL), Allergy, BMI, Smoking, IDH1, 1p/19q, EGFR
National Category
Cancer and Oncology Public Health, Global Health, Social Medicine and Epidemiology
Identifiers
urn:nbn:se:umu:diva-157597 (URN)10.1007/s10552-018-1120-2 (DOI)000459153800007 ()30560391 (PubMedID)
Available from: 2019-03-28 Created: 2019-03-28 Last updated: 2019-03-28Bibliographically approved
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