Estimates of lung and pancreatic cancer survival in Sweden with and without inclusion of death certificate initiated (DCI) cases.

INTRODUCTION: International differences in cancer incidence and survival may partly reflect differences in cancer registration practices. As opposed to most other National Cancer Registries, Death Certificate Initiated (DCI) cases are not included in the Swedish Cancer Register. We characterized cases not reported to the Swedish Cancer Register and assessed the impact of inclusion of DCI cases on the completeness and estimates of one-year lung and pancreatic cancer survival. METHODS: We used information in the Swedish Cause of Death Register to identify individuals in two Health Care Regions (West and Uppsala Örebro) with lung or pancreatic cancer as cause of death in 2013. These records were cross-linked to the Cancer Register to identify individuals without a corresponding cancer registration, i.e. Death Certificate Notified (DCN) cases. DCN cases were cross-linked to the Patient Register to retrieve hospital discharge information to confirm the diagnosis. In a separate step, trace-back of DCN cases was performed to access medical records to validate the diagnosis. RESULTS: Following validity checks, an estimated 16% and 34% of individuals with a diagnosis of lung or pancreatic cancer, respectively, had not been reported to the SCR. Non-reported patients were older and had a considerable poorer survival than those included in the SCR. Inclusion of DCI cases decreased one-year lung cancer overall survival from 45% to 41%. The corresponding decrease for pancreatic cancer was five percentage points, from 29% to 24%. CONCLUSIONS: Lung and pancreatic cancers are underreported to the SCR yielding too low incidence rates and upward biased survival estimates. We conclude that implementation of systematic death certificate processing with trace-back is feasible also within the Swedish system with regionalized cancer reporting. Verifying registrability by use of information in the Patient Register provided a good approximation of "corrected" survival estimates based on chart review.

Socioeconomic factors and penile cancer risk and mortality; a population-based study.

OBJECTIVE: To investigate possible associations between socioeconomic status (SES) and penile cancer risk, stage at diagnosis, and mortality. PATIENTS/SUBJECTS AND METHODS: A population-based register study including men in Sweden diagnosed with penile cancer between 2000 and 2012 (1676 men) and randomly chosen controls (9872 men). Data were retrieved from the National Penile Cancer Register (NPECR) and several other population-based healthcare and sociodemographic registers. Educational level, disposable income, marital status, and number of individuals in the household, were assessed as indicators of SES. The risk of penile cancer and penile cancer death in relation to SES were estimated using logistic regression and proportional hazards models, respectively. Cumulative cause-specific mortality (CSM) estimates by SES were calculated using the Kaplan-Meier method. RESULTS: A low educational level and low disposable income were associated with an increased risk of invasive penile cancer. Furthermore, low educational level was associated with more advanced primary tumour stage. Divorced and never married men had a generally increased risk of penile cancer and were diagnosed with more advanced primary tumour stages. However, neither educational level nor marital status was associated with lymph node or distant metastases. Also, men in single-person households had an increased risk of both non-invasive and invasive disease. In men with invasive penile cancer, there were no significant associations of indicators of SES and CSM. CONCLUSIONS: Low educational level, low disposable income, being divorced or never married, and living in a single-person household, all increase the risk of advanced stage penile cancer, but not lymph node or distant metastases. The assessed indicators of SES did not influence penile CSM. In conclusion, our findings indicates that SES influences the risk and stage of penile cancer, but not survival.

Evaluation of data quality in the National Prostate Cancer Register of Sweden.

BACKGROUND: Data in cancer quality registers are increasingly used for quality assurance, benchmarking, and research. MATERIALS AND METHODS: Data in the National Prostate Cancer Register (NPCR) of Sweden were evaluated for completeness, timeliness, comparability and validity. Completeness and timeliness were assessed by cross-linkage to the Swedish Cancer Register, comparability was examined by comparing registration routines in NPCR with national and international guidelines, and validity was assessed by re-abstraction of data from medical charts for 731 men diagnosed with prostate cancer (Pca) in 2009. Furthermore, data on treatment were validated by record linkage to the Swedish Patient Register and The Prescribed Drug Register. RESULTS: NPCR captured 98% of Pca cases in the Cancer Register and the mean value for completeness of the 48 evaluated variables was 90% (range 64-100%). Timeliness increased substantially from 2008 to 2012 with 95% of cases reported within 12 months after diagnosis in 2012. NPCR complied with national and international coding routines. Overall, the agreement between original data and re-abstracted data from 731 charts was high. For example, the correlation between original and re-abstracted data was 1.00 for date of surgery, and 0.97 for serum levels of prostate specific antigen and exact agreement was 97% for Gleason score at biopsy, 83% for clinical local T stage and more than 95% of the androgen deprivation therapies registered in NPCR had a corresponding filled prescription. CONCLUSION: Record linkages with other data sources and re-abstraction of data showed that data quality in NPCR is high.

Serum glucose and fructosamine in relation to risk of cancer.

BACKGROUND: Impaired glucose metabolism has been linked with increased cancer risk, but the association between serum glucose and cancer risk remains unclear. We used repeated measurements of glucose and fructosamine to get more insight into the association between the glucose metabolism and risk of cancer. METHODS: We selected 11,998 persons (>20 years old) with four prospectively collected serum glucose and fructosamine measurements from the Apolipoprotein Mortality Risk (AMORIS) study. Multivariate Cox proportional hazards regression was used to assess standardized log of overall mean glucose and fructosamine in relation to cancer risk. Similar analyses were performed for tertiles of glucose and fructosamine and for different types of cancer. RESULTS: A positive trend was observed between standardized log overall mean glucose and overall cancer risk (HR= 1.08; 95% CI: 1.02-1.14). Including standardized log fructosamine in the model resulted in a stronger association between glucose and cancer risk and aninverse association between fructosamine and cancer risk (HR = 1.17; 95% CI: 1.08-1.26 and HR: 0.89; 95% CI: 0.82-0.96, respectively). Cancer risks were highest among those in the highest tertile of glucose and lowest tertile of fructosamine. Similar findings were observed for prostate, lung, and colorectal cancer while none observed for breast cancer. CONCLUSION: The contrasting effect between glucose, fructosamine, and cancer risk suggests the existence of distinct groups among those with impaired glucose metabolism, resulting in different cancer risks based on individual metabolic profiles. Further studies are needed to clarify whether glucose is a proxy of other lifestyle-related or metabolic factors.

Cohort Profile: the National Prostate Cancer Register of Sweden and Prostate Cancer data Base Sweden 2.0.

In 1987, the first Regional Prostate Cancer Register was set up in the South-East health-care region of Sweden. Other health-care regions joined and since 1998 virtually all prostate cancer (PCa) cases are registered in the National Prostate Cancer Register (NPCR) of Sweden to provide data for quality assurance, bench marking and clinical research. NPCR includes data on tumour stage, Gleason score, serum level of prostate-specific antigen (PSA) and primary treatment. In 2008, the NPCR was linked to a number of other population-based registers by use of the personal identity number. This database named Prostate Cancer data Base Sweden (PCBaSe) has now been extended with more cases, longer follow-up and a selection of two control series of men free of PCa at the time of sampling, as well as information on brothers of men diagnosed with PCa, resulting in PCBaSe 2.0. This extension allows for studies with case-control, cohort or longitudinal case-only design on aetiological factors, pharmaceutical prescriptions and assessment of long-term outcomes. The NPCR covers >96% of all incident PCa cases registered by the Swedish Cancer Register, which has an underreporting of <3.7%. The NPCR is used to assess trends in incidence, treatment and outcome of men with PCa. Since the national registers linked to PCBaSe are complete, studies from PCBaSe 2.0 are truly population based.

Impact of comorbidity on management and mortality in women diagnosed with breast cancer.

To investigate associations between comorbidity burden, management, and mortality in women with breast cancer. A total of 42,646 women diagnosed with breast cancer between 1992 and 2008 were identified in two Clinical Quality Registers in Central Sweden. Breast cancer-specific, conditional breast cancer, competing-cause and all-cause mortality were estimated in relation to comorbidity burden assessed by the Charlson comorbidity index. All analyses were stratified by stage at diagnosis using competing risk analyses, and all-cause mortality was estimated as a function of follow-up time. Following adjustment for age and calendar period, breast conserving surgery was significantly less likely to be offered to women with severe comorbidity (OR 0.63; 95 % CI 0.58-0.69). Similarly, the proportion treated with radiotherapy, tamoxifen, or chemotherapy was lower in women with severe compared to those with no comorbidity. In women with early stage disease, breast cancer-specific mortality was higher among patients with severe comorbidity (sHR 1.47; 95 % CI 1.11-1.94). In all stages of breast cancer, conditional breast cancer and competing-cause mortality were elevated in women with severe comorbidity. For all stages, the relative risk of all-cause mortality between women with severe versus no comorbidity varied by time since diagnosis, and was most pronounced at early follow-up. Comorbidity affects treatment decisions and mortality. In women with early stage breast cancer, severe comorbidity was associated not only with conditional breast cancer, competing-cause and all-cause mortality, but also breast cancer-specific mortality. The observed differences in breast cancer-specific mortality may be due to less extensive treatment, impaired tumor defense and differences in general health status and lifestyle factors.

Lipid profiles and the risk of endometrial cancer in the Swedish AMORIS study.

BACKGROUND: While the association between obesity and endometrial cancer (EC) is well established, the underlying mechanisms require further study. We assessed possible links between lipid profiles and EC risk, while also taking into account BMI, parity, and menopausal status at baseline. METHODS: Using the information available from the Swedish Apolipoprotein MOrtality RISk (AMORIS) study we created a cohort of 225,432 women with baseline values for glucose, triglycerides (TG), and total cholesterol (TC). Two subgroups of 31,792 and 26,317 had, in addition, baseline measurements of HDL, LDL, apolipoprotein A-I and apoB and BMI, respectively. We used Multivariate Cox proportional hazards models to analyze quartiles and dichotomized values of these lipid components for a link to EC risk. RESULTS: During mean follow-up of 12 years (SD: 4.15), 1,144 persons developed endometrial cancer. A statistically significant association was found between TG and EC risk when using both quartiles and a clinical cut-off (Hazard Ratio (HR): 1.10 (95%CI: 0.88-1.37), 1.34 (1.09-1.63), and 1.57 (1.28-1.92)) for the 2(nd), 3(rd), and 4(th) quartile, compared to the 1(st), with P-value for trend: <0.001). The association remained after exclusion of the first three years of follow-up. Also total cholesterol and TG/HDL ratio were positively associated with EC risk, but no link was found for the other lipid components studied. CONCLUSION: This detailed analysis of lipid components showed a consistent relation between TG levels and EC risk. Future research should continue to analyze the metabolic pathway and its relation to EC risk, as a pathway to further understand the relation of obesity and disease.

Lipid profiles and risk of breast and ovarian cancer in the Swedish AMORIS study.

BACKGROUND: Obesity is a risk factor for breast and ovarian cancer; the mechanisms of action are not completely understood. Perturbed lipid metabolism often accompanies obesity; we therefore ascertained the associations between lipid components and breast and ovarian cancer risk in a prospective cohort study. METHODS: A total of 234,494 women with baseline measurements of triglycerides and total cholesterol and glucose were selected from the AMORIS database.A total of 27,394 had measurements of high-density lipoprotein, low-density lipoprotein, apolipoprotein (Apo) B, and A-I. Associations between quartiles and dichotomized values of lipid components and breast and ovarian cancer risk were analyzed using Cox proportional hazard models. RESULTS: We identified 6,105 women diagnosed with breast cancer and 808 women diagnosed with ovarian cancer. A weak trend was observed between triglycerides and breast cancer (HR, 1.01, 95% Confidence Interval, 0.94-1.09; 0.93 (0.86-1.00) 0.91 (0.84-0.99), second, third, and fourth quartiles; P = 0.01). No other associations between lipid components and risk of breast cancer or ovarian cancer showed statistical significance. CONCLUSIONS: A weak protective association was found between levels of triglycerides and risk of breast cancer. IMPACT: An analysis including information on tumour characteristics of ovarian cancer and breast cancer may provide more insight in possible links between lipid metabolism and the risk of these cancers.

Adherence and discontinuation of adjuvant hormonal therapy in breast cancer patients: a population-based study.

Adherence to long-term pharmacological treatment for chronic conditions is often less than optimal. Till date, a limited number of population-based studies have assessed adherence to adjuvant hormonal therapy in breast cancer, a therapy with proven benefits in terms of reductions of recurrence and mortality. We aimed to examine rates of adherence and early discontinuation in Sweden where prescribed medications are subsidized for all residents and made available at reduced out-of-pocket costs. Individual-level data were obtained from Regional Clinical Quality Breast Cancer Registers, the Swedish Prescribed Drug Register, and several other population-based registers. Multivariate logistic regression was used to analyze factors associated with adherence to prescribed medication for a period of 3 years. Between January 1 and December 31, 2005, 1,741 patients in central Sweden were identified with estrogen receptor positive breast cancer, and at least one prescription dispensation of either tamoxifen or an aromatase inhibitor. Of these women, 1,193 (69%) were fully adherent to therapy for 3 years (medication possession ratio of 80% or higher and a maximum of 180 days between refills). During the 3-year follow-up, 215 women (12%) had prematurely discontinued therapy. Adherence was positively associated with younger age, large tumor size, being married, and being born in the Nordic countries, while no clear association was observed with education or income. During the 3 years of follow-up, 31% of women were non-adherent to therapy. Further efforts must be undertaken to promote adherence over the entire recommended treatment period.

Pancreatic cancer; reporting and long-term survival in Sweden.

BACKGROUND: The overall completeness of the Swedish Cancer Register is high, although underreporting for certain sites must be acknowledged. The aims of the present study were twofold. Firstly to assess the completeness of reporting of pancreatic cancer to the Swedish Cancer Register, and secondly to identify and characterise long-term survivors based on information from two separate population-based register resources. MATERIAL AND METHODS: To assess the completeness of the Cancer Register, pancreatic cancer cases registered in the National Patient Register between 1987 and 1999 were compared to cases reported to the Cancer Register. For estimations of long-term survival, the study population was restricted to 4321 cases identified both in the Cancer Register and the Patient Register with a histopathologically confirmed diagnosis of pancreatic ductal adenocarcinoma. A complete follow-up of survival in this group was performed till December 31, 2004. RESULTS: There was a considerable underreporting of pancreatic cancer to the Cancer Register. During the period under study, a total of 19 745 patients were identified with a diagnosis of pancreatic cancer. Of these, only 73% had been reported to the Cancer Register. The underreporting increased markedly with age at diagnosis and was more pronounced during the second period under study. Only 2.8% of patients with a histopathologically confirmed diagnosis of pancreatic ductal adenocarcinoma survived five years or longer. The likelihood of long-term survival was strongly associated with younger age and surgery. Pancreatic resection was reported in 20.4% of all patients. Median survival among those operated on was 12 months compared to 4.6 months in all patients. CONCLUSIONS: Underreporting of pancreatic cancer to the Swedish Cancer Register was pronounced and increased with older age. Less than 3% of patients with a record of pancreatic cancer both in the Cancer Register and the Patient Register survived five years or longer.

Impaired glucose metabolism and diabetes and the risk of breast, endometrial, and ovarian cancer.

BACKGROUND: Epidemiological evidence indicates that individuals with type 2 diabetes are at an increased risk of cancer. Elevated glucose levels, below the diagnostic threshold for diabetes, have also been suggested to be associated with increased cancer risks. METHODS: We investigated possible associations between glucose levels and the risk of breast, endometrial, and ovarian cancer in a cohort of more than 230,000 women, for which information on outcome and potential confounders was obtained by record linkage to population-based registers. RESULTS: Diabetes was associated with an increased risk of postmenopausal breast cancer (HR = 1.22, 95% CI 1.04-1.43). An indication of a slightly elevated breast cancer risk was also found in postmenopausal women with impaired glucose metabolism (HR = 1.11, 95% CI 0.96-1.28). Diabetes (HR = 1.46, 95% CI 1.09-1.96) and impaired glucose metabolism (HR = 1.41, 95% CI 1.08-1.85) were associated with an increased risk of endometrial cancer. No associations were found between glucose levels and ovarian cancer risk. Following adjustment for BMI, estimates were attenuated for endometrial cancer, while point estimates for breast and ovarian cancer remained essentially unchanged. CONCLUSIONS: Our results indicate that glucose levels below the diagnostic threshold for diabetes modify the risk not only of endometrial cancer but possibly also of postmenopausal breast cancer.

Breast cancer, sickness absence, income and marital status. A study on life situation 1 year prior diagnosis compared to 3 and 5 years after diagnosis.

BACKGROUND: Improved cancer survival poses important questions about future life conditions of the survivor. We examined the possible influence of a breast cancer diagnosis on subsequent working and marital status, sickness absence and income. MATERIALS: We conducted a matched cohort study including 4,761 women 40-59 years of age and registered with primary breast cancer in a Swedish population-based clinical register during 1993-2003, and 2,3805 women without breast cancer. Information on socioeconomic standing was obtained from a social database 1 year prior and 3 and 5 years following the diagnosis. In Conditional Poisson Regression models, risk ratios (RRs) and 95% confidence intervals (CIs) were estimated to assess the impact of a breast cancer diagnosis. FINDINGS: Three years after diagnosis, women who had had breast cancer more often had received sickness benefits (RR = 1.49, 95% CI 1.40-1.58) or disability pension (RR = 1.47, 95% CI 1.37-1.58) than had women without breast cancer. We found no effect on income (RR = 0.99), welfare payments (RR = 0.98), or marital status (RR = 1.02). A higher use of sickness benefits and disability pension was evident in all stages of the disease, although the difference in use of sickness benefits decreased after 5 years, whereas the difference in disability pension increased. For woman with early stage breast cancer, the sickness absence was higher following diagnosis among those with low education, who had undergone mastectomy, and had received chemo- or hormonal therapy. Neither tumour size nor presence of lymph nodes metastasis was associated with sickness absence after adjustment for treatment. INTERPRETATION: Even in early stage breast cancer, a diagnosis negatively influences working capacity both 3 and 5 years after diagnosis, and it seems that the type of treatment received had the largest impact. A greater focus needs to be put on rehabilitation of breast cancer patients, work-place adaptations and research on long-term sequelae of treatment.

Non-participant characteristics and the association between socioeconomic factors and brain tumour risk.

BACKGROUND: The aim of the study was to identify demographic and socioeconomic characteristics of participants and non-participants in a Swedish population-based case-control study on brain tumours and to analyse the association between socioeconomic factors and glioma and meningioma risk. METHODS: Record linkage was made to an official register to gather information on socioeconomic status, income, education and demography for all participating and non-participating cases and controls. RESULTS: 494 glioma cases, 321 meningioma cases and 955 controls were eligible and 74%, 85% and 70%, respectively, participated. Working status and income level were positively associated with participation among cases and controls. Among both cases and controls, being married, and having a high education were also associated with participation. Having a family income level in the highest quartile was associated with an increased glioma risk (OR 1.5, 95% CI 1.1 to 2.1). This risk increase diminished when only participating individuals were included in the analysis. Socioeconomic factors were not associated with meningioma risk. CONCLUSIONS: Non-participation, related to socioeconomic factors, is a potential source of bias in case-control studies that should be acknowledged; however, the effect was not large in the present study due to the fact that the level of participation was comparable between cases and controls and participation was similarly influenced by socioeconomic factors among cases and controls. The association between a high income level and an increased glioma risk and possible underlying factors needs to be explored further.

Interaction between 5 genetic variants and allergy in glioma risk.

The etiology of glioma is barely known. Epidemiologic studies have provided evidence for an inverse relation between glioma risk and allergic disease. Genome-wide association data have identified common genetic variants at 5p15.33 (rs2736100, TERT), 8q24.21 (rs4295627, CCDC26), 9p21.3 (rs4977756, CDKN2A-CDKN2B), 11q23.3 (rs498872, PHLDB1), and 20q13.33 (rs6010620, RTEL1) as determinants of glioma risk. The authors investigated whether there is interaction between the effects of allergy and these 5 variants on glioma risk. Data from 5 case-control studies carried out in Denmark, Finland, Sweden, and the United Kingdom (2000-2004) were used, totaling 1,029 cases and 1,668 controls. Risk was inversely associated with asthma, hay fever, eczema, and "any allergy," significantly for each factor except asthma, and was significantly positively associated with number of risk alleles for each of the 5 single nucleotide polymorphisms. There was interaction between asthma and rs498872 (greater protective effect of asthma with increasing number of risk alleles; per-allele interaction odds ratio (OR) = 0.65, P = 0.041), between "any allergy" and rs4977756 (smaller protective effect; interaction OR = 1.27, P = 0.047), and between "any allergy" and rs6010620 (greater protective effect; interaction OR = 0.70, P = 0.017). Case-only analyses provided further support for atopy interactions for rs4977756 and rs498872. This study provides evidence for possible gene-environment interactions in glioma development.

Reductions in use of hormone replacement therapy: effects on Swedish breast cancer incidence trends only seen after several years.

Studies from Western countries have found evidence of a recent decline in breast cancer incidence rates in postmenopausal women, findings which have been hypothesized to reflect a reduced use of hormonal replacement therapy (HRT). We examined breast cancer incidence trends in Sweden between 1997 and 2007, a period characterized by a drop in the use of HRT. Incidence trends were assessed using data from three population-based Regional Clinical Registries on breast cancer covering 2/3 of the Swedish population. Information on HRT sales was obtained from national pharmacy data. The prevalence of HRT use in age group 50-59 years decreased from a peak of 36% in 1999 to 27% in 2002 and further to 9% in 2007. Incidence rates of breast cancer in women 50 years and older increased between 1997 and 2003. A significant decrease in incidence between 2003 and 2007 was confined to women 50-59 years of age, the group in which the prevalence of HRT use has been highest and the decrease in use most pronounced. As opposed to the immediate effects reported from the United States and other regions, there was a time lag between the drop in HRT use and clear reductions in breast cancer incidence. This may reflect between country differences with regard to types of HRT used, and the rate, magnitude and pattern of change in use. The present findings give further support to the notion that HRT use is a driver of breast cancer incidence trends on the population level.

Reproductive factors and risk of meningioma and glioma.

Female sex hormones have previously been suggested as possible risk factors for brain tumors, but published studies have reported conflicting results. We conducted a population-based case-control study of glioma (n=626) and meningioma (n=906) cases and randomly selected controls stratified on age and geographic region (n=1,774) in Denmark, Finland, Norway, Sweden, and the United Kingdom. Unconditional logistic regression was used to estimate odds ratios (OR) for glioma and meningioma in relation to reproductive factors. A decreased glioma risk was associated with ever-pregnancy compared with never-pregnancy [OR, 0.8; 95% confidence interval (95% CI), 0.6-1.0]. Meningioma risk among women ages <50 years was increased in relation to number of pregnancies leading to a live birth (OR, 1.8; 95% CI: 1.1-2.8 for giving birth to 3 children compared with nulliparous women; P(trend) among parous women=0.01). This relation was not found for older women. Breast-feeding among parous women increased the glioma risk (OR, 2.2; 95% CI, 1.3-3.9 for breast-feeding 36 months or more compared with breast-feeding 3 months or less). Menopausal status and age at menopause were not associated with meningioma or glioma risk. Our findings imply that reproductive hormones may influence the occurrence of meningioma and glioma.

An international case-control study of interleukin-4Ralpha, interleukin-13, and cyclooxygenase-2 polymorphisms and glioblastoma risk.

Previous studies found that allergies are inversely related to risk of glioma. In an earlier publication, using data from a Swedish case-control study, Schwartzbaum et al. report an inverse relation between risk of glioblastoma and four single nucleotide polymorphisms (SNP) on two genes [interleukin (IL)-4Ralpha, IL-13] that are associated with allergies. In addition, recent studies suggest that IL-4 and IL-13 induce cyclooxygenase-2 (COX-2) to resolve brain inflammation. To see whether previous Swedish results (110 cases, 430 controls) would be replicated, we estimated the association between glioblastoma and two IL-4Ralpha (rs1805015, rs1801275) and two IL-13 (rs20541, rs1800925) SNPs and their haplotypes and one COX-2 SNP (-765GC) using additional English, Danish, and Finnish data (217 cases, 1,171 controls). Among general population controls, we evaluated associations between these haplotypes, the COX-2 SNP, and self-reported allergies. Our data did not support our original observations relating individual IL-4Ralpha, IL-13, or COX-2 SNPs to glioblastoma risk. However, the T-G IL-4Ralpha haplotype was associated with glioblastoma risk (odds ratio, 2.26; 95% confidence interval, 1.13-4.52) and there was a suggestion of an inverse relation between this haplotype and hayfever prevalence among controls (odds ratio, 0.38; 95% confidence interval, 0.14-1.03). The lack of support for a link between four IL-4Ralpha and IL-13 SNPs and glioblastoma may reflect the absence of associations or may result from uncontrolled confounding by haplotypes related both to those that we examined and glioblastoma. Nonetheless, the association between the T-G IL-4Ralpha haplotype and glioblastoma risk may indicate a role of immune factors in glioblastoma development.

Allergic conditions and brain tumor risk.

An inverse association between allergic conditions and glioma risk has been reported previously. In this large population-based case-control study, the authors identified cases diagnosed with glioma or meningioma in Denmark, Norway, Finland, Sweden, and southeast England between 2000 and 2004. Detailed information on self-reported physician-diagnosed allergic conditions was collected from 1,527 glioma cases, 1,210 meningioma cases, and 3,309 randomly selected controls. Logistic regression showed an odds ratio of 0.70 (95% confidence interval: 0.61, 0.80) for glioma associated with a diagnosis of any of asthma, hay fever, eczema, or other type of allergy. The risk estimates for glioma were around 0.65 for each allergic condition (asthma, eczema, hay fever, and food allergy), and the 95% confidence intervals were equally consistent, at around 0.55, 0.80. The reduced risks of glioma related to eczema, hay fever, and allergy overall, but not asthma, were confined to current rather than past conditions. Meningioma risk was not associated with allergic conditions, except for eczema (odds ratio = 0.74, 95% confidence interval: 0.60, 0.91). Our results show a reduced risk for glioma associated primarily with current allergic conditions. If this is etiologic, it has implications for the understanding of how allergic conditions might reduce the tumor risk.

Risk of brain tumors associated with exposure to exogenous female sex hormones.

The etiology of brain tumors is largely unknown. Prior observations have implicated gender-specific hormones in the pathogenesis of these tumors. In a population-based case-control study, the authors identified all women aged 20-69 years who had been diagnosed with meningioma or glioma during 2000-2002 in four regions of Sweden. Controls were randomly selected from the study base. Detailed information on hormone usage, including use of hormonal contraceptives, hormonal treatment for gynecologic problems, and hormone replacement therapy, was collected from 178 meningioma cases, 115 glioma cases, and 323 controls. Data were analyzed using unconditional logistic regression, adjusting for age, residential area, education, and parity. An increased relative risk of meningioma was found among postmenopausal women for ever use of hormone replacement therapy, with an odds ratio of 1.7 (95% confidence interval: 1.0, 2.8). Women who had used long-acting hormonal contraceptives (subdermal implants, injections, or hormonal intrauterine devices) had an increased risk of meningioma; the odds ratio for at least 10 years of use was 2.7 (95% confidence interval: 0.9, 7.5). Hormone usage was not associated with glioma risk in this study. The findings suggest that the use of female sex steroids may increase the risk of meningioma.