The aim of the present study was to investigate if use of antidepressants is related to the risk of developing lower (WHO grade 2-3) and higher grade (WHO grade 4) glioma. A registry-based case-control study was performed using 1283 glioma cases and 6400 age-, sex- and geographically matched controls, diagnosed in Sweden 2009-2013. Conditional logistic regression was used to analyze whether Selective Serotonin Reuptake Inhibitors (SSRIs) or non-SSRIs were associated with the risk of developing lower- or higher-grade glioma in the study population. Our results show that use of antidepressant medication was not associated with the risk of developing glioma. We also performed a meta-analysis in which the dataset from the present study was combined with results from two previous epidemiological studies to answer the same questions. The meta-analysis showed a modest risk reduction of developing glioma in relation to antidepressant treatment (OR 0.90 [95% CI 0.83-0.97]), when all glioma subgroups and all forms of antidepressant medications were combined. In conclusion, it remains possible that antidepressants may have common monoaminergic mechanism(s) that reduce the risk of developing glioma.

We performed the next-generation sequencing (NGS) analysis of a rare grade 1 brain meningioma (angiomatous type) and a common grade 1 spinal meningioma (psammomatous type) and compared their mutation profiling. The data were analysed using the Ion Reporter 5.16 programme (Thermo Fisher Scientific, Waltham, MA). Sequencing analysis identified 10 novel variants and two previously reported variants that were common between these two tumours. Nine variants were missense, which included an insertion in EGFR c.1819_1820insCA, causing frameshifting, and a single nucleotide deletion in HRAS and HNF1A genes, causing frameshifting in these genes. These were common variants identified for both tumours. Also, 10 synonymous variants and 10 intronic variants were common between these two tumours. In intronic variants, two were splice site_5\' variants (acceptor site variants). Typical of the angiomatous type tumour, there were 11 novel and six previously reported variants that were not found in the psammomatous tumour; three variants were synonymous, 11 were missense mutations, and three were deletions causing frameshifting. The deletion variants were in the SMARCB1, CDH1, and KDR genes. In contrast, eight novel and five previously reported variants were found in the psammomatous meningioma tumour. In this tumour, two variants were synonymous: a deletion causing a frameshifting in [(c.3920delT; p. (Ile1307fs)], and a two-base pair insertion and deletion (INDEL) [(c.3986_3987delACinsGT; p. (His1329Arg)] both in the APC gene were also found. Among our findings, we have identified that ALK, VHL, CTNNB1, EGFR, ERBB4, PDGFRA, KDR, SMO, ABL1, HRAS, ATM, HNF1A, FLT3, and RB1 mutations are common for psammomatous meningioma and angiomatous tumours. Variants typical for angiomatous (brain) meningioma are PIK3CA, KIT, PTPN11, CDH1, SMAD4, and SMARCB1; the variants typical for psammomatous meningioma are APC, FGFR2, HNF1A, STK11, and JAK3. The RET splice variant (c.1880-2A>C) found in both meningioma tumours is reported (rs193922699) as likely pathogenic in the Single Nucleotide Polymorphism Database (dbSNP). All missense variants detected in these two meningiomas are found in the cancer-driver genes. The eight variants we found in genes such as EGFR, PDGFRA, SMO, FLT3, PIK3CA, PTPN11, CDH1, and RB1 are glioma-driver genes. We did not find any mutations in genes such as BRAF, IDH1, CDKN2A, PTEN, and TP53, which are also listed as cancer-driver genes in gliomas. Mutation profiling utilising NGS technology in meningiomas could help in the accurate diagnosis and classification of these tumours and also in developing more effective treatments.

BACKGROUND: Despite considerable research effort, causes of brain cancer are largely unknown. Male brain cancer predominance and reduced brain cancer risk with increasing parity among women, however, support a favourable role of pregnancy. We set out to determine whether fetal-origin microchimerism, namely the presence and long-term persistence of fetal cells, likely obtained via natural trafficking across the placenta during pregnancy, associates with reduced risk of brain cancer in women.
METHODS: Using a case-cohort design, we sampled 505 middle-aged women randomly at baseline in the Diet, Cancer and Health cohort (controls), and 73 women with incident brain cancer diagnosed during follow-up in the Danish Cancer Registry (cases). Male origin microchimerism was determined by presence of Y chromosome sequences in female blood samples. Data were analysed using weighted proportional Hazards regression, yielding Hazard Ratios with 95% confidence intervals.
RESULTS: Compared with male origin microchimerism negative women, positive women had half the risk of developing brain cancer (Hazard Ratio = 0.50 [0.33-0.77]). Sensitivity analyses support that our findings are unlikely due to bias or chance.
CONCLUSIONS: Here, for the first time, we demonstrate half the risk of brain cancer in male origin microchimerism positive compared with negative women. Our findings resemble those of previous studies of male origin microchimerism and other female cancers.

There remains controversy as to whether cell phones cause cancer. We evaluated whether temporal changes in cell phone use and the incidence of glioma in Canada were consistent with the hypothesis of an increased risk.
We used data from the Canadian Cancer Registry to calculate annual incidence rates for glioma between 1992 and 2015. The annual number of new cell phone subscribers was determined using national industry statistics. The number of newly diagnosed gliomas was compared to the predicted number by applying risks from epidemiological studies to age-specific population estimates. Specifically, we calculated the \"predicted\" number of incident gliomas by determining the annual prevalence of cell phone users and years of use. These estimates were multiplied by the corresponding risk estimates to determine the predicted number of gliomas.
The number of cellular subscriptions in Canada increased from nil in the early-1980s to approximately 29.5 million in 2015. In contrast, age-standardized glioma incidence rates remained stable between 1992 and 2015. When applying risk estimates from i) a recent pooled analysis of Swedish case-control studies, ii) the 13 country INTERPHONE study, and iii) more recent results from data collected from the Canadian component of the INTERPHONE these risks overestimated the observed number of glioma cases diagnosed in Canada in 2015 by 50%, 86%, and 63%, respectively.
Predictions of glioma incidence counts using estimates of the relative risk of glioma due to cell phone use from case-control studies over-estimated the incidence rates of glioma in Canada. The absence of an elevation in incidence rates of glioma in conjunction with marked increases in cell phone use suggests that there may not be a causal link between cellphones and glioma.

UNASSIGNED: Diagnoses of anaplastic oligodendrogliomas are rare. For cancer rehabilitation practitioners, anaplastic oligodendroglioma may impact on the development and maintenance of prescriptive exercise. Exercise interventions for healthy individuals and cancer patients have been shown to increase functional capacity, psychosocial functioning, and aspects of cognitive function. However, there is a lack of research into exercise interventions among patients with anaplastic oligodendroglioma. This case report of a patient with anaplastic oligodendroglioma, measures the effects of aerobic and flexibility training on physiological, psychosocial, and cognitive functioning.
UNASSIGNED: A 44-year old woman diagnosed with class III anaplastic oligodendroglioma with 1p19q genetic co-deletion underwent left-frontal craniotomy, chemotherapy, and radiation treatment. Comprehensive physical, psychosocial, and cognitive assessments were completed before and after a 36-session exercise intervention.
UNASSIGNED: Following the intervention improvements were observed in 9 of the 14 physiological measures. Fatigue decreased by 20% and quality of life increased by almost 70%. Improvements were also observed in 6 of the 12 cognitive assessment variables.
UNASSIGNED: The 36 sessions of aerobic and flexibility training were well-tolerated by the subject. The results demonstrate the feasibility and importance of aerobic and flexibility training for the attenuation of cancer-related decrements in physiological and psychosocial variables in patients with anaplastic oligodendroglioma. The effects on cognitive function were uncertain.

We explored the association between ionizing radiation (IR) from pre-natal and post-natal radio-diagnostic procedures and brain cancer risk within the MOBI-kids study.
MOBI-kids is an international (Australia, Austria, Canada, France, Germany, Greece, India, Israel, Italy, Japan, Korea, New Zealand, Spain, The Netherlands) case-control study including 899 brain tumor (645 neuroepithelial) cases aged 10-24 years and 1,910 sex-, age-, country-matched controls. Medical radiological history was collected through personal interview. We estimated brain IR dose for each procedure, building a look-up table by age and time period. Lifetime cumulative doses were calculated using 2 and 5 years lags from the diagnostic date. Risk was estimated using conditional logistic regression. Neurological, psychological and genetic conditions were evaluated as potential confounders. The main analyses focused on neuroepithelial tumors.
Overall, doses were very low, with a skewed distribution (median 0.02 mGy, maximum 217 mGy). ORs for post-natal exposure were generally below 1. ORs were increased in the highest dose categories both for post and pre-natal exposures: 1.63 (95% CI 0.44-6.00) and 1.55 (0.57-4.23), respectively, based on very small numbers of cases. The change in risk estimates after adjustment for medical conditions was modest.
There was little evidence for an association between IR from radio-diagnostic procedures and brain tumor risk in children and adolescents. Though doses were very low, our results suggest a higher risk for pre-natal and early life exposure, in line with current evidence.

Klippel-Feil syndrome (KFS) is an exceedingly rare constitutional disorder in which a paucity of knowledge exists about the disease and its associated morbidity and mortality. We present a 4-year-old male with KFS, who notably was also diagnosed with large-cell anaplastic medulloblastoma. We evaluated the genetic basis of co-occurring KFS and medulloblastoma and the role of MYO18B as related to medulloblastoma. Constitutional and somatic variant and copy number analyses were performed from DNA-based exome studies, along with RNA-sequencing of tumor tissue, to elucidate the genetic etiology of the co-existing disease states. We identified novel constitutional compound heterozygous frameshift variants (NM_032608.5: p.Leu2257SerfsTer16 and p.Arg2220SerfsTer74) each encoding a premature stop of translation in MYO18B, consistent with a diagnosis of KFS. We did not identify any somatic variants of known relevance or disease-relevant therapeutic targets in the tumor. The somatic copy number profile was suggestive of Group 3γ medulloblastoma. Relative to pediatric brain tumors, medulloblastoma, particularly, Group 3, had increased gene expression of MYO18B. In summary, coexisting constitutional and somatic diagnoses in this patient enabled the elucidation of the genetic etiology of KFS and provided support for the role of MYO18B in tumor suppression.

BACKGROUND: Astrocytomas are the most common malignant glial tumors. With improved prognosis, it is possible for patients to pursue pregnancy post-treatment. However, with potential gonadotoxicity of oncology treatments, fertility preservation prior to chemotherapy and/or radiation therapy should be considered. This requires close collaboration between the oncologist and reproductive endocrinologist. To our knowledge this is the first report of successful pregnancies following fertility preservation for AA.
METHODS: 33-year-old nulligravid woman with newly diagnosed anaplastic astrocytoma (AA; WHO grade III, IDH1-negative) sought fertility preservation. Prior to chemotherapy and radiation for AA, the patient underwent in vitro fertilization (IVF) for fertility preservation, resulting in 8 vitrified embryos. Following chemo-radiation, the patient underwent two rounds of frozen embryo transfers (FET), each resulting in a successful singleton pregnancy.
CONCLUSIONS: This case illustrates the realistic possibility, in carefully selected patients with brain tumors, of oocyte or embryo cryo-preservation prior to chemo-radiation and subsequent pregnancies.

OBJECTIVE: To identify and describe patients\' experiences and care needs throughout the diagnostic phase of an integrated brain cancer pathway.
BACKGROUND: A malignant brain tumour is a devastating diagnosis, which may cause psychical symptoms and cognitive deficits. Studies have shown that the shock of the diagnosis, combined with the multiple symptoms, affects patients\' ability to understand information and express needs of care and support. Unmet needs have been reported within this group of patients; however, the experiences and care needs of patients going through the diagnostic phase of a standardised integrated brain cancer pathway have not previously been explored.
METHODS: A case study design was used to provide detailed information of the complex needs of patients being diagnosed with a malignant brain tumour.
METHODS: Research interviews and direct participant observation of four patients during hospital admission, brain surgery and discharge were conducted in a Danish university hospital. Systematic text condensation was used to analyse the data material.
RESULTS: Four major themes were identified: information needs, balancing hope and reality while trying to perceive the unknown reality of brain cancer, not knowing what to expect and participants\' perceptions of the relationship with the healthcare providers. The analysis revealed that participants were in risk of having unmet information needs and that contextual factors seemed to cause fragmented care that led to feelings of uncertainty and loss of control.
CONCLUSIONS: Brain tumour patients have complex care needs and experience a particular state of vulnerability during the diagnostic phase. Through personal relationships based on trust with skilled healthcare providers, participants experienced an existential recognition and alleviation of emotional distress.
CONCLUSIONS: Patients receiving a brain tumour diagnosis experience unmet care needs in several areas during their hospital stay. There is a need for interventions from healthcare providers.

Stroke and brain cancer are two distinct diseases. However, the relationship between both diseases has rarely been examined. This study investigated the longitudinal risk for developing brain cancer in stroke patients. To study this, we first reviewed the malignant gliomas previously with or without stroke using brain magnetic resonance imaging (MRI) images and the past histories. Two ischemic stroke patients before the malignant glioma were identified and belonged to the glioblastoma mutiforme (GBM). Particularly, both GBM specimens displayed strong hypoxia-inducible factor 1α (HIF-1α) expression in immunohistochemical (IHC) staining. To elucidate the significance of this relationship, we then used a nationwide population-based cohort in Taiwan to investigate the risk for the incidence of brain cancer in patients previously with or without stroke. The incidence of all tumors in the stroke group was lower than that in the control group with an adjusted hazard ratio (HR) of 0.79 (95% confidence interval [CI]: 0.74-0.84) in both gender and age older than 60 years. But the stroke patients had higher risk of developing only brain cancer with an adjusted HR of 3.09 (95% CI: 1.80-5.30), and otherwise had lower risk of developing head and neck, digestive, respiratory, bone and skin, as well as other tumors, all with p<0.05. After stratification by gender and age, the female and aged 40-60 year old stroke patients had higher risk of developing brain cancer with an adjusted HR of 7.41 (95% CI: 3.30-16.64) and 16.34 (95% CI: 4.45-62.13), respectively, both with p<0.05. Patients with stroke, in particular female and age 40-60 years old, have an increased risk for developing brain cancer.