a b s t r a c tSleep disturbances are highly prevalent in women with breast cancer; side effects of cancer treatment may worsen pre-existing sleep problems and have been pointed to as important determinants of their incidence. Therefore, we aimed to assess the association between different types of breast cancer treatment and sleep disturbances, through a systematic review. Medline (using PubMed), CINAHL Plus with full text, PsycINFO and Cochrane Central Register of Controlled Trials (Central) were searched from inception to January 2014. Studies that evaluated samples of women with breast cancer, assessed sleep disturbances with standardized sleep-specific measures, and provided data for different cancer treatments were eligible. A total of 12 studies met the inclusion criteria. Three studies evaluated insomnia, five studies assessed sleep quality, two provide data on general sleep disturbances and two analysed specific sleep parameters. Women submitted to chemotherapy, or radiotherapy, tended to report higher levels of sleep disturbances. More heterogeneous findings were observed regarding the effect of surgical treatment and hormonal therapy. However, a sound assessment of the impact of these treatments was hampered by differences across studies regarding the outcomes assessed, reporting bias and the fact that most studies did not control for the effect of potential confounders. The present review highlights the potential relation between breast cancer treatments and sleep disturbances, particularly of chemotherapy, though more robust evidence is needed for a proper understanding of these associations.

Background Significant advances in the molecular profiling of gliomas, led the 2016 World Health Organization (WHO) Classification to include, for the first-time, molecular biomarkers in glioma diagnosis: IDH mutations and 1p/19q codeletion. Here, we evaluated the effect of this new classification in the stratification of gliomas previously diagnosed according to 2007 WHO classification. Then, we also analyzed the impact of TERT promoter mutations, PTEN deletion, EGFR amplification and MGMT promoter methylation in diagnosis, prognosis and response to therapy in glioma molecular subgroup. Methods A cohort of 444 adult gliomas was analyzed and reclassified according to the 2016 WHO. Mutational analysis of IDH1 and TERT promoter mutations was performed by Sanger sequencing. Statistical analysis was done using SPSS Statistics 21.0. Results The reclassification of this cohort using 2016 WHO criteria led to a decrease of the number of oligodendrogliomas (from 82 to 49) and an increase of astrocytomas (from 49 to 98), while glioblastomas (GBM) remained the same (n = 256). GBM was the most common diagnosis (57.7%), of which 55.2% were IDH-wildtype. 1p/19q codeleted gliomas were the subgroup associated with longer median overall survival (198 months), while GBM IDH-wildtype had the worst outcome (10 months). Interestingly, PTEN deletion had poor prognostic value in astrocytomas IDH-wildtype (p = 0.015), while in GBM IDH-wildtype was associated with better overall survival (p = 0.042) as well as MGMT promoter methylation (p = 0.009). EGFR amplification and TERT mutations had no impact in prognosis. Notably, EGFR amplification predicted a better response to radiotherapy (p = 0.011) and MGMT methylation to chemo-radiotherapy (p = 0.003). Conclusion In this study we observed that the 2016 WHO classification improved the accuracy of diagnosis and prognosis of diffuse gliomas, although the available biomarkers are not enough. Therefore, we suggest MGMT promoter methylation should be added to glioma classification. Moreover, we found two genetic/clinical correlations that must be evaluated to understand their impact in the clinical setting: i) how is PTEN deletion a favorable prognostic factor in GBM IDH wildtype and an unfavorable prognostic factor in astrocytoma IDH wildtype and ii) how EGFR amplification is an independent and strong factor of response to radiotherapy.

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Our study, which is one of the largest to date on the topic, shows that FHD lesions are a common complication after radiotherapy for childhood PCNST. The young brain is probably more susceptible to radiation-induced late cerebrovascular injury. Diffuse small vessel disease and ceiling effect may account for the low topographic concordance we found. The clinical implications of FHD lesions in this specific population are yet to be clarified.