BackgroundAdaptation to hypoxia and consequent pro-inflammatory gene expression of prostate and breast carcinomas have been implicated in the progression toward cancer malignant phenotype. Only partial data are available for the human tumor glioblastoma multiforme (GBM). The aim of our study was to analyze the hypoxic and pro-inflammatory microenvironment in GBMs and to demonstrate that in a stem/progenitor cell line derived from human glioblastoma (GBM-SCs), hypoxia activates a coordinated inflammatory response, evidencing an invasive and migratory phenotype.MethodsFrom each of 10 human solid glioblastomas, clinically and histopathologically characterized, we obtained three surgical samples taken from the center and the periphery of the tumor, and from adjacent host normal tissue. Molecular and morphological analyses were carried out using quantitative real-time PCR and western blot (WB). GBM stem and differentiated cells were incubated under hypoxic conditions and analyzed for pro-inflammatory gene expression and for invasive/migratory behavior.ResultsA panel of selected representative pro-inflammatory genes (RAGE and P2X7R, COX2, NOS2 and, PTX3) were analyzed, comparing tumor, peritumor and host normal tissues. Tumors containing leukocyte infiltrates (as assessed using CD45 immunohistochemistry) were excluded. Selected genes were overexpressed in the central regions of the tumors (i.e. in the more hypoxic areas), less expressed in peripheral regions, and poorly expressed or absent in adjacent normal host tissues. Western blot analysis confirmed that the corresponding pro-inflammatory proteins were also differently expressed. Hypoxic stem cell lines showed a clear time-dependent activation of the entire panel of pro-inflammatory genes as compared to differentiated tumor cells. Biological assays showed that invasive and migratory behavior was strengthened by hypoxia only in GBM stem cells.ConclusionsIn human solid glioblastoma we have observed a coordinated overexpression of a panel of pro-inflammatory genes as compared to host normal tissue. We have also evidenced a similar pattern of overexpressed genes in GBM-SCs after hypoxic treatment, showing also a gain of invasive and migratory function that was lost when these stem cells differentiated. We suggest that, as has been previously described for prostatic and mammary carcinoma, in human glioblastoma acquisition of a proinflammatory phenotype may be relevant for malignant progression.

A growing body of evidence consistently describes the side‐effects of coronavirus disease 2019 lockdown on mental health and sleep quality. We conducted a longitudinal web‐based survey of 217 Italian participants at two time points: lockdown and subsequent follow‐up. To thoroughly investigate lockdown‐related changes in sleep quality, we first evaluated variations in overall sleep quality assessed by the Pittsburgh Sleep Quality Index. We then examined sleep changes in specific components of sleep quality. Results revealed a clear dissociation of sleep effects, as a function of the specific domain considered, with longer sleep latency, worse sleep efficiency, and massive sleep medication use during forced confinement. On the other hand, we simultaneously observed an increased sleep duration and better daytime functioning. Our present findings highlight the importance of an accurate examination of sleep quality during lockdown, as the effects were not uniform across populations and different sleep domains.

These data support the evidence that molecules typical of the innate immune system, similar to that of activated leukocytes, are produced by prostate epithelial cells and that their expression is up-regulated in malignant cells. We suggest that the observed pro-inflammatory and repair process activation may represent an important molecular mechanism in the progression of prostate cancer.

Experimental and epidemiological studies have revealed that chronic inflammation contributes to cancer progression and even predisposes to cellular transformation. Inflammatory infiltrates in papillary thyroid cancer include lymphocytes, macrophages and cytokines. High-mobility group box 1 protein (HMGB1) is a late inflammatory cytokine that signals danger to the immune system through the receptor for advanced glycation end-products (RAGE) and Toll-like receptor. The activation of the above receptors results in the secretion of growth, chemotactic and angiogenic factors that contribute to chronic inflammation. In this study, we suggest that apart from the activation of signal transduction pathways by the activation of RAGE, the indirect inhibition of cell cycle regulators [such as phosphatase and tensin homolog (PTEN)] may also cause an increase in cell growth and motility. MicroRNAs (miRNAs) have increasingly been implicated in regulating the malignant progression of cancer. MiR-221 and miR-222 have been found to be deregulated in human papillary thyroid carcinomas. They are involved in cell proliferation through the inhibition of the cell cycle regulator, p27kip1, in human papillary carcinomas. In this study, we show that HMGB1 increases the expression of miR-221 and miR-222 in primary cultures of excised papillary lesions and in an established papillary cancer cell line (BC PAP). The overexpression of oncogenic miR-221 and miR-222 caused by HMGB1 is associated with an increase in malignancy scores, namely cell growth and motility.

Social isolation is considered one of the main risk factors leading to intimate partner violence episodes; this evidence also emerged during the application of stay-at-home policies to contain the COVID-19 pandemic. For this reason, we aimed to collect data on intimate partner violence over the last year, comparing data reported by victims with data collected by help professionals. In accordance with PRISMA guidelines, through keywords related to abuse, pandemic and containment measures, 3174 articles were identified for screening. After full-text reading and risk of bias analysis, 19 studies were included, and a thematic synthesis was conducted according to two categories: “studies with victims” and “studies with help professionals”. The results of the present review showed that there were significant differences between the data provided by victims and the data collected by health care facilities and police departments; additionally, differences among different forms and severity of victimization emerged. The results have been discussed according to the literature; in particular, we reflected on how containment measures have apparently made it more difficult for victims to report, thus making the existence of the dark figure of crime even more salient.