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The determinants of higher education policy have their sources in various spheres, such as economic, social, educational, national policy, administrative, and demographic. Problems for the development of higher education also stem from these spheres. One of them is the challenging demographic situation that is a significant element of developing higher education in southern Poland (particuarly in the Silesia region). Given this context, this article aims to indicate the policies of the universities in the region which respond to the existing demographic threats. This relationship is to confront student opinions regarding their vision for their education and future career within the current demographic situation. Using research-based on an analysis of university and regional local government strategic documents and surveys carried out among students, we conclude that higher education development policy is responding to the demographic transformation. Meanwhile, students’ attitudes to the challenges of the demographic situation is quite “flexible” and relatively ambivalent. This article presents the contrast between the increasingly tricky demographic situation in Silesia, Poland, and the limited response in the two main groups of stakeholders – academic authorities and students – that require shaping higher education ipolicy towards future demographic challenges.

Castration-resistant prostate cancer (CRPC) is defined by resistance of the tumor to androgen deprivation therapy (ADT). Several molecular changes, particularly in the AR signaling cascade, have been described that may explain ADT resistance. The variety of changes may also explain why the response to novel therapies varies between patients. Testing the specific molecular changes may be a major step towards personalized treatment of CRPC patients. The aim of our study was to evaluate the molecular changes in the AR signaling cascade in CRPC patients. We have developed and validated several methods which are easy to use, and require little tissue material, for exploring AR signaling pathway changes simultaneously. We found that the AR signaling pathway is still active in the majority of our CRPC patients, due to molecular changes in AR signaling components. There was heterogeneity in the molecular changes observed, but we could classify the patients into 4 major subgroups which are: AR mutation, AR amplification, active intratumoral steroidogenesis, and combination of AR amplification and active intratumoral steroidogenesis. We suggest characterizing the AR signaling pathway in CRPC patients before beginning any new treatment, and a recent fresh tissue sample from the prostate or a metastatic site should be obtained for the purpose of this characterization. [ABSTRACT FROM AUTHOR]

Leydig cell ovarian tumors constitute not only a medical problem for clinicians but also a social problem - which is why women with symptoms of hirsutism relatively quickly contact physicians for medical consultation. Leydig cell ovarian tumor is a rare sex cord-gonadal stromal tumor which constitutes less than 0.5% of ovarian tumors. These cancers appear at all ages but the majority of the cases concern women in the perimenopause. In the majority of cases (70-85%), the growth is accompanied by androgen secretion, together with virilization and hirsutism. The presence of hormonally active ovarian cancers should be suspected in cases of rapidly growing symptoms of masculinization, especially when the level of free testosterone in the blood exceeds the upper limit for the given age more than three times. In diagnosing postmenopausal hyperandrogenism, it is necessary to take into account hormonally active ovarian tumors, as well as adrenal cancers. It is important to exclude other causes of hyperandrogenism, e.g. endocrinopathies (acromegaly or hypothyroidism), or iatrogenic and idiopathic factors. In order to make the diagnosis and implement the proper treatment method faster, an interdisciplinary team of physicians specializing in endocrinology, gynecology and oncology is crucial. This paper contains a study of two cases concerning Leydig cell ovarian tumors in women of postmenopausal age with symptoms of masculinization and hirsutism. [ABSTRACT FROM AUTHOR]

Head and neck cancer is a serious clinical and social problem. Surgery and radiotherapy play the most important role in treatment and give the chance of cure. Optimal treatment of patients with head and neck cancer should provide for the maximum destruction of cancerous tissue, saving as much healthy tissue as possible. Despite this, due to radiotherapy still almost 90% of patients develop skin symptoms. It seems that the mechanism of radiodermatitis is quite clear, but studies assume that its pathogenesis is not fully understood and there is much to be clarified. Acute and chronic dermatitis caused by radiotherapy is usually diagnosed according to clinical criteria. It seems that it would be useful to have a photographic classification that would facilitate and unify the clinical evaluation. In this article we shall summarize the current knowledge about the mechanisms of formation, risk factors, clinical classifications and methods for the prevention and treatment of acute and chronic radiation dermatitis. We have included clinical photos that depict individual stages according to the clinical classification of RTOG. [ABSTRACT FROM AUTHOR]

Abstract: Approximately 20% of patients with bladder cancer are diagnosed with muscle‐invasive disease (MIBC). The treatment involves radical cystectomy, but almost 50% of patients with MIBC eventually relapse and develop metastasis. The use of platinum‐based chemotherapy in the neoadjuvant setting or for metastatic patients has been shown to improve the overall survival in a subset of patients. Unfortunately, no biomarkers are available to select patients with MIBC who will benefit from chemotherapy or to monitor the efficacy of the treatment. Recently, long noncoding RNAs (lncRNAs) were shown to regulate a variety of processes involved in the development and progression of cancer, including bladder cancer. Moreover, several lncRNAs have been shown to play a role in chemotherapy resistance. Here, we analyzed lncRNA expression associated with response to platinum‐based chemotherapy in metastatic MIBC using data from the MiTranscriptome lncRNA expression database. Expression of the lncRNA, LINC00857, was found to be upregulated in tumors from patients that did not respond to platinum‐based chemotherapy. Moreover, high expression of LINC00857 is correlated with shorter recurrence‐free and overall survival of patients with MIBC. Knockdown of LINC00857 significantly decreased cell viability of bladder cancer cell lines through the induction of apoptosis. Furthermore, LINC00857 knockdown sensitized UM‐UC‐3 and T24 bladder cancer cells to cisplatin, via the negative regulation of the LMAN1 gene. Our data indicate that LINC00857 plays an important role in the regulation of response to platinum‐based chemotherapy. LINC00857 potentially could serve as a novel prognostic and predictive biomarker and might be a therapeutic target to overcome cisplatin resistance in patients with MIBC. [ABSTRACT FROM AUTHOR]

In the last few years, susceptibility loci have been identified for urinary bladder cancer (UBC) through candidate-gene and genome-wide association studies. Prognostic relevance of most of these loci is yet unknown. In this study, we used data of the Nijmegen Bladder Cancer Study (NBCS) to perform a comprehensive evaluation of the prognostic relevance of all confirmed UBC susceptibility loci. Detailed clinical data concerning diagnosis, stage, treatment, and disease course of a population-based series of 1,602 UBC patients were collected retrospectively based on a medical file survey. Kaplan-Meier survival analyses and Cox proportional hazard regression were performed, and log-rank tests calculated, to evaluate the association between 12 confirmed UBC susceptibility variants and recurrence and progression in non-muscle invasive bladder cancer (NMIBC) patients. Among muscle-invasive or metastatic bladder cancer (MIBC) patients, association of these variants with overall survival was tested. Subgroup analyses by tumor aggressiveness and smoking status were performed in NMIBC patients. In the overall NMIBC group (n = 1,269), a statistically significant association between rs9642880 at 8q24 and risk of progression was observed (GT vs. TT: HR = 1.08 (95% CI: 0.76–1.54), GG vs. TT: HR = 1.81 (95% CI: 1.23–2.66), P for trend = 2.6×10−3). In subgroup analyses, several other variants showed suggestive, though non-significant, prognostic relevance for recurrence and progression in NMIBC and survival in MIBC. This study provides suggestive evidence that genetic loci involved in UBC etiology may influence disease prognosis. Elucidation of the causal variant(s) could further our understanding of the mechanism of disease, could point to new therapeutic targets, and might aid in improvement of prognostic tools. [ABSTRACT FROM AUTHOR]

Dendritic cells (DCs) are the sentinel antigen-presenting cells of the immune system; such that their productive interface with the dying cancer cells is crucial for proper communication of the "non-self" status of cancer cells to the adaptive immune system. Efficiency and the ultimate success of such a communication hinges upon the maturation status of the DCs, attained following their interaction with cancer cells. Immature DCs facilitate tolerance towards cancer cells (observed for many apoptotic inducers) while fully mature DCs can strongly promote anticancer immunity if they secrete the correct combinations of cytokines (observed when DCs interact with cancer cells undergoing immunogenic cell death (ICD)). However, an intermediate population of DC maturation, called semi-mature DCs exists, which can potentiate either tolerogenicity or pro-tumourigenic responses (as happens in the case of certain chemotherapeutics and agents exerting ambivalent immune reactions). Specific combinations of DC phenotypic markers, DC-derived cytokines/chemokines, dying cancer cell-derived danger signals and other less characterized entities (e.g. exosomes) can define the nature and evolution of the DC maturation state. In the present review, we discuss these different maturation states of DCs, how they might be attained and which anticancer agents or cell death modalities (e.g. tolerogenic cell death vs. ICD) may regulate these states. [ABSTRACT FROM AUTHOR]

Genome-wide association studies (GWAS) have been successful in the identification of the several urinary bladder cancer (UBC) susceptibility loci, pointing towards novel genes involved in tumor development. Despite that, functional characterization of the identified variants remains challenging, as they mostly map to poorly understood, non-coding regions. Recently, two of the UBC risk variants (PSCA and UGT1A) were confirmed to have functional consequences. They were shown to modify bladder cancer risk by influencing gene expression in an allele-specific manner. Although the role of the other UBC risk variants is unknown, it can be hypothesized--based on studies from different cancer types--that they influence cancer susceptibility by alterations in regulatory networks. The insight into UBC heritability gained through GWAS and further functional studies can impact on cancer prevention and screening, as well as on the development of new biomarkers and future personalized therapies. [ABSTRACT FROM AUTHOR]

The inspection of the mechanisms through which autophagy modulates immunogenic cell death revealed that the autophagic response of cancer cells to reactive oxygen species-dependent endoplasmic reticulum stress suppresses the exposure of calreticulin on the cell surface, the phenotypic maturation of dendritic cells (DCs) as well as their ability to release interleukin-6 and to support the proliferative expansion of (interferon γ-producing) CD4+ and CD8+ T lymphocytes. These findings unveil an unprecedented role for therapy-induced autophagy in suppressing key mechanisms that underlie anticancer immune responses as elicited by immunogenic cell death. [ABSTRACT FROM AUTHOR]

For many years, research on the biology underlying bladder cancer focused on protein-coding genes which cover only about 3% of the human genome. Recently, it was discovered that a large part of the human genome is actively transcribed as long non-coding RNAs (lncRNAs). LncRNAs are master regulators of gene expression and several lncRNAs were shown to play a role in bladder cancer development and progression. Here, we analyzed lncRNA expression in muscle-invasive bladder cancer (MIBC) using the MiTranscriptome database of cancer lncRNA expression profiles, and we studied their function in bladder cancer-derived tumor cells. Analysis of the MiTranscriptome lncRNA expression data revealed four MIBC subgroups, which partially overlapped with the four mRNA clusters identified by The Cancer Genome Atlas consortium. Up-regulation of three lncRNAs CAT266, CAT1297, and CAT1647 in bladder cancer, in comparison to normal urothelium, was confirmed in an independent series of normal, non-muscle invasive (NMIBC) and MIBC tissue samples. Furthermore, expression levels of CAT1297 were found to be correlated with disease-free and overall survival in MIBC. Knockdown of CAT266, CAT1297, and CAT1647 decreased cell viability and colony formation, due to the induction of apoptosis. In conclusion, our data show that lncRNAs expression is de-regulated in MIBC and three aberrantly expressed transcripts regulate proliferation and apoptosis. Our data indicate that lncRNAs play an important role in MIBC development and progression and are a treasure chest for the discovery of new biomarkers.

We argue that the field of extracellular vesicle (EV) biology needs more transparent reporting to facilitate interpretation and replication of experiments. To achieve this, we describe EV-TRACK, a crowdsourcing knowledgebase (http://evtrack.org) that centralizes EV biology and methodology with the goal of stimulating authors, reviewers, editors and funders to put experimental guidelines into practice.

Background: Many studies investigated the prognostic or predictive relevance of single nucleotide polymorphisms (SNPs) in biologically plausible genes in urinary bladder cancer (UBC) patients. Most published SNP associations have never been replicated in independent patient series., Objective: To independently replicate all previously reported associations between germline SNPs and disease prognosis or treatment response in UBC., Methods: A Pubmed search was performed to identify studies published by July 1, 2014 reporting on germline SNP associations with UBC prognosis or treatment response. For the replication series, consisting of 1,284 non-muscle-invasive bladder cancer (NMIBC) and 275 muscle-invasive or metastatic bladder cancer (MIBC) patients recruited through the Netherlands Cancer Registry, detailed clinical data were retrieved from medical charts. Patients were genotyped using a genome-wide SNP array. SNP association with recurrence-free, progression-free, and overall survival (OS) within specific patient and treatment strata was tested using Cox regression analyses., Results: For only six of the 114 evaluated SNPs, the association with either UBC prognosis or treatment response was replicated at the p  <  0.05 level: rs1799793 ( ERCC2 ) and rs187238 ( IL18 ) for BCG recurrence; rs6678136 ( RGS4 ) and rs11585883 ( RGS5 ) for NMIBC progression; rs12035879 ( RGS5 ) and rs2075786 ( TERT ) for MIBC OS., Conclusions: Non-replicated genetic associations in the literature require cautious interpretation. This single replication does not provide definitive proof of association for the six SNPs, and non-replication of other SNPs may result from population-specific effects or the retrospective patient enrollment.