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Science communication training plays a crucial role in enabling scientists to effectively connect with the public, emphasizing essential skills such as building trust in scientific and technological advancements. Despite significant progress, some studies show a notable deficiency in higher education (HE) institutional structures and mechanisms dedicated to science communication training, addressing a diverse audience including researchers, teachers, and science monitors. This study delves into the key characteristics of current science communication postgraduate training programs within the HE landscape of Portugal. Our analysis is based on a comprehensive examination of the curricula of five science communication doctoral programs offered by four public universities in Portugal. The research involves a meticulous review of course documents and insights gathered from five directors through a detailed questionnaire. The primary objectives of this research are to discern the specific goals pursued by each course, uncover the content and development of competencies within their curricula, and explore the market opportunities envisioned by each offering. The results underscore that these programs equip students with the necessary competencies to effectively address challenges in science communication, notably enhancing public understanding of science. Significant findings suggest that Portugal's current higher education scenario predominantly emphasizes cultivating postgraduate training activities in authentic settings, fostering collaborative partnerships with society. This article is a foundational resource for further exploration into the discipline-specific applications of science communication, aiming to elevate academic engagement with society. [ABSTRACT FROM AUTHOR]

Simple Summary: Triple-negative breast cancer (TNBC) is an aggressive BC that highly metastasizes to the brain, constituting a major hurdle and with poor survival after diagnosis. This strongly contributes to the lack of well-defined molecular targets, limiting effective TNBC therapeutic options. Nevertheless, TNBC has been associated with epidermal growth factor receptor (EGFR) overexpression and downstream phosphoinositide 3-kinase (PI3K) signaling activation. We hypothesized that blood–brain barrier (BBB)-permeant molecules with the predicted ability to inhibit the EGFR/PI3Kp110β pathway could be strong candidates to tackle metastatic TNBC. A screening of EGFR, PI3Kp110β, and dual inhibitors was performed to validate their efficacy in biological assays. We used TNBC cells with brain tropism to test the drugs' effects in downstream players of the EGFR/PI3Kp110β pathway, as well as in cell death, morphology, proliferation, and migration. We found that two dual inhibitors presented the strongest anti-tumor effects, pointing to their usefulness in abrogating TNBC cells' tumorigenic properties. Triple-negative breast cancer (TNBC) is a devastating BC subtype. Its aggressiveness, allied to the lack of well-defined molecular targets, usually culminates in the appearance of metastases that account for poor prognosis, particularly when they develop in the brain. Nevertheless, TNBC has been associated with epidermal growth factor receptor (EGFR) overexpression, leading to downstream phosphoinositide 3-kinase (PI3K) signaling activation. We aimed to unravel novel drug candidates for TNBC treatment based on EGFR and/or PI3K inhibition. Using a highly metastatic TNBC cell line with brain tropism (MDA-MB-231 Br4) and a library of 27 drug candidates in silico predicted to inhibit EGFR, PI3K, or EGFR plus PI3K, and to cross the blood–brain barrier, we evaluated the effects on cell viability. The half maximal inhibitory concentration (IC50) of the most cytotoxic ones was established, and cell cycle and death, as well as migration and EGFR pathway intervenient, were further evaluated. Two dual inhibitors emerged as the most promising drugs, with the ability to modulate cell cycle, death, migration and proliferation, morphology, and PI3K/AKT cascade players such as myocyte enhancer factor 2C (MEF2C) and forkhead box P1 (FOXP1). This work revealed EGFR/PI3K dual inhibitors as strong candidates to tackle brain metastatic TNBC cells. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) remains a challenging disease, as it is the most common and deadly brain tumour in adults and has no curative solution and an overall short survival time. This incurability and short survival time means that, despite its rarity (average incidence of 3.2 per 100,000 persons), there has been an increased effort to try to treat this disease. Standard of care in newly diagnosed glioblastoma is maximal tumour resection followed by initial concomitant radiotherapy and temozolomide (TMZ) and then further chemotherapy with TMZ. Imaging techniques are key not only to diagnose the extent of the affected tissue but also for surgery planning and even for intraoperative use. Eligible patients may combine TMZ with tumour treating fields (TTF) therapy, which delivers low-intensity and intermediate-frequency electric fields to arrest tumour growth. Nonetheless, the blood–brain barrier (BBB) and systemic side effects are obstacles to successful chemotherapy in GBM; thus, more targeted, custom therapies such as immunotherapy and nanotechnological drug delivery systems have been undergoing research with varying degrees of success. This review proposes an overview of the pathophysiology, possible treatments, and the most (not all) representative examples of the latest advancements. [ABSTRACT FROM AUTHOR]

Cadherins are calcium-binding proteins with a pivotal role in cell adhesion and tissue homeostasis. The cadherin-dependent mechanisms of cell adhesion and migration are exploited by cancer cells, contributing to tumor invasiveness and dissemination. In particular, cadherin switch is a hallmark of epithelial to mesenchymal transition, a complex development process vastly described in the progression of most epithelial cancers. This is characterized by drastic changes in cell polarity, adhesion, and motility, which lead from an E-cadherin positive differentiated epithelial state into a dedifferentiated mesenchymal-like state, prone to metastization and defined by N-cadherin expression. Although vastly explored in epithelial cancers, how these mechanisms contribute to the pathogenesis of other non-epithelial tumor types is poorly understood. Herein, the current knowledge on cadherin expression in normal development in parallel to tumor pathogenesis is reviewed, focusing on epithelial to mesenchymal transition. Emphasis is taken in the unascertained cadherin expression in CNS tumors, particularly in gliomas, where the potential contribution of an epithelial-to-mesenchymal-like process to glioma genesis and how this may be associated with changes in cadherin expression is discussed. [ABSTRACT FROM AUTHOR]