There are several well-described molecular mechanisms that influence cell growth and are related to the development of cancer. Chemokines constitute a fundamental element that is not only involved in local growth but also affects angiogenesis, tumor spread, and metastatic disease. Among them, the C-X-C motif chemokine ligand 12 (CXCL12) and its specific receptor the chemokine C-X-C motif receptor 4 (CXCR4) have been widely studied. The overexpression in cell membranes of CXCR4 has been shown to be associated with the development of different kinds of histological malignancies, such as adenocarcinomas, epidermoid carcinomas, mesenchymal tumors, or neuroendocrine neoplasms (NENs). The molecular synapsis between CXCL12 and CXCR4 leads to the interaction of G proteins and the activation of different intracellular signaling pathways in both gastroenteropancreatic (GEP) and bronchopulmonary (BP) NENs, conferring greater capacity for locoregional aggressiveness, the epithelial–mesenchymal transition (EMT), and the appearance of metastases. Therefore, it has been hypothesized as to how to design tools that target this receptor. The aim of this review is to focus on current knowledge of the relationship between CXCR4 and NENs, with a special emphasis on diagnostic and therapeutic molecular targets.

Background: Continuous glucose monitoring (CGM) may overcome the limitations of intermittent point-of-care (POC) testing by providing real-time glucose trends and reducing treatment delays. This study aimed to evaluate the efficacy of CGM versus POC capillary testing in improving glycemic control among hospitalized non-Intensive Care Unit (non-ICU) adults with type 2 diabetes mellitus (T2DM). Methods: We conducted a systematic review and meta-analysis following PRISMA 2020 guidelines. We searched PubMed for randomized controlled trials published in English or Spanish that compared CGM with POC testing in hospitalized non-ICU adults ≥ 18 years old with T2DM and assessed risk of bias using the Cochrane RoB2 tool. The primary outcome was time in range (TIR). Secondary outcomes included time below range (TBR), time above range (TAR), mean glucose (MG), and glycemic variability (GV). Results: Seven randomized controlled trials (RCTs) including 1106 patients were analyzed. CGM significantly improved TIR (mean difference [MD] +8.15%; 95% confidence interval [CI]: +5.76, +10.55; p < 0.001) and reduced TAR > 180 mg/dL (MD −7.11%; 95% CI: −9.43, −4.78; p < 0.001) and TAR > 250 mg/dL (MD −3.96%; 95% CI: −5.29, −2.62; p < 0.001) compared with POC testing. MG also decreased with CGM (MD −11.27 mg/dL; 95% CI: −14.74, −7.81; p < 0.001). A modest reduction in TBR <70 mg/dL was observed (MD −0.29%; p < 0.001), whereas no significant differences were found for TBR < 54 mg/dL or GV. Conclusions: CGM improves inpatient glycemic control in non-ICU adults with type 2 diabetes, demonstrating advantages over POC testing across multiple randomized trials. However, further multicenter research is needed to clarify workflow implications, cost-effectiveness, and optimal implementation strategies.

Inhibitors of DNA-binding (Id) proteins constitute a family of repressor factors that modulate a multitude of cellular processes and have been linked to tumor aggressiveness, resistance to chemotherapy, angiogenesis, and worse prognosis in numerous malignancies. This review explores the role of Id proteins in the pathogenesis of neuroendocrine neoplasms (NENs). The findings revealed that this family of proteins shows significant overexpression in tumors such as small cell lung carcinoma (SCLC), neuroendocrine prostate carcinoma (NEPC), and medullary thyroid carcinoma (MTC), although the role of epigenetics in regulating Id proteins within NENs remains poorly understood, with most evidence limited to NEPC. These results underscore the potential of Id proteins not only as diagnostic biomarkers and promising therapeutic targets for the management of NENs, but also highlight the need for further research to better understand their epigenetic regulation and broader role in these tumors.

There are several well-described molecular mechanisms that influence cell growth and are relat-ed to the development of cancer. Chemokines constitute a fundamental element which are not only involved in local growth but also affect angiogenesis, tumor spread and metastatic disease. Among them, the C-X-C motif chemokine ligand 12 (CXCL12) and its specific receptor the chemo-kine C-X-C motif receptor 4 (CXCR4) have been widely studied. The overexpression in cell mem-branes of CXCR4 has been shown to be associated with the development of different kinds of his-tological malignancies, such as adenocarcinomas, epidermoid carcinomas, mesenchymal tumors or neuroendocrine neoplasms (NENs). The molecular synapsis between CXCL12 and CXCR4 leads to the interaction of G proteins and activation of different intracellular signaling pathways in both gastroenteropancreatic (GEP) and bronchopulmonary (BP) NENs conferring greater ca-pacity for locoregional aggressiveness, epithelial-mesenchymal transition (EMT) and the ap-pearance of metastases. Therefore, it has been hypothesized how to design tools that target this receptor. The aim of this review is to focus on current knowledge of the relationship between CXCR4 and NENs, with a special emphasis on diagnostic and therapeutic molecular targets.

The pituitary gland, as a central regulator of endocrine function, may be affected by a wide range of biologically derived harmful substances present in nature. While most available literature focuses on neoplasms, trauma or autoimmune disorders, the potential impact of natural toxins and poisons on pituitary function remains underexplored. This narrative review addresses the effects of acute or chronic exposure to harmful agents originating from the five biological kingdoms—Animalia, Plantae, Fungi, Monera, and Protista—on the hypothalamic–pituitary axis. Drawing on clinical reports, experimental data, and physiological insights, we describe how various biological substances may alter hormonal regulation, leading to temporary or persistent dysfunction. Importantly, this review does not cover direct infectious involvement of the pituitary, such as pituitary abscess, but focuses instead on biologically active compounds produced by living organisms. The review highlights a dispersed body of knowledge with implications not only for endocrinologists and pituitary specialists, but also for clinicians in toxicology, emergency medicine, infectious diseases, and global health. Recognizing the pituitary as a vulnerable target in diverse environmental and ecological contexts may aid in the early diagnosis and management of otherwise unexpected endocrine disorders.