Lung cancer (LC) remains the leading cause of cancer-related deaths worldwide, characterized by high mortality rates and limited treatment options. MicroRNAs (miRNAs) are critical regulators of gene expression and play significant roles in the development of LC. This review aimed to provide a comprehensive analysis of oncogenic miRNAs involved in LC, focusing on their dysregulation, functional roles, and potential implications for diagnosis and therapy. In this review, we collected data from published literature, specifically selecting English articles closely related to the topic. We conducted a thorough review of studies published between 2013 and 2023, utilizing prominent academic databases such as PubMed, Scopus, and Google Scholar to gather relevant data. Our investigation highlights several oncogenic miRNAs that have been shown to play critical roles in lung cancer biology, including miR-9-5p, miR-21, and miR-31. These miRNAs are known to facilitate various key processes, such as tumor cell proliferation, enhanced migratory capabilities, and the development of resistance to chemotherapeutic agents. Additionally, miRNAs present significant diagnostic and therapeutic potential. In conclusion, the unique roles and regulatory networks of miRNAs in LC warrant extensive further research. Further research is essential to uncover the complex networks of miRNAs and to develop innovative miRNA-based therapies for lung cancer.

Intrahepatic cholangiocarcinoma (iCCA) is the second most prevalent primary liver cancer, characterized by insidious onset and high malignancy. Many patients are diagnosed at an inoperable stage, and the effectiveness of chemotherapy and radiotherapy remains limited. This study aimed to provide a comprehensive review of the histological classification, genetic alterations, molecular subtypes, and corresponding imaging signatures of iCCA, highlighting its heterogeneity and offering insights into targeted therapy and personalized treatment. The heterogeneity of iCCA poses significant challenges to both targeted therapy and immunotherapy, necessitating in-depth exploration at the molecular and subtyping levels. Investigating genetic variations, signaling pathway alterations, and molecular subtypes can aid in patient stratification. Stratifying iCCA patients allows for more precise treatment selection, ultimately improving survival outcomes. Imaging, as a non-invasive tool, holds substantial potential for predicting subtypes and molecular profiles. It is possible to infer histological and molecular features from imaging, or to interpret imaging signatures in light of known histological and molecular data. This integrative approach, combining external imaging with internal molecular insights, fosters a comprehensive understanding of iCCA’s characteristics and enhances clinical management.

Endometrial cancer is a common malignant tumor of the female reproductive system, and its incidence is increasing worldwide. The underlying causes of endometrial cancer are multifactorial. In recent years, the role of diet and lifestyle has received considerable attention and has become a key area of research for cancer prevention. Available literature suggests that different dietary patterns, such as the Mediterranean diet or a plant-based diet, along with moderate physical activity, are associated with a reduced risk of this cancer. Despite these findings, significant gaps in knowledge remain, particularly regarding the specific foods, lifestyle choices, and mechanisms of action that can help mitigate the risk of cancer. Furthermore, the effects of cultural and genetic differences among subpopulations make this issue even more complex. In this context, this review aimed to assess the existing literature on the potential role of diet and lifestyle factors in preventing endometrial cancer, evaluate the available data, and highlight areas that require further investigation to provide concrete evidence and recommendations for prevention.

Acetaminophen (APAP) is one of the most commonly used analgesic and antipyretic medications and is generally considered safe at therapeutic doses. However, overdose remains a leading cause of acute liver failure, primarily characterized by centrilobular (zone 3) hepatic necrosis, oxidative stress, mitochondrial dysfunction, and sterile inflammation. The hepatotoxic effects of APAP are localized to the centrilobular region, where cytochrome P450 2E1 is highly expressed. Cytochrome P450 2E1 catalyzes the conversion of APAP to a toxic metabolite, N-acetyl-p-benzoquinone imine. During overdose, the liver’s detoxification capacity is overwhelmed and excess N-acetyl-p-benzoquinone imine binds to cellular proteins, initiating oxidative stress and mitochondrial injury that culminate in hepatocyte death. A central component of APAP-induced hepatotoxicity is the activation of innate immune responses, particularly via inflammasome pathways. Inflammasomes are cytosolic multiprotein complexes that detect cellular damage and trigger inflammation. Among these, the NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) inflammasome plays a significant role in APAP-induced liver injury. Upon activation, the NLRP3 inflammasome promotes autocatalytic cleavage of procaspase-1 into its active form, caspase-1, which subsequently processes the pro-inflammatory cytokines pro-interleukin-1β and pro-interleukin-18 into their mature forms. These cytokines recruit additional immune cells and amplify liver inflammation, exacerbating tissue injury. Thus, the NLRP3 inflammasome serves as a key mechanistic link between the initial toxic insult and the ensuing inflammatory response in APAP hepatotoxicity. This review aimed to explore the molecular mechanisms underlying APAP-induced liver injury, particularly inflammasome activation, and evaluate the current and emerging therapeutic strategies.

Autoimmune hepatitis (AIH) is a chronic, progressive inflammatory liver disease characterized by autoimmune-mediated hepatic injury. Currently, glucocorticoid drugs, primarily prednisone, with or without azathioprine, are commonly recommended as first-line therapeutic agents in treatment guidelines by many scientific associations. However, the primary objective of treatment is to achieve a complete biochemical response, which is defined as the normalization of both transaminases and immunoglobulin G levels within six to twelve months. Ideally, this should also be accompanied by histological remission. Nevertheless, corticosteroid therapy is associated with significant adverse effects, potentially resulting in treatment discontinuation. In this context, it has become evident that standard treatment is inadequate for a proportion of patients, leading to the emergence of other treatment options and lines. Novel immunomodulatory agents, a class of drugs that regulate the body’s immune functions, have been confirmed to possess properties that modulate immune balance and induce immune tolerance. In recent years, these agents have played an increasingly significant role in the clinical management of AIH. This article provided an in-depth review of recent advancements in the development of novel immunomodulators, including immune cell nucleic acid inhibitors, calmodulin phosphate inhibitors, mammalian target of rapamycin inhibitors, tumor necrosis factor-α inhibitors, interleukin-2, anti-CD20 monoclonal antibodies, and B cell-activating factor inhibitors, for the treatment of AIH.

Chronic liver cirrhosis (LC) and acute-on-chronic liver failure (ACLF) are interconnected hepatic disorders associated with substantial morbidity and mortality. Despite their distinct clinical characteristics, both conditions share common pathogenic pathways that remain inadequately understood. This study aimed to identify shared gene signatures and elucidate underlying molecular mechanisms.

In this study, we employed Weighted Gene Co-Expression Network Analysis to explore transcriptomic data from the Gene Expression Omnibus for LC and ACLF.

Key co-expression modules enriched with genes involved in glycolysis and gluconeogenesis pathways were identified, implicating metabolic dysfunction as a central feature in both conditions. Furthermore, microRNA analysis revealed that hsa-miR-122 and hsa-miR-194 play pivotal roles in regulating these metabolic pathways, potentially contributing to immune dysregulation.

Our findings indicate that these shared molecular mechanisms are critical in the progression from LC to ACLF, providing novel insights into potential therapeutic targets for mitigating disease severity and improving clinical outcomes.

Mesonephric carcinoma (MC) is a rare type of cervical carcinoma that arises from mesonephric remnants. It is characterized by a mixture of a wide variety of growth patterns and typically exhibits positive immunoreactivity for GATA binding protein 3, thyroid transcription factor 1, and apical common acute lymphoblastic leukemia antigen. A subset of adenocarcinomas in the uterine corpus and ovary with similar morphology and immunophenotype is classified as mesonephric-like adenocarcinoma (MLA) in the current World Health Organization classification. This review aimed to summarize the clinicopathological features of mesonephric remnants, mesonephric hyperplasia, and MC, provide an update on the current understanding of MLA, and highlight the molecular differences between MC and MLA.

A literature review was conducted on mesonephric remnants, mesonephric hyperplasia, MC, and MLA. The clinicopathological and molecular features were summarized from previously published studies and compared across these entities.

Both MC and MLA exhibit a mixture of growth patterns and show immunoreactivity for GATA binding protein 3, thyroid transcription factor 1, and common acute lymphoblastic leukemia antigen. They commonly harbor genetic alterations in KRAS and NRAS. However, key differences exist between these two entities. MC is associated with mesonephric remnants, whereas no such association has been identified for MLA. Additionally, although KRAS and NRAS mutations are common in both, a subset of MLA cases also harbors PIK3CA and/or PTEN mutations, genetic alterations commonly seen in endometrioid adenocarcinoma.

Although the exact pathogenesis of MLA remains unclear, it is favored to originate from Müllerian-derived epithelium undergoing differentiation along the mesonephric pathway, rather than from true mesonephric remnants. Both MC and MLA tend to follow a relatively aggressive clinical course, underscoring the importance of accurate diagnosis.

Portal hypertension can cause serious complications such as upper gastrointestinal bleeding, primarily due to esophageal and gastric varices. The risk of mortality from variceal hemorrhage is significant, particularly when the hepatic venous pressure gradient exceeds 12 mmHg. Established treatments generally include endoscopic variceal band ligation and cyanoacrylate glue for gastric varices; however, challenges such as limited availability and a lack of technical expertise can hinder the use of glue, leading to preventable complications. This study investigates the efficacy of using a 50% glucose solution for injection sclerotherapy in cases of gastric varices. We present three unique patient cases. The first case involves a 21-year-old with persistent upper gastrointestinal bleeding and a portal vein thrombus, who experienced temporary relief after receiving injection sclerotherapy but tragically succumbed to significant bleeding later. The second case describes a 24-year-old who successfully managed his bleeding with the same treatment but was subsequently lost to follow-up. Lastly, a 72-year-old patient with recurrent painless hematemesis remained free of symptoms following injection sclerotherapy. Overall, while cyanoacrylate glue remains the preferred treatment, injection sclerotherapy with 50% dextrose shows promise as an effective alternative, particularly in settings where conventional treatments are not readily available, potentially reducing the risks associated with untreated variceal bleeding.

Cardiovascular diseases (CVDs) remain the leading cause of global morbidity and mortality, highlighting the urgent need for innovative diagnostic and prognostic approaches to address their complex pathophysiology. Recent advances in molecular cardiology have unveiled immune-derived microRNAs (miRNAs), or immuno-miRs, as pivotal regulators in the interplay between immune responses and cardiovascular pathology. Secreted by immune cells such as T lymphocytes, macrophages, and neutrophils, these small non-coding RNAs modulate critical signaling pathways by regulating gene expression. Immuno-miRs influence essential processes, including inflammation, endothelial dysfunction, and fibrotic remodeling—core mechanisms underlying conditions such as atherosclerosis, myocardial infarction, and heart failure. Moreover, their presence in systemic circulation within extracellular vesicles underscores their role in intercellular communication, impacting both immune and non-immune cardiovascular cells, such as cardiomyocytes and endothelial cells. This dual functionality renders immuno-miRs promising candidates as diagnostic biomarkers for early disease detection and as prognostic tools for assessing disease progression and therapeutic efficacy. Furthermore, emerging miRNA-based interventions—such as miRNA mimics and inhibitors—show considerable promise in modulating immune dysregulation in CVDs, although clinical translation remains a significant challenge. In this review, we comprehensively examine the regulatory roles of immuno-miRs in both innate and adaptive immune responses and explore recent advancements in miRNA-based therapies. By consolidating current knowledge and identifying existing gaps, we provide a comprehensive overview of the transformative potential of immuno-miRs in CVD management. Integrating these molecules into personalized medicine may pave the way for more effective, targeted, and minimally invasive strategies to combat one of the world’s most pressing health challenges.