Mesothelioma is an aggressive tumor with a poor prognosis. Histological diagnosis of mesothelioma using limited tissue samples can be challenging. Carbonic anhydrase IX (CAIX) is a transmembrane protein that is overexpressed in a variety of solid tumors. This study aimed to investigate the clinical utility of CAIX expression in the differential diagnosis of pleural mesothelioma from non-small cell lung carcinoma (NSCLC).

Unstained tissue microarray slides composed of 56 cases of pleural mesothelioma and 82 cases of NSCLC were subjected to immunohistochemical staining using a mouse anti-human antibody against CAIX.

Of the 38 epithelioid mesothelioma cases, 34 (89%) displayed diffuse and strong cytoplasmic membrane reactivity, while the remaining four cases (11%) showed weak to moderate staining in tumor cells. Five out of sixteen (5/16) sarcomatoid mesothelioma cases were negative. Among the non-small cell lung carcinoma cases, 76% (32/42) of adenocarcinomas and 57% (21/37) of squamous cell carcinomas were completely negative, whereas the remaining cases showed focal weak expression of CAIX.

Our study demonstrates that CAIX expression has a high sensitivity (100%) in detecting pleural epithelioid mesothelioma, which is comparable to or better than currently used mesothelial markers. The specificity of CAIX is within a comparable range to that of commonly used mesothelial markers for differentiating epithelioid mesothelioma from NSCLC. Therefore, we recommend that CAIX immunohistochemistry staining be considered as an additional tool for the differential diagnosis of mesothelioma, particularly pleural epithelioid mesothelioma, from its common mimicker, NSCLC.

A growing body of literature has demonstrated improved quality of life in cancer patients who utilize web-based patient portals; however, no studies have investigated their impact on objective clinical measures. The study aimed to evaluate the impact of patient portal utilization on clinical outcomes in cancer care. Patient portal platforms provide patients with direct access to their providers through messaging, medication requests, and other tools. There is a knowledge gap in the literature regarding whether electronic patient portals enhance outcomes in cancer care.

This study is a retrospective analysis of 791 patients with multiple myeloma within the Scripps Health system. The effect of MyScripps electronic patient portal use on unplanned hospital visits and mortality was assessed. Outcomes were also evaluated in relation to the age-adjusted Charlson comorbidity index and chemotherapy use.

Results showed that older, male, Hispanic, and Spanish-speaking patients had lower portal utilization. Those with inactive portal status had higher rates of unplanned hospital visits and mortality. Inactive portal status was an independent predictor of unplanned hospital visits in two multivariable logistic regression analyses. A logistic regression model investigating the interaction between patient portal use and age-adjusted Charlson comorbidity index revealed that active portal status remained a predictor of unplanned hospital visits.

This study highlights the potential to improve clinical outcomes among patients with multiple myeloma, particularly in vulnerable communities, by increasing access to electronic patient portals.

Diagnosing and treating cytopenic myelofibrosis in children is challenging due to the wide spectrum of clinical and pathological features, underlying etiologies, and variable therapeutic responses. In this review, we summarize the related literature and present our diagnostic algorithm to differentiate pediatric myelofibrosis and guide therapy. In brief, primary myelofibrosis is extremely rare in children, while myelofibrosis secondary to non-neoplastic or neoplastic disorders should be thoroughly ruled out in ambiguous cases. Moreover, it is reasonable to closely follow up patients and repeat bone marrow biopsy before reaching a definitive diagnosis.

Metabolic dysfunction-associated steatotic liver disease (MASLD), is the most common form of chronic liver disease worldwide. This study aimed to explore the role of TM6SF2 in high-fat diet (HFD)-induced MASLD through the gut-liver axis.

The TM6SF2 gut-specific knockout (TM6SF2 GKO) mouse was constructed using CRISPR/Cas9 technology. TM6SF2 GKO and wild-type (CON) mice were fed either a HFD or a control diet for 16 weeks to induce MASLD. Blood, liver, and intestinal lipid content, as well as gut microbiota and serum metabolites, were then analyzed.

TM6SF2 GKO mice fed an HFD showed elevated liver and intestinal lipid deposition compared to CON mice. The gut microbiota of HFD-fed TM6SF2 GKO mice exhibited a decreased Firmicutes/Bacteroidetes ratio compared to HFD-fed CON mice. The HFD also reduced the diversity and abundance of the microbiota and altered its composition.Aspartate aminotransferase, alanineaminotransferase, and total cholesterol levels were higher in HFD-fed TM6SF2 GKO mice compared to CON mice, while triglyceride levels were lower. Serum metabolite analysis revealed that HFD-fed TM6SF2 GKO mice had an increase in the expression of 17 metabolites (e.g., LPC [18:0/0-0]) and a decrease in 22 metabolites (e.g., benzene sulfate). The differential metabolites of LPC (18:0/0-0) may serve as HFD-fed TM6SF2 serum biomarkers, leading to MASLD exacerbation in GKO mice.

TM6SF2 GKO aggravates liver lipid accumulation and liver injury in MASLD mice. TM6SF2 may play an important role in regulating intestinal flora and the progression of MASLD through the gut-liver axis.

Inherited metabolic liver diseases (IMLDs) have complex etiologies and vary widely in clinical presentation, with a significant overall incidence. With the advancements in diagnostic and treatment technologies, an increasing number of children with inherited metabolic diseases are surviving into adolescence and adulthood. These advancements have improved our understanding of the IMLD disease spectrum and clinical outcomes. This study aimed to analyze changes in the disease spectrum and epidemiological characteristics of inherited metabolic liver diseases (IMLD) over the past 20 years in two specialized liver disease hospitals in northern China.

A retrospective analysis was conducted on IMLD cases diagnosed between January 1, 2002, and December 31, 2023, at two liver disease specialty hospitals in Beijing. Data were obtained from inpatient and outpatient hospital information systems, with diagnoses based on national and international IMLD diagnosis and treatment guidelines.

A total of 2,103 IMLD patients were analyzed, including 1,213 adults and 890 children. IMLD accounted for 4.58‰ of hospitalized liver disease patients during this period. The most common IMLD was Wilson’s disease, comprising 68% of all IMLD cases. The number of diagnosed IMLD types increased from 15 to 32 across two 11-year periods (2002–2012 and 2013–2023). Among pediatric patients, glycogen storage disease and Alagille syndrome were more prevalent in those under one year of age, while Wilson’s disease was prevalent across all age groups. In adult IMLD patients, Wilson’s disease, polycystic liver disease, and hereditary hyperbilirubinemia were more frequently observed.

Over the past 20 years, both the number of diagnosed IMLD cases and disease diversity have significantly increased, with Wilson’s disease remaining the most prevalent IMLD. These findings provide valuable insights for the long-term management of IMLD patients and the allocation of healthcare resources.

Among all tumors worldwide, digestive tract tumors have a higher incidence rate and a significant disease burden. Esophageal cancer, gastric cancer, liver cancer, and colorectal cancer are often diagnosed at an advanced stage, and the prognosis remains poor. Currently, tumor treatment resistance is a major global challenge, with many underlying mechanisms. Ferroptosis has been shown to reverse drug resistance. This article reviews the mechanisms and recent advancements in ferroptosis related to reversing treatment resistance in gastrointestinal tumors, aiming to provide theoretical insights and research directions for the diagnosis and treatment of digestive tract tumors.

Gelsemium elegans Benth (G. elegans) is a traditional medicinal plant; however, it is highly toxic, and toxicity varies significantly between species. The cause of this difference has not been clarified. Humantenirine is an important toxic alkaloid in G. elegans, and its metabolism has been poorly studied. This study aimed to compare the different metabolites formed by human liver microsomes, pig liver microsomes, and goat liver microsomes.

High-performance liquid chromatography/quadrupole time-of-flight mass spectrometry was used to study the metabolism of humantenirine in human liver microsomes, pig liver microsomes, and goat liver microsomes.

A total of eight metabolites (M1-M8) were identified, and three major metabolic pathways were found: demethylation (M1), dehydrogenation (M2, M3, M7), and oxidation (M4, M5, M6, M8).

Based on these results, it is hypothesized that demethylation is the major detoxification pathway for humantenirine, providing important information to better understand the metabolism and toxicity differences between species of G. elegans.

Mitochondria are highly dynamic organelles that adapt to cellular stress and metabolic demands through processes such as fission, fusion, mitophagy, and transport, all of which are vital for maintaining cellular signaling and metabolic homeostasis. Fission facilitates mitochondrial division and biogenesis, while fusion enhances mitochondrial fitness and metabolic flexibility by mitigating damage. Together, these processes play a critical role in regulating cellular stress responses and apoptosis. Dysregulation of mitochondrial dynamics has been linked to impaired development and cancer progression, including breast cancer metastasis. A comprehensive understanding of mitochondrial dynamics in breast cancer progression is essential for advancing precision medicine. This review delves into the intricate molecular mechanisms governing mitochondrial biogenesis, fission, fusion, and mitophagy, with a particular focus on the role of mitophagy in maintaining mitochondrial homeostasis and its connection to metastasis progression. Furthermore, it discusses potential therapeutic strategies targeting mitochondrial dynamics and highlights the critical steps necessary to translate these approaches into clinical trials.

The tumor microenvironment (TME) consists of a complex mix of cellular and non-cellular components, including immune cells, stromal cells, extracellular matrix, cytokines, and growth factors. These elements interact with tumor cells to influence tumorigenesis, growth, invasion, and metastasis. Long noncoding RNAs (lncRNAs)—a class of non-coding RNAs longer than 200 nucleotides—have attracted considerable attention for their roles in regulating gene expression at the epigenetic, transcriptional, and post-transcriptional levels. Emerging evidence suggests that lncRNAs are crucial in shaping the TME by modulating processes such as immune evasion, angiogenesis, metabolic reprogramming, and the maintenance of cancer stem cells. This review provides an overview of the current understanding of lncRNAs in the TME, focusing on their involvement in key signaling pathways and cellular interactions that drive tumor progression. We discussed how lncRNAs contribute to extracellular matrix remodeling, facilitate communication between tumor and stromal cells, and regulate immune cell infiltration and function within the TME. Additionally, we explore the potential of lncRNAs as biomarkers for early cancer detection and prognosis, as well as their promise as therapeutic targets to disrupt tumor-microenvironment crosstalk. The review also addresses challenges in targeting lncRNAs therapeutically, such as ensuring specificity, minimizing off-target effects, and achieving effective in vivo delivery of lncRNA-targeted therapies. Strategies to overcome these challenges include the development of highly specific lncRNA knockout technologies and the use of advanced delivery systems, such as nanoparticles and viral vectors, to precisely target tumor-associated cells. Overall, this review underscores the significant role of lncRNAs in the TME and their potential as novel tools for enhancing cancer diagnosis and treatment. By elucidating the multifaceted roles of lncRNAs in the TME, we aimed to provide insights that could lead to more effective, targeted therapeutic strategies, ultimately advancing cancer research and improving patient care.