Solute carrier (SLC) family transporters are crucial transmembrane proteins responsible for transporting various molecules, including amino acids, electrolytes, fatty acids, and nucleotides. To date, more than fifty SLC transporter subfamilies have been identified, many of which are linked to the progression of hepatic steatosis and fibrosis. These conditions are often caused by factors such as non-alcoholic fatty liver disease and non-alcoholic steatohepatitis, which are major contributors to the global liver disease burden. The activity of SLC members regulates the transport of substrates across biological membranes, playing key roles in lipid synthesis and metabolism, mitochondrial function, and ferroptosis. These processes, in turn, influence the function of hepatocytes, hepatic stellate cells, and macrophages, thereby contributing to the development of hepatic steatosis and fibrosis. Additionally, some SLC transporters are involved in drug transport, acting as critical regulators of drug-induced hepatic steatosis. Beyond substrate transport, certain SLC members also exhibit additional functions. Given the pivotal role of the SLC family in hepatic steatosis and fibrosis, this review aimed to summarize the molecular mechanisms through which SLC transporters influence these conditions.

Hepatocellular carcinoma (HCC) is a significant global health issue, ranking as the sixth most prevalent malignancy and the fourth leading cause of cancer-related mortality worldwide. Despite advancements in therapeutic strategies, mortality rates for HCC remain high. The tumor immune microenvironment (TIME) plays a vital role in HCC progression by influencing tumor cell survival and growth. Recent studies highlight the essential role of exosomes in mediating intercellular communication within the TIME, particularly in interactions among tumor cells, immune cells, and fibroblasts. These interactions drive critical aspects of tumor development, including immune escape, angiogenesis, drug resistance, and metastasis. A detailed understanding of the molecular mechanisms by which exosomes modulate the TIME is essential for developing targeted therapies. This review systematically evaluated the roles and regulatory mechanisms of exosomes within the TIME of HCC, examining the impact of both HCC-derived and non-HCC-derived exosomes on various cellular components within the TIME. It emphasized their regulatory effects on cell phenotypes and functions, as well as their roles in HCC progression. The review also explored the potential applications of exosome-based immunotherapies, offering new insights into improving therapeutic strategies for HCC.

Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related death worldwide. Multiple treatment modalities are available for the management of HCC, depending on its stage as determined by the Barcelona Clinic Liver Cancer staging system. Because liver transplantation (LT) theoretically removes the cancer and replaces the organ at risk for future malignancy, LT is often considered the most definitive and one of the most efficacious treatment options for HCC. Nevertheless, the success and efficacy of liver transplantation depend on various tumor characteristics. As a result, multiple criteria have been developed to assess the appropriateness of a case of HCC for LT, with the pioneering Milan Criteria established in 1996. Over the past 20 to 30 years, these criteria have been critically evaluated, expanded, and often liberalized to make LT for patients with HCC a more universally applicable option. Furthermore, the development of other treatment modalities has enabled downstaging and bridging strategies for HCC prior to LT. In this narrative and comprehensive review, we provided an update on recent trends in the epidemiology of HCC, selection criteria for LT, implementation of LT across different regions, treatment modalities available as bridges, downstaging strategies, alternatives to LT, and, finally, post-LT surveillance.

The prevalence and fatality rates of cutaneous malignant melanoma (CMM) have been rising, particularly among the elderly. This study analyzes CMM incidence trends in the United States elderly population from 1987 to 2016 to inform prevention and management strategies.

Using incidence data from the Surveillance, Epidemiology, and End Results database spanning 1989 to 2008, we calculated the age-adjusted standardized population incidence rates for CMM in elderly individuals. The Joinpoint software was employed to estimate annual percent change and analyze trends in CMM incidence among elderly individuals from 1987 to 2016.

The study included 56,997 elderly CMM patients from eight Surveillance, Epidemiology, and End Results registries, of whom 36,726 were male (64.4%). The age-adjusted CMM incidence rate from 2012 to 2016 was 0.99 per 1,000, a 2.8-fold increase from 1987–1991 (95% confidence interval: 2.7–2.9). Incidence rates increased with age and birth cohort, peaking at 1.53 per 1,000 males and 0.59 per 1,000 females aged 85+ during 2012–2016. Birth cohort effects also showed a continuous increase.

This study reveals a substantial increase in CMM incidence rates among the elderly from 1987 to 2016, particularly between 2012 and 2016. Incidence rates escalated with age and birth cohort, with the highest rates observed in individuals aged 85 and older.

FMS-like tyrosine kinase 3 (FLT3) mutations are among the most common genetic alterations in acute myeloid leukemia (AML) and play a pivotal role in leukemogenesis. The two primary mutation types, internal tandem duplications (ITDs) and tyrosine kinase domain point mutations, serve as key prognostic markers and therapeutic targets. Advances in next-generation sequencing (NGS) have revolutionized FLT3 mutation detection by providing precise insights into mutation architecture, enhancing risk stratification, and enabling personalized treatment strategies. Additionally, these advancements have facilitated molecular minimal residual disease (MRD) testing, which is instrumental in guiding post-remission management. This review summarizes the molecular characteristics, diagnostic approaches, and therapeutic implications of FLT3 mutations in hematologic malignancies.

A narrative review of the current literature on FLT3 mutations was conducted, incorporating data from original research articles, clinical trials, and recent reviews. Relevant studies were identified through a PubMed literature search and manually curated.

FLT3 mutations are detected in approximately 30% of AML cases and occur at lower frequencies in myelodysplastic syndromes, chronic myelomonocytic leukemia, acute lymphoblastic leukemia, and mixed phenotype acute leukemia. NGS enables comprehensive mutation profiling, revealing rare variants and subclonal complexity while supporting MRD detection with high analytic sensitivity. FLT3-ITD-based MRD positivity is strongly associated with relapse and poor survival in AML. Clinical trial data support FLT3 inhibitors, including midostaurin, gilteritinib, and quizartinib, in FLT3-mutated AML. Additionally, MRD-guided therapy and combination treatment strategies are promising approaches to overcoming resistance.

FLT3 mutations play a central role in the pathogenesis and treatment of AML and related malignancies. NGS-based testing and MRD monitoring transform clinical decision-making by refining risk stratification and enabling personalized therapeutic interventions. Establishing standardized testing protocols and the broader integration of FLT3-targeted therapies will be essential for optimizing patient outcomes.

Chronic hepatitis B (CHB) remains a significant global health challenge, and effective antiviral therapies are essential for long-term management. This study aimed to evaluate the real-world effectiveness and safety of tenofovir amibufenamide (TMF) in a cohort of patients with chronic hepatitis B (CHB).

In this multicenter, prospective, real-world cohort study, 194 CHB patients were recruited from four hospitals between August 2021 and August 2022. Patients were divided into treatment-naïve (TN, n = 123) and treatment-experienced (TE, n = 71) groups. The TN group was further subdivided into TMF (n = 63) and tenofovir disoproxil fumarate (TDF, n = 60) subgroups. In the TE group, patients transitioned from prior antiviral therapies (entecavir or TDF) to TMF after meeting criteria for poor virological response or safety concerns. Treatment response was evaluated in terms of virological effectiveness and alanine transaminase normalization rates. Virological response (VR), ALT normalization rates, renal function markers, and lipid profiles were monitored.

In the TN cohort, VR rates at 24 and 48 weeks were 42.86% and 90.48% for TMF, and 60.00% and 83.33% for TDF. ALT normalization rates at 24 and 48 weeks for TMF were 56.82% and 70.45% (according to AASLD 2018 standards). In the TE group, VR rates at 24 and 48 weeks were 83.1% and 91.55%, respectively. ALT normalization rates were 86.67% and 93.33% (local standards), and 66.67% and 76.67% (AASLD 2018 standards) (z = −2.822, P = 0.005). Additionally, TMF showed improved renal safety over TDF, with no significant differences in lipid concentrations.

TMF is comparable to TDF in terms of CHB treatment effectiveness, with better renal safety and no impact on lipid levels. In TE patients, transitioning to TMF therapy does not affect antiviral treatment outcomes.

Type 2 diabetes mellitus (T2DM) is a prevalent yet complex metabolic disorder that has shown a rising incidence over the past few decades. Recent research has identified flavonoids as compounds capable of both preventing and managing T2DM through various mechanisms. These mechanisms include enhancing insulin sensitivity, stimulating insulin secretion, modulating intestinal microbiota, inhibiting glucose absorption, and reducing gluconeogenesis. Moreover, numerous studies have suggested that flavonoids may influence gut hormones. Therefore, we propose that flavonoids could serve as effective therapeutic agents for T2DM by modulating intestinal hormone levels. This review aimed to elucidate the potential pathways through which flavonoids may impact T2DM, with a particular emphasis on their role in regulating the enteroendocrine system.

Hyperuricemia (HU), characterized by elevated uric acid (UA) levels in the blood, is a global health concern associated with various conditions, including cardiovascular diseases, gout, hypertension, metabolic syndrome, renal dysfunction, and neurodegenerative diseases. Recent studies highlight the multifaceted origins of HU, implicating genetic predisposition, dietary patterns, lifestyle choices, and environmental influences. Genetic variations affecting enzymes and transporters involved in purine metabolism and UA excretion have been identified, paving the way for personalized treatment strategies. Advances in diagnostic imaging and omics technologies provide enhanced precision in detecting and evaluating risks. While pharmacological interventions remain central to managing HU, persistent challenges such as treatment resistance necessitate the exploration of novel drug targets and lifestyle modifications. Chinese herbal medicines present a potential alternative with fewer side effects. Emerging research on the impact of gut microbiota on UA metabolism opens new therapeutic avenues. Despite progress, challenges such as optimizing treatment duration and understanding long-term effects remain. Collaborative efforts are essential to address these challenges and advance our comprehension of HU. Integrating precision medicine and holistic patient care approaches holds promise for improving outcomes and enhancing the quality of life for individuals with HU. This review provided a contemporary analysis of HU, covering its causes, associated health risks, diagnosis, treatment, and future outlook.

Clostridioides difficile infection (CDI) is associated with significant morbidity and mortality and carries a high risk of recurrence. Given the substantial healthcare burden and the evolving nature of CDI, understanding the role of emerging treatment strategies is essential. While oral vancomycin remains a mainstay of CDI treatment, the past decade has brought several notable advances in agents and practices that may be used for CDI treatment and prevention. Fidaxomicin or vancomycin are now recommended for an initial episode of CDI, with several guidelines giving preference to fidaxomicin based on its demonstrated ability to reduce recurrent CDI. Promising developments have emerged regarding the use of fecal microbiota-based therapies in the management of CDI, including conventional fecal microbiota transplantation and the approved live biotherapeutic products, Rebyota and Vowst. These therapies help restore the microbiota of the colon to treat severe CDI and prevent recurrence in select patients. Several strategies have emerged to prevent recurrent CDI, including bezlotoxumab, a single-dose, weight-based IgG1 monoclonal antibody that may be given to patients at high risk of recurrence. Additional pipeline therapies, such as vaccines, beta-lactamases, and bacteriophages, may provide future opportunities for CDI management. This narrative review aimed to summarize societal guideline recommendations for CDI management, describe the evidence for key therapies used in CDI treatment, and review recent updates on emerging treatment modalities.