Chronic kidney disease (CKD) poses a global health challenge, engendering various physiological and metabolic shifts that significantly impact health and escalate the susceptibility to severe illnesses. This comprehensive review delves into the intricate complexities of CKD, scrutinizing its influence on cellular growth homeostasis, hormonal equilibrium, wasting, malnutrition, and its interconnectedness with inflammation, oxidative stress, and cardiovascular diseases. Exploring the genetic, birth-related, and comorbidity factors associated with CKD, alongside considerations of metabolic disturbances, anemia, and malnutrition, the review elucidates how CKD orchestrates cellular growth control. A pivotal focus lies on the nexus between CKD and insulin resistance, where debates persist regarding its chronological relationship with impaired kidney function. The prevalence of insulin abnormalities in CKD is emphasized, contributing to glucose intolerance and raising questions about its role as a precursor or consequence. Moreover, the review sheds light on disruptions in the growth hormone and insulin-like growth factor axis in CKD, underscoring the heightened vulnerability to illness and mortality in cases of severe growth retardation. Wasting, a prevalent concern affecting up to 75% of end-stage renal disease (ESRD) patients, is analyzed, elucidating the manifestations of cachexia and its impact on appetite, energy expenditure, and protein reserves. Taste disturbances in CKD, affecting sour, umami, and salty tastes, are explored for their implications on food palatability and nutritional status. Independent of age and gender, these taste alterations have the potential to sway dietary choices, further complicating the management of CKD. The intricate interplay between CKD, inflammation, oxidative stress, and cardiovascular diseases is unraveled, emphasizing the profound repercussions on overall health. Additionally, the review extends its analysis to CKD’s broader impact on cognitive function, emotional well-being, taste perception, and endothelial dysfunction. Concluding with an emphasis on dietary interventions as crucial components in CKD management, this comprehensive review navigates the multifaceted dimensions of CKD, providing a nuanced understanding essential for developing targeted therapeutic strategies.

The Melanoma Antigen Gene (MAGE) is a large family of highly conserved proteins that share a common MAGE homology domain. Interestingly, many MAGE family members exhibit restricted expression in reproductive tissues but are abnormally expressed in various human malignancies, including bladder cancer, which is a common urinary malignancy associated with high morbidity and mortality rates. The recent literature suggests a more prominent role for MAGEA family members in driving bladder tumorigenesis. This review highlights the role of MAGEA proteins, the potential for them to serve as diagnostic or prognostic biomarker(s), and as therapeutic targets for bladder cancer.

Prostate cancer is a complex heterogeneous disease that affects millions of males worldwide. Despite rapid advances in molecular biology and innovation in technology, few biomarkers have been forthcoming in prostate cancer. The currently available biomarkers for the prognosis of prostate cancer are inadequate and face challenges, thus having limited clinical utility. To date, there are a number of prognostic and predictive biomarkers identified for prostate cancer but lack specificity and sensitivity to guide clinical decision making. There is still tremendous scope for specific biomarkers to understand the natural history and complex biology of this heterogeneous disease, and to identify early treatment responses. Accumulative studies indicate that aquaporins (AQPs) a family of membrane water channels may serve as a prognostic biomarker for prostate cancer in monitoring disease advancement. In the present review, we discuss the existing prostate cancer biomarkers, their limitations, and aquaporins as a prospective biomarker of prognostic significance in prostate cancer.

Introduction Cancer is not just a genetic disease but is deeply entangled with trillions of microbes that live in and on our bodies. The human microbiome has emerged as a critical regulator of cellular metabolism and, increasingly, as a driver of carcinogenesis across multiple organ systems. In this editorial, we provide a concise overview of the intricate relationship between the microbiome and carcinogenesis, underscoring several unifying insights crucial for understanding this emerging field. The ten papers published in frontiers research editorial topic titled "Understanding the Role of Microbiome in Alteration of Cellular Metabolism and Cancer Development," explored the surprising connection between human microbiome and cancer-ranging from narrative and systematic reviews to original mendelian randomization and multi-omics studies. These studies guide us, how microbial communities and their metabolites modulate tumor initiation, progression, and treatment response. Here, we have summarized each contribution and suggested future directions for this rapidly evolving field. Sabour and colleagues comprehensively reviewed, how anaerobic bacteria including Fusobacterium nucleatum, Enterotoxigenic Bacteroides fragilis, Peptostreptococcus, Prevotella, Clostridium spp., and others initiate and exacerbate colorectal cancer (CRC). Under low-oxygen conditions of a tumor, these bacteria release toxins and metabolites that activate multiple mechanisms by which anaerobic bacteria drive carcinogenesis: activation of Wnt/β-catenin signaling, disruption of epithelial architecture, proinflammatory cytokine induction, and direct genotoxic DNA damage in hypoxic tumor niches, essentially providing a local environment to favor tumor growth. The authors underscore the role of dysbiosis and aberrant microbial metabolites (e.g., secondary bile acids, short-chain fatty acids) in shaping a pro-tumorigenic microenvironment (Sabour et al., 2025). Chen and co-workers provided a comprehensive review that links the gut and intratumorally microbiota dysbiosis and gastric cancer (GC). They have highlighted the pivotal role of microbial dysbiosis in the initiation and progression of GC, wherein; imbalance in the microbial community notably Helicobacter pylori alongside enrichment of Citrobacter, Clostridium, Fusobacterium, and others contribute to GC by promoting genomic instability, impaired DNA repair, exacerbating tumor hypoxia, and fostering an immunosuppressive microenvironment. The authors evaluate the translational aspect of potential microbiota-based interventions including probiotics, prebiotics, antibiotics, fecal transplantation, and traditional Chinese medicine to improve the chemotherapeutic and immunotherapeutic outcomes. The authors also highlighted the need for rigorous preclinical and clinical validation of these strategies (Chen et al., 2025). Jin et al. (2024) integrated the transcriptomic profiles with gut microbiome data to colorectal cancer. Based on their analysis they classified colorectal cancer into two biologically and clinically distinct tumor subtypes and constructed a risk score model. The one group, marked by favorable prognosis, in contrasts to another group, which harbors a richer gut microbiota and poorer outcomes. The authors risk-scoring model effectively stratifies survival and links microbial composition to immune microenvironment features and therapeutic sensitivity. Distinct taxa including Robiginitomaculum and Myxococcus in the low-risk group, and Sutterella and Zymomonas in the high-risk group emerge as potential biomarkers. This work represents a meaningful step toward the critical importance of personalized treatment. A mendelian randomization study investigates whether gut microbes can causally influence the risk of ovarian cancer through metabolic changes. Using large‐scale Genome-Wide Association Study (GWAS) datasets for gut microbiota, blood metabolites, and ovarian cancer, the authors identify turicibacter sp001543345 as a protective player. Its presence appears to affect lipid metabolism by (1) lowering free cholesterol in small HDL and raising saturated fatty acid ratios to total fatty acids, (2) increasing total cholesterol and cholesteryl esters to total lipids ratio in very‐small VLDL particles changes that collectively reduce cancer risk. Additionally, they mapped the genetic-microbial-metabolic chain that pinpoints lipoprotein subclasses and fatty acid ratios as key mediators. Such specificity suggests a future where microbial profiling and targeted lipid modulation could form part of ovarian cancer prevention strategies. By bridging genetics, microbiology, and lipid biochemistry, the study offers a compelling glimpse of precision cancer prevention grounded in the microbiome (Zhang et al., 2024). Gu et al., (2024) use mendelian randomization to show a causal link between specific oral bacteria and CRC risk using data from two large east Asian databanks including China national gene bank and biobank Japan. Using multi-omics approach, they identify 19 taxa that exhibit strong causal associations, with some such as RUG343 appearing protective and others like HOT-345_umgs_976 and W5053_sp000467935_mgs_712 increasing susceptibility. Single-cell RNA sequencing reveals that high-risk microbial profiles are associated with activation of JAK-STAT signaling and tyrosine metabolism in tumor-adjacent endothelial cells. These findings suggest that oral microbes may influence CRC development through metabolic and inflammatory pathways. They performed in silico drug screening and predicted potential therapeutic agents, including menadione sodium bisulfite and raloxifene, that could target these mechanisms and interrupt the microbe driven pathways. This integrated genetic, cellular, and drug-prediction approach opens new possibilities for CRC prevention and treatment. In a study, Han et al., (2024) unfold the complexity of how shifts in vaginal...

Dialysis-dependent chronic kidney disease (DD-CKD), a severe form of end-stage renal disease (ESRD), currently affects more than three million patients globa... Dialysis-dependent chronic kidney disease (DD-CKD), a severe form of end-stage renal disease (ESRD), currently affects more than three million patients globa...

Sex differences play a fundamental role in cancer incidence, progression, and treatment response, yet their influence remains underexplored in many aspects of oncology. Emerging research suggests that biological factors such as sex hormones, genetic variations, immune system differences, and metabolic pathways contribute to distinct tumor behaviors and therapeutic outcomes between males and females. Understanding these disparities is critical for advancing precision medicine and improving patient care. This special issue, Advancements in the Heterogeneity of Sex for Tumors, brings together ten cutting-edge studies that investigate the impact of sex on cancer biology across a range of malignancies. These investigations examine molecular mechanisms, prognostic markers, and therapeutic targets, revealing how sex affects tumor initiation, progression, immune responses, and treatment resistance, paving the way for personalized therapies.The first review published by Zhu and Zhao (2024), their review explores the influence of sex on bladder cancer, from incidence to biology and outcomes. They asses risk factors like smoking, occupational exposures, and genetic mutations, alongside sex-based differences in cancer development. They provide comprehensive insights into the roles of hormones, chromosomes, metabolism, and the microbiome, while also highlighting gender gaps in diagnosis and prognosis. Their work underscores the need for more research and sex-specific treatments to improve care for all patients. Li et al. (2024) analyze cutaneous melanoma using TCGA and GEO data, integrating mutation, clinical, and single-cell sequencing to identify key genes. They developed a prognostic model using LASSO, linking genes to immune responses through functional and immunological analyses. They showed GMR6's role in melanoma cell proliferation, invasion, and migration. These findings identify potential therapeutic targets, offering new avenues to improve patient outcomes in cutaneous melanoma, particularly through targeting GMR6-mediated mechanisms.A mini review published by Su et al., 2024 explores gender differences in hepatocellular carcinoma, emphasizing on sex hormones, genetics, and environmental factors. They highlight the liver's sexual dimorphism and gender-specific risks like alcohol and obesity in cancer development. The review explores molecular mechanisms, including androgen and estrogen signaling, influencing tumor biology; and highlighting the need for genderspecific research to improve diagnostics, treatment precision, and personalized therapies, aiming to enhance outcomes for liver cancer patients. 2024) investigate AIB1's role in endometrial cancer, focusing on its impact on aerobic glycolysis and tumor progression. AIB1 is linked to poor prognosis and identified as a potential therapeutic target. Using cell lines and mouse models, researchers confirmed AIB1's high expression and its role in tumor proliferation and invasion. Mechanistically, AIB1 is acetylated by PCAF, binds to c-myc, and regulates glycolysisrelated genes. These findings suggest targeting AIB1-mediated glycolysis could offer a novel strategy for treating estrogen-dependent endometrial cancer, advancing personalized therapies.In another study Xia et al., 2024 investigated the chromatin accessibility in peripheral blood mononuclear cells (PBMCs) of breast cancer patients to assess its diagnostic and prognostic potential. Using ATAC sequencing and bioinformatics analysis, they identified 1,906 differentially accessible regions and 1,632 differentially expressed genes. Nine key genes (e.g., JUN, CDC42, TRIB1) and five transcription factors (NFY, Sp2, ELK1) were linked to breast cancer progression. The findings suggest chromatin accessibility in PBMCs as a promising biomarker for early detection and therapeutic innovation in breast cancer. 2024) investigate BYL-719, a PI3K p110α inhibitor, for targeting breast cancer stem cells (BCSCs) and overcoming drug resistance. Using a 3D mammosphere model, they found BYL-719 inhibits BCSC proliferation, stemness, and epithelial-tomesenchymal transition (EMT). The drug suppresses key pathways like PI3K/AKT/mTOR, Notch, JAK-STAT, and MAPK/ERK, which regulate tumor microenvironment dynamics. They demonstrated that BYL-719 overcomes resistance in eribulin-resistant breast cancer cells. These results suggest combining BYL-719 with other therapies could enhance breast cancer treatment strategies. 2024) explore cell communication in hepatocellular carcinoma (HCC) using single-cell sequencing and clustering analysis. They identified malignant and cancerassociated fibroblast subpopulations, emphasizing SPP1-mediated interactions. Two clusters, C1 and C2, were distinguished, with C1 showing higher cytotoxicity and invasion. A gene risk model revealed increased immune pathway activity in C1, while high-risk scores correlated with poorer prognosis. They showed that ABCA1 promotes HCC progression by enhancing proliferation, invasion, and migration while reducing apoptosis. These findings provide critical insights into HCC pathogenesis and prognosis.Hong et al. ( 2025) investigated WNT signaling genes in melanoma, identifying 19 prognostic-related genes and developing a 13-gene model using LASSO regression. Key findings linked CSNK1E and RAC3 to epithelial-to-mesenchymal transition and immune evasion. They identified role of CSNK1E in melanoma progression via the TGF-β pathway. These results suggest targeting CSNK1E and WNT/TGF-β pathways could enhance melanoma treatment and address therapy resistance. Wang et al. (2025) investigated inflammatory gene expression in epithelial ovarian cancer and its role in immunotherapy resistance. Transcriptome analysis revealed two inflammatory gene patterns, differing in immune infiltration, prognosis, and treatment response. The high-risk group showed elevated M2 macrophage infiltration, increased tumor stemness, poorer prognosis, and reduced...