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Interaction between gut microbiota and immune system. Gut microbiota metabolites and dietary factors constitute the main antigen load of the GIT. Macrophages (CXCR1 +) and dendritic cells (DCs) are stimulated, and T regulatory (Treg) cells are activated by metabolic products such as short-chain fatty acid (SCFA). Follicular T cells activate B cells, inducing the production of IgA antibodies.
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Gut microbiota substantially impacts pathogenic and normal immune responses and is associated with common chronic diseases. Moreover, it has a considerable effect on the efficacy of cancer therapy. Variant gut microbiota is linked with immune checkpoint inhibitors, chemo drugs, and radiotherapy resistance. Therefore, a comprehensive interpretation...
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Cancer remains a significant global health concern, and understanding factors that regulate cancer development is important. The microbiome, with its potential role in cancer development, progression, and treatment, has garnered increasing attention in recent years. The cervicovaginal and gastrointestinal microbiomes in females constitute complex b...
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... Equally, gut dysbiosis may impair anti-tumor immunity by altering the balance of regulatory and pro-inflammatory immune cells, thereby promoting brain tumor progression [9]. Furthermore, recent studies have demonstrated that gut microbiota can impact the efficacy of brain cancer therapies, including immunotherapy and chemotherapy [10]. Certain bacterial species enhance the responsiveness to immune checkpoint inhibitors, while others contribute to resistance by modulating host immune pathways [11]. ...
The gut–brain–cancer axis represents a novel and intricate connection between the gut microbiota, neurobiology, and cancer progression. Recent advances have accentuated the significant role of gut microbiota metabolites in modulating systemic processes that influence both brain health and tumorigenesis. This paper explores the emerging concept of metabolite-mediated modulation within the gut–brain–cancer connection, focusing on key metabolites such as short-chain fatty acids (SCFAs), tryptophan derivatives, secondary bile acids, and lipopolysaccharides (LPS). While the gut microbiota’s impact on immune regulation, neuroinflammation, and tumor development is well established, gaps remain in grasping how specific metabolites contribute to neuro–cancer interactions. We discuss novel metabolites with potential implications for neurobiology and cancer, such as indoles and polyamines, which have yet to be extensively studied. Furthermore, we review preclinical and clinical evidence linking gut dysbiosis, altered metabolite profiles, and brain tumors, showcasing limitations and research gaps, particularly in human longitudinal studies. Case studies investigating microbiota-based interventions, including dietary changes, fecal microbiota transplantation, and probiotics, demonstrate promise but also indicate hurdles in translating these findings to clinical cancer therapies. This paper concludes with a call for standardized multi-omics approaches and bi-directional research frameworks integrating microbiome, neuroscience, and oncology to develop personalized therapeutic strategies for neuro-cancer patients.
... Some gut microbes also produce genotoxic metabolites that can damage DNA, leading to mutations, chromosomal instability, and eventually cancer [60]. Such genotoxic metabolites are often overproduced in dysbiosis, heightening the risk of cancer through direct DNA damage and impairing the body's ability to detoxify harmful substances [61]. In sum, dysbiosis can contribute to cancer development through a multitude of mechanisms, including immune dysregulation, hormonal imbalances, and direct genetic damage. ...
... Some gut microbes also produce genotoxic metabolites that can da age DNA, leading to mutations, chromosomal instability, and eventually cancer [60]. Su genotoxic metabolites are often overproduced in dysbiosis, heightening the risk of can through direct DNA damage and impairing the body's ability to detoxify harmful s stances [61]. In sum, dysbiosis can contribute to cancer development through a multitu of mechanisms, including immune dysregulation, hormonal imbalances, and direct netic damage. ...
The human microbiome, which encompasses microbial communities and their genetic material, significantly influences health and disease, including cancer. The urogenital microbiota, naturally present in the urinary and genital tracts, interact with factors such as age, lifestyle, and health conditions to affect homeostasis and carcinogenesis. Studies suggest that alterations in this microbiota contribute to the development and progression of genitourinary cancers, emphasizing the concept of oncobiome, which refers to microbial genetic contributions to cancer. Similarly, gut microbiota can influence hormone levels and systemic inflammation, impacting cancers such as cervical and prostate cancer. Advanced studies indicate that microbial communities in genitourinary cancers have distinct profiles that may serve as diagnostic biomarkers or therapeutic targets. Dysbiosis of the urinary microbiota correlates with bladder and kidney cancer. Additionally, gut microbiota influence the effectiveness of cancer treatments. However, further research is necessary to clarify causality, the role of microbial metabolites, and hormonal regulation. The aim of this review is to understand that these dynamics present opportunities for innovative cancer diagnostics and therapies, highlighting the need for integration of microbiology, oncology, and genomics to explore the role of microbiota in genitourinary cancers. For this, a comprehensive search of relevant databases was conducted, applying specific inclusion and exclusion criteria to identify studies examining the association between microbiota and urogenital cancers. Research into the mechanisms by which microbiota influence urogenital cancers may pave the way for new diagnostic and therapeutic approaches, ultimately improving patient outcomes.
With nearly half of colorectal cancer (CRC) patients diagnosed at advanced stages where surgery alone is insufficient, chemotherapy remains a cornerstone for this cancer treatment. To prevent infections and improve outcomes, antibiotics are often co-administered. However, chemotherapeutic interactions with the gut microbiota cause significant non-selective toxicity, affecting not only tumor and normal epithelial cells but also the gut microbiota. This toxicity triggers the bacterial SOS response and loss of microbial diversity, leading to bacterial mutations and dysbiosis. Consequently, pathogenic overgrowth and systemic infections increase, necessitating broad-spectrum antibiotics intervention. This review underscores how prolonged antibiotic use during chemotherapy, combined with chemotherapy-induced bacterial mutations, creates selective pressures that drive de novo antimicrobial resistance (AMR), allowing resistant bacteria to dominate the gut. This compromises the treatment efficacy and elevates the mortality risk. Restoring gut microbial diversity may mitigate chemotherapy-induced toxicity and improve therapeutic outcomes, and emerging strategies, such as fecal microbiota transplantation (FMT), probiotics, and prebiotics, show considerable promise. Given the global threat posed by antibiotic resistance to cancer treatment, prioritizing antimicrobial stewardship is essential for optimizing antibiotic use and preventing resistance in CRC patients undergoing chemotherapy. Future research should aim to minimize chemotherapy’s impact on the gut microbiota and develop targeted interventions to restore microbial diversity affected during chemotherapy.
