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Evidence suggests that gut microbiota composition and microbial metabolites can affect the effectiveness and adverse effects of immunotherapy, chemotherapy, and radiotherapy, yet links to targeted agents remain insufficiently clarified. This review connects gut microbiota and metabolites such as butyrate, propionate, and ursodeoxycholic acid with regulation of tumor-related signaling, contrasting potential pro-tumor influences from deoxycholic acid, lipopolysaccharide, and trimethylamine N-oxide.",{"@graph":14,"@context":73},[15,34,56],{"@type":16,"itemListElement":17},"BreadcrumbList",[18,23,27,31],{"item":19,"name":20,"@type":21,"position":22},"https://docshare.wps.com","Home","ListItem",1,{"item":24,"name":25,"@type":21,"position":26},"https://docshare.wps.com/document/","Document",2,{"item":28,"name":29,"@type":21,"position":30},"https://docshare.wps.com/document/research-report/","Research & 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are EGFR, VEGF, and KRAS important in targeted cancer therapy?","Question",{"text":63,"@type":64},"They are key oncogenic targets that guide the development of targeted agents aimed at controlling tumor growth through specific receptors and signaling pathways.","Answer",{"name":66,"@type":61,"acceptedAnswer":67},"How can gut microbiota influence the effectiveness of targeted therapies?",{"text":68,"@type":64},"Gut microbiota and their metabolites can interact with oncogenic pathways, modulating anti-tumor effects and potentially shaping both therapeutic responses and side effects.",{"name":70,"@type":61,"acceptedAnswer":71},"What roles may different gut microbial metabolites play in tumor progression?",{"text":72,"@type":64},"Some metabolites such as butyrate, propionate, and ursodeoxycholic acid are discussed as modulators of anti-tumor effects, while deoxycholic acid, lipopolysaccharide, and trimethylamine N-oxide may exert pro-tumor 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10.20892/j.issn.2095-3941.2024.0320  \nREVIEW  \nModulation of gut microbiota in targeted cancer therapy: insights on the EGFR/VEGF/KRAS pathways  \nLi Gong1,2, Shixue Yang3, Junli Huang2, Yongsheng Li1  \n1 Department of Phase I Clinical Trial Ward, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing 400030, China; 2 Key Laboratory of Biorheological Science and Technology of Ministry of Education, Bioengineering College, Chongqing University, Chongqing 400044, China; 3 Department of Medical Oncology, Chongqing Key Laboratory of Translational Research for Cancer Metastasis and Individualized Treatment, Chongqing University Cancer Hospital, Chongqing 400030, China  \n\n| ABSTRACT | The rise in the incidence of cancer globally has led to a heightened interest in targeted therapies as a form of anticancer treatment. Key oncogenic targets, including epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and kirsten rat sarcoma viral oncogene homologue (KRAS), have emerged as focal points in the development of targeted agents. Research has investigated the impact of gut microbiota on the efficacy of various anticancer therapies, such as immunotherapy, chemotherapy, and radiotherapy. However, a notable gap exists in the literature regarding the relationship between gut microbiota and targeted agents. This review emphasizes how specific gut microbiota and gut microbiota metabolites, including butyrate, propionate, and ursodeoxycholic |\n| --- | --- |\n| KEYWORDS | acid, interact with oncogenic pathways to modulate anti-tumor effects. Conversely, deoxycholic acid, lipopolysaccharide, and trimethylamine n-oxide may exert pro-tumor effects. Furthermore, modulation of the gut microbiota influences glucose and lipid metabolism, thereby enhancing the response to anti-KRAS agents and addressing diarrhea induced by tyrosine kinase inhibitors. By elucidating the connection between gut microbiota and the EGFR/VEGF/KRAS pathways, this review provides valuable insights for advancing targeted cancer therapy and optimizing treatment outcomes in clinical settings.\u003Cbr>Gut microbiota; metabolites; targeted therapy; tumorigenesis pathway; EGFR; VEGF; KRAS |\n\nIntroduction  \nCancer represents a significant public health challenge globally with the rapid advance of various anti-cancer pharmacotherapies, including chemotherapy, targeted therapy, and immunotherapy. Targeted therapy, which specifically aims to eliminate tumor cells, has emerged as a valuable treatment option for many cancer patients1. The development of targeted agents focuses on the regulation of specific receptors, signal transduction pathways, neovascularization, and critical targets,  \nCorrespondence to: Junli Huang and Yongsheng Li  \nE-mail: [huangjunli@cqu.edu.cn](huangjunli@cqu.edu.cn) and [lys@cqu.edu.cn](lys@cqu.edu.cn)[ ](lys@cqu.edu.cn)ORCID ID: [https://orcid.org/0000-0002-4583-4637](https://orcid.org/0000-0002-4583-4637)  \nand [https://orcid.org/0000-0003-2175-9449](https://orcid.org/0000-0003-2175-9449)  \nReceived August 4, 2024; accepted November 4, 2024;  \npublished online November 25, 2024. Available [at www.cancerbiomed.org](at www.cancerbiomed.org)  \n©2024 The Authors. Creative Commons Attribution-NonCommercial 4.0 International License  \nsuch as the epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), and kirsten rat sarcoma viral oncogene homologue (KRAS)2,3. Nevertheless, resistance to targeted agents poses a significant clinical challenge that adversely affects treatment response and patient prognosis1. Mechanisms contributing to drug resistance include DNA damage repair, altered signaling pathways, abnormal metabolism, and the tumor microenvironment3. The limitations of single-target drugs in cancer treatment arise from the complexity of resistance mechanisms, highlighting the necessity for e","cbCaidohMpNOOQoK","https://ap.wps.com/l/cbCaidohMpNOOQoK","pdf",1720730,15,"English","# Introduction\n## Targeted therapy and major oncogenic targets\n## Gut microbiota as a regulator of cancer outcomes\n# Gut microbiota impacts on targeted therapy\n## Microbial metabolites and oncogenic pathway modulation\n## Effects on anti-tumor activity versus pro-tumor mechanisms\n# EGFR/VEGF/KRAS pathway connections\n## Clinical relevance for therapy optimization","[{\"question\":\"Why are EGFR, VEGF, and KRAS important in targeted cancer therapy?\",\"answer\":\"They are key oncogenic targets that guide the development of targeted agents aimed at controlling tumor growth through specific receptors and signaling pathways.\"},{\"question\":\"How can gut microbiota influence the effectiveness of targeted therapies?\",\"answer\":\"Gut microbiota and their metabolites can interact with oncogenic pathways, modulating anti-tumor effects and potentially shaping both therapeutic responses and side effects.\"},{\"question\":\"What roles may different gut microbial metabolites play in tumor progression?\",\"answer\":\"Some metabolites such as butyrate, propionate, and ursodeoxycholic acid are discussed as modulators of anti-tumor effects, while deoxycholic acid, lipopolysaccharide, and trimethylamine N-oxide may exert pro-tumor effects.\"}]","Modulation of gut microbiota in targeted cancer therapy - insights on the EGFR/VEGF/KRAS pathways | PDF",1790000126,38]