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Current pharmaceutical biotechnology. 2025 Apr 18. doi: 10.2174/0113892010356542250407143257 Q32.62025

Microbial Influences: The Microbiome's Impact on Pancreatic Cancer Development and Progression

微生物影响:肠道微 biome 对胰腺癌发生和发展的作用 翻译改进

Md Fakruddin  1, Zarifah Chowdhury  1, Suraiya Nasrin Suprova  1, Bakhtiar Ul Islam  1, Jinath Sultana Jime  1, Nayeema Bulbul  1, Mohammad Badrul Anam  2, Shahnewaj Bin Mannan  3, Md Asaduzzaman Shishir  4

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作者单位

  • 1 Department of Biochemistry & Microbiology, North South University, Bashundhara, Dhaka-1229, Bangladesh.
  • 2 Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, New York-13210.206.
  • 3 H Lee Moffitt Cancer Center and Research Institute, Tampa, Florida, USA.
  • 4 Department of Microbiology, Dhaka International University, Badda, Dhaka, Bangladesh.
  • DOI: 10.2174/0113892010356542250407143257 PMID: 40257025

    摘要 中英对照阅读

    Pancreatic ductal adenocarcinoma (PDAC) presents significant challenges due to its dense stromal environment, which impedes treatment efficacy. Recent molecular and phenotypic analyses have enhanced our understanding of PDAC, driving the development of targeted therapies. Emerging research highlights the crucial role of the pancreatic tumor microbiome in PDAC initiation and progression. However, the specific mechanisms influencing the tumor microenvironment (TME) and systemic immunity remain incompletely understood. Studies have elucidated various genetic mutations, signaling pathways, and cellular interactions driving PDAC progression, aiding the development of targeted therapies. Despite these advances, overall survival rates for PDAC patients remain low, necessitating novel therapeutic strategies. Therapeutic strategies targeting the microbiome hold significant potential. Therapeutic strategies aimed at modulating microbiomes demonstrate significant potential for treating diseases and enhancing human well-being. Early research indicates that manipulating the microbiome could alter the TME to enhance the efficacy of existing treatments and lead to new therapeutic modalities. Modulating microbiomes might improve the delivery and effectiveness of chemotherapeutic agents or sensitize the tumor to immunotherapy, potentially revolutionizing PDAC treatment paradigms. Microbes can indirectly contribute to pancreatic cancer by inducing chronic inflammation and immune dysregulation. Microbes create a pro-inflammatory environment conducive to cancer development. This persistent inflammation can lead to genetic mutations and a suppressed immune response, fostering an environment where cancer cells can thrive. This review synthesizes current evidence on how the microbiome influences PDAC development and progression, emphasizing its potential for early disease detection and novel therapeutic strategies. Early detection, particularly in premalignant conditions such as chronic pancreatitis and intraductal papillary mucinous neoplasm (IPMN), is crucial for improving patient outcomes through timely intervention.

    Keywords: Chronic inflammation; Early detection; Immunotherapy; Microbiome; Pancreatic ductal adenocarcinoma (PDAC); Targeted therapies.; Tumor microenvironment (TME).

    Keywords:microbial influences; microbiome impact; pancreatic cancer development

    胰腺导管腺癌(PDAC)由于其密集的间质环境,给治疗带来了重大挑战。最近的分子和表型分析增强了我们对 PDAC 的理解,并推动了靶向疗法的发展。新兴的研究强调了胰腺肿瘤微生物组在 PDAC 发病和进展中的关键作用。然而,影响肿瘤微环境(TME)和全身免疫的具体机制仍不完全清楚。已有研究阐明了驱动 PDAC 进展的各种基因突变、信号通路和细胞相互作用,这有助于靶向疗法的发展。尽管取得了这些进步,PDAC 患者的总体生存率仍然很低,需要新的治疗策略。针对微生物组的治疗方法具有很大的潜力。旨在调节微生物组的治疗方法在治疗疾病和提高人类健康方面显示出巨大的潜力。早期研究表明,通过操纵微生物组可以改变 TME,从而增强现有疗法的效果,并可能带来新的治疗模式。调节微生物组可能会改善化疗药物的递送和有效性,或使肿瘤对免疫疗法敏感化,这有可能彻底革新 PDAC 的治疗方法。微生物可以通过诱导慢性炎症和免疫失调间接导致胰腺癌。微生物创造了一个有利于癌症发展的促炎环境。这种持续性炎症可能导致基因突变,并抑制免疫反应,为癌细胞的生长提供有利条件。本综述综合了当前有关微生物组如何影响 PDAC 发展和进展的证据,强调其在早期疾病检测和新治疗策略方面的潜力。对于慢性胰腺炎和导管内乳头状黏液性肿瘤(IPMN)等癌前病变中的早期检测尤为重要,这可以通过及时干预来改善患者的预后。

    关键词:慢性炎症;早期检测;免疫疗法;微生物组;胰腺导管腺癌(PDAC);靶向治疗;肿瘤微环境(TME)。

    关键词:微生物影响; 微生态影响; 胰腺癌发生发展

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    期刊名:Current pharmaceutical biotechnology

    缩写:CURR PHARM BIOTECHNO

    ISSN:1389-2010

    e-ISSN:1873-4316

    IF/分区:2.6/Q3

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