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- W4385071457 endingPage "188959" @default.
- W4385071457 startingPage "188959" @default.
- W4385071457 abstract "More recently, microbiota was detected in several tumorous tissues including multiple myeloma (MM), but the roles of which is still under-studied as paucity of research on tumor biology. Moreover, we also detected the presence of microbiota in the bone marrow of patients with MM by 2bRAD-M sequencing technology, which is an incurable hematological malignancy characterized by accumulation of abnormal plasma cells in the bone marrow. However, the roles of intratumor microbiota in tumor disease remains poorly understood. In this review, we critically reviewed recent literature about microbiota in the tumorigenesis and progression of MM. Importantly, we proposed that the emergence of microbiota in the microenvironment of multiple myeloma may be attributed to microbial dysbiosis and impaired intestinal barrier, due to the increased prevalence of MM in patients with obesity and diabetes, of which the characteristic phenotype is gut microbial dysbiosis and impaired intestinal barrier. When the intestinal barrier is damaged, dysbiotic microbiota and their metabolites, as well as dysregulated immune cells, may participate in the reshaping of the local immune microenvironment, and play pivotal roles in the tumorigenesis and development of multiple myeloma, probably by migrating to the bone marrow microenvironment from intestine. We also discuss the emerging microbiological manipulation strategies to improve long-term outcomes of MM, as well as the prospective of the state-of-the-art techniques to advance our knowledge about the biological implication in the microbiome in MM." @default.
- W4385071457 created "2023-07-23" @default.
- W4385071457 creator A5003787100 @default.
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- W4385071457 creator A5090038131 @default.
- W4385071457 date "2023-09-01" @default.
- W4385071457 modified "2023-09-23" @default.
- W4385071457 title "Intratumor microbiota: Occult participants in the microenvironment of multiple myeloma" @default.
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