Search

An intricate relationship exists, and interactions occur between the gut microbiota and colorectal cancer (CRC). Recent studies have indicated that inflammatory reactions stimulated by Fusobacterium nucleatum (Fn) lead to the development of CRC. Radical surgery combined with adjuvant chemotherapy is the primary treatment approach for most CRC patients. This study was designed to evaluate the abundance of Fn as part of the gut microbiota in patients with CRC compared to healthy individuals and to assess the effect of the gut microbiota Fn on patients undergoing adjuvant chemotherapy and those experiencing CRC relapse. There were 201 participants, comprising 50 healthy controls and 151 CRC patients. Stool samples were collected from three CRC groups (postoperatively, chemotherapy and relapse), and the fourth was the healthy control group. The amount of Fn in each sample was analyzed using quantitative loop-mediated isothermal amplification-phenol red (QLAMP-PhR), a novel biomolecular method that targets regions encoding the specific Fn FadA gene. Compared with healthy control stool samples, the Fn levels were significantly elevated in all CRC patient groups (P < 0.001), and it was significantly more frequent in the CRC relapse patients (group C) (P < 0.001). In addition, Fn abundance increased significantly in the distal colon compared to the proximal colon (P < 0.001). Both CRC relapse and chemotherapy exert significant reciprocal effects on the gut microbiota Fn of CRC patients. Microbiota-based intervention may be beneficial for patients during postoperative care, especially in CRC relapsing cases. Registration: This study of the clinical trial has been registered in the ISRCTN registry with study registration number ISRCTN53358464. https://www.isrctn.com/ISRCTN53358464 [ABSTRACT FROM AUTHOR]

Copyright of Basic & Clinical Medicine is the property of Editorial Office of Basic & Clinical Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Abstract: Wilms tumors (WT) with WT1 mutations do not respond well to preoperative chemotherapy by volume reduction, suggesting resistance to chemotherapy. The histologic pattern of this tumor subtype indicates an intrinsic mesenchymal differentiation potential. Currently, it is unknown whether cytotoxic treatments can induce a terminal differentiation state as a direct comparison of untreated and chemotherapy‐treated tumor samples has not been reported so far. We conducted gene expression profiling of 11 chemotherapy and seven untreated WT1‐mutant Wilms tumors and analyzed up‐ and down‐regulated genes with bioinformatic methods. Cell culture experiments were performed from primary Wilms tumors and genetic alterations in WT1 and CTNNB1 analyzed. Chemotherapy induced MYF6 165‐fold and several MYL and MYH genes more than 20‐fold and repressed many genes from cell cycle process networks. Viable tumor cells could be cultivated when patients received less than 8 weeks of chemotherapy but not in two cases with longer treatments. In one case, viable cells could be extracted from a lung metastasis occurring after 6 months of intensive chemotherapy and radiation. Comparison of primary tumor and metastasis cells from the same patient revealed up‐regulation of RELN and TBX2, TBX4 and TBX5 genes and down‐regulation of several HOXD genes. Our analyses demonstrate that >8 weeks of chemotherapy can induce terminal myogenic differentiation in WT1‐mutant tumors, but this is not associated with volume reduction. The time needed for all tumor cells to achieve the terminal differentiation state needs to be evaluated. In contrast, prolonged treatments can result in genetic alterations leading to resistance. [ABSTRACT FROM AUTHOR]

Copyright of Progress in Modern Biomedicine is the property of Publishing House of Progress in Modern Biomedicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)