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Results The AUC of the Faster RCNN operating system was 0.93, and the recognition accuracies for T2, T3, and T4 were 90, 93, and 95%, respectively. The time required to automatically recognize a single image was 0.2 s, while the interpretation time of an imaging expert was ~10 s. Conclusion In enhanced CT images of gastric cancer before treatment, the application of Faster RCNN to diagnosis the T stage of gastric cancer has high accuracy and feasibility.Background No consensus exists regarding the superiority of either of the two types of gastrointestinal anastomosis, which are isoperistaltic and antiperistaltic. This study aimed to compare the clinical outcomes between isoperistaltic and antiperistaltic anastomoses after total laparoscopic distal gastrectomy (TLDG) in patients with gastric cancer. Methods We retrospectively reviewed the medical records of patients with gastric cancer who underwent TLDG with Billroth II anastomosis between January 2014 and December 2018. The patients were divided into two groups according to the peristaltic direction of gastrointestinal anastomosis after TLDG. One group underwent isoperistaltic anastomosis (Iso group), and the other underwent antiperistaltic anastomosis (Anti group). Clinical outcomes were compared between the groups. Results Of the 148 patients who underwent TLDG with Billroth II anastomosis, 124 were included in the Iso group and 24 were included in the Anti group. The Anti and Iso groups showed no significant difference with regard to the incidence of internal hernia (0.0 vs. 6.5%, respectively; p = 0.355). The incidence of bile reflux was more frequent in the Iso group than in the Anti group (p = 0.010), but food stasis was more common in the Anti group than in the Iso group (p = 0.006). Conclusion In gastric cancer patients who underwent TLDG in which postoperative adhesion was minimized, antiperistaltic anastomosis may have created a physiologic barrier in gastrointestinal continuity. However, a large-scale study is necessary to validate the relationship between the digestive stream and the peristaltic direction.New therapeutic strategies and paradigms are direly needed for the treatment of cancer. While the surgical removal of tumors is favored in most cancer treatment plans, resection options are often limited based on tumor localization. Over the last two decades, multiple tumor ablation strategies have emerged as promising stand-alone or combination therapeutic options for patients. These strategies are often employed to treat tumors in areas where surgical resection is not possible or where chemotherapeutics have proven ineffective. The type of cell death induced by the ablation modality is a critical aspect of therapeutic success that can impact the efficacy of the treatment and systemic anti-tumor immune system responses. Electroporation-based ablation technologies include electrochemotherapy, irreversible electroporation, and other modalities that rely on pulsed electric fields to create pores in cell membranes. These pores can either be reversible or irreversible depending on the electric field parameters and can induce cell death either alone or in combination with a therapeutic agent. click here However, there have been many controversial findings among these technologies as to the cell death type initiated, from apoptosis to pyroptosis. As cell death mechanisms can impact treatment side effects and efficacy, we review the main types of cell death induced by electroporation-based treatments and summarize the impact of these mechanisms on treatment response. We also discuss potential reasons behind the variability of findings such as the similarities between cell death pathways, differences between cell-types, and the variation in electric field strength across the treatment area.Epithelial-to-mesenchymal transition (EMT) is one of the important underlying molecular mechanisms for most types of cancers including bladder cancer. The precise underlying molecular mechanism in EMT-mediated bladder cancer progression is far from completed. LSD1, a histone lysine-specific demethylase, is known to promote cancer cell proliferation, metastasis, and chemoresistance. We found in this study that LSD1 is highly upregulated in bladder cancer specimens, especially those underwent chemotherapy, and the elevated levels of LSD1 are highly associated with bladder cancer grades, metastasis status, and prognosis. Inhibiting or knockdown LSD1 repressed not only EMT process but also cancer progression. Mechanistically, LSD1 complexes with β-catenin to transcriptionally upregulate LEF1 and subsequently enhances EMT-mediated cancer progression. More importantly, LSD1 specific inhibitor GSK2879552 is capable of repressing tumor progression in patient-derived tumor xenograft. These findings altogether suggest that LSD1 can serve as not only a prognostic biomarker but also a promising therapeutic target in bladder cancer treatment.Breast carcinomas are characterized by anomalous gene regulatory programs. As is well-known, gene expression programs are able to shape phenotypes. Hence, the understanding of gene co-expression may shed light on the underlying mechanisms behind the transcriptional regulatory programs affecting tumor development and evolution. For instance, in breast cancer, there is a clear loss of inter-chromosomal (trans-) co-expression, compared with healthy tissue. At the same time cis- (intra-chromosomal) interactions are favored in breast tumors. In order to have a deeper understanding of regulatory phenomena in cancer, here, we constructed Gene Co-expression Networks by using TCGA-derived RNA-seq whole-genome samples corresponding to the four breast cancer molecular subtypes, as well as healthy tissue. We quantify the cis-/trans- co-expression imbalance in all phenotypes. Additionally, we measured the association between co-expression and physical distance between genes, and characterized the ratio of intra/inter-cytoband interactions per phenotype. We confirmed loss of trans- co-expression in all molecular subtypes. We also observed that gene cis- co-expression decays abruptly with distance in all tumors in contrast with healthy tissue. We observed co-expressed gene hotspots, that tend to be connected at cytoband regions, and coincide accurately with already known copy number altered regions, such as Chr17q12, or Chr8q24.3 for all subtypes. Our methodology recovered different alterations already reported for specific breast cancer subtypes, showing how co-expression network approaches might help to capture distinct events that modify the cell regulatory program.
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