Notes

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Furthermore, high CHODL expression in CRC was a predictor of improved survival, though CHODL hypermethylation was a poor prognostic factor for CRC patients, especially those with early-stage CRC. Significance CHODL promoter hypermethylation silences CHODL expression in CRC, and CHODL suppresses CRC tumorigenesis. CHODL methylation and expression levels can be used as potential markers to evaluate the prognosis of CRC patients. © The author(s).Background It has been rarely reported whether 18F-fluorodeoxyglucose (18F-FDG) uptake in colorectal cancer cells is associated with the expression of PD-L1. We performed a clinical pathology study to evaluate PD-L1 expression in patients undergoing surgical resection of colorectal cancer with preoperative 18F-FDG PET/CT imaging, with the aim of predicting the response of CRC patients to immune checkpoint inhibitors. Material and Methods A retrospective analysis of patients with CRC who underwent FDG-PET imaging before surgery was performed to measure the parameters of FDG-PET imaging the maximum standardized uptake value (SUVmax), the metabolic tumor volume (MTV), and the total lesion glycolysis (TLG) were evaluated to determine whether each parameter was associated with clinical pathology. Tumor specimens were subjected to PD-L1 staining by immunohistochemistry. Analysis of whether there is a correlation between PD-L1 expression and 18F-FDG uptake parameters in CRC. Results PD-L1 expression level was significantly correlated with SUVmax, MTV3.0 and TLG3.0. Multivariate analysis showed that PD-L1 and TLG3.0 were independent predictors of poor DFS in patients with CRC (P=0.009; P=0.016), PD-L1 expression is closely related to the patient's lesion (TLG3.0) (P less then 0.01). Conclusion The results of this study indicate that there was a significant correlation between PD-L1 expression and TLG3.0 which suggested that FDG-PET could serve as a noninvasive tool to assess the tumor microenvironment and as a predictor of PD-L1 inhibitor activity to determine the optimal therapeutic strategy for CRC. High PD-L1 expression levels and high TLG3.0 are independent risk factors for DFS differences in CRC patients. © The author(s).Background Nucleolar and spindle-associated protein 1 (NUSAP1) was previously reported to be associated with poor prognosis in multiple cancers. In the present study, we comprehensively investigated the clinicopathological features and potential prognostic value of NUSAP1 in cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC). Methods The expression profiles of the genes were extracted from Gene Expression Omnibus (GEO), The Cancer Genome Atlas (TCGA), International Cancer Genome Consortium (ICGC), Cancer Cell Line Encyclopedia (CCLE), Gene Expression Profiling Interactive Analysis (GEPIA), and The Human Protein Atlas databases. The association between clinicopathological characteristics and NUSAP1 was analyzed using logistic regression in TCGA patients and receiver operating characteristic (ROC) curve analysis for GSE7803, GSE9750, and GSE63514 datasets. The prognostic value of NUSAP1 in TCGA patients was evaluated using the Kaplan-Meier method and Cox regression. Gene set enrichment analay serve as a valuable indicator of poor survival in CESC. © The author(s).Objectives Small-size lung lesions suspected of being cancer are now often being identified on computed tomography. Correspondingly, a new lung cancer staging system has been proposed by the International Association for the Study of Lung Cancer (IASLC), in which the T1 factor and adenocarcinoma are re-subclassified. Previously, we proposed an intraoperative cytological diagnosis and its classification of small-size lung adenocarcinoma, which correlated significantly with clinical malignancy, to be used for selecting the surgical strategy. In the current study, the correlation of our intraoperative cytological classification with the new 8th IASLC classification was investigated. Materials and Methods A total of 139 consecutive small-size lung adenocarcinoma cases were surgically resected from 2000 to 2006 and included in this study. Intraoperative stump imprint cytology using these specimens was performed, and the cases were classified into 5 groups based on our classification. The cytological classification was compared with the IASLC classification and the WHO histopathological grading. Results According to our classification, 32 patients were in Group I, 38 in Group II, 24 in Group III, 27 in Group IV, and 18 in Group V. Compared with the IASLC classification, most of Group I was pTis or pT1mi, and most of Group II was pT1mi or pT1a (p less then 0.001). There was also a significant relationship between lymph node metastasis and our cytological classification (p less then 0.001). The histological patterns according to the WHO classification also had a significant relationship with our classification (p less then 0.001). Conclusion Our cytological classification correlated not only with the T classification, but also with the adenocarcinoma subclassification of the 8th IASLC classification. © The author(s).Cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) has been reported in cancers but its role and potential molecular mechanism in hepatocellular carcinoma (HCC) is unclear. Therefore, we aimed to investigate the clinical value and molecular mechanism of CELSR3 in HCC using an in vitro experiment, a meta-analysis and bioinformatics. The in vitro experiment determined the promoting effect of CELSR3 in the proliferation, invasion, and migration of HCC cells. CELSR3 knockout causes S-phage arrest in HCC cells. Sodium L-lactate supplier CELSR3 can also inhibit the apoptosis of HCC cells. The expression of the CELSR3 gene and protein was significantly elevated in HCC. Elevated CELSR3 was correlated to the bigger tumor size, higher pathological stage, and the worse overall survival of HCC. Methylation analysis revealed that the hypomethylation of CELSR3 regulated by DNMT1, DNMT3A, and DNMT3B may be the underlying mechanism of upregulated CELSR3. Biological enrichment analysis uncovered that the cell cycle, DNA replication, and PI3K-Akt signaling pathways were important pathways regulated by CELSR3 and its co-expressed genes in HCC.
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