Prognostic and Clinicopathological Significance of C-Reactive Protein to Albumin Ratio in Patients with Bile Duct Cancer: A Meta-Analysis.

Recent studies have explored the prognostic role of the C-reactive protein to albumin ratio (CAR) in patients with bile duct cancer (BTC), but the results have been inconsistent. This study aimed to provide insight into the prognostic significance of the CAR in BTC prior to treatment using a meta-analysis. Summarized hazard ratios (HRs) or odds ratios (ORs) and 95% confidence intervals (CIs) were calculated for prognosis and clinicopathological features using fixed or random effects models. Fourteen studies with a total of 1,543 subjects were included in this meta-analysis. Elevated CAR was significantly associated with poor overall survival (HR = 2.17, 95% CI = 1.81-2.60, P < 0.001) and decreased disease-free survival or recurrence-free survival (HR = 2.53, 95% CI = 1.98-3.25, P < 0.001) in BTC. In addition, high CAR was significantly associated with the presence of lymph node metastasis (OR = 1.54, 95% CI = 1.12- 2.13, P = 0.008), bile duct invasion (OR = 2.64, 95% CI = 1.54-4.54, P < 0.001), and tumor stages III-IV (OR = 3.11, 95% CI = 1.05-9.20, P = 0.040). However, there was no significant association between CAR and sex, microvascular invasion, or resection. An elevated CAR was significantly related to worse long-term and short-term survival and advanced clinicopathological features of BTC. CAR could serve as a valuable, noninvasive prognostic marker in patients with BTC.

SOX2 knockdown slows cholangiocarcinoma progression through inhibition of transcriptional activation of lncRNA PVT1.

Cholangiocarcinoma (CCA) has accounted for a high rate of mortality and morbidity in the recent years. Long non-coding RNAs (lncRNAs) play an important role in different cellular environments, including cancer. As such, they have been used as potential targets during CCA therapy. The objective of this study was to investigate the effects of lncRNA PVT1 on CCA and its mechanisms behind lncRNA PVT1 regulation. The interactions among SOX2, lncRNA PVT1, miR-186 and SEMA4D were verified by chromatin immunoprecipitation, RNA immunoprecipitation and dual luciferase reporter gene assay. Gain- and loss-of-function experiments were conducted to explore the modulatory effects of SOX2, lncRNA PVT1, miR-186 and SEMA4D on cell viability, migration and invasion of CCA by CCK-8 and Transwell assays. In vivo effects of lncRNA PVT1 or SEMA4D were studied in a nude mouse model. MiR-186 was poorly expressed while SOX2, lncRNA PVT1 and SEMA4D were highly expressed in CCA cells. SOX2 induced the transcriptional activation of lncRNA PVT1 expression to promote proliferation, migration and invasion of CCA cells. LncRNA PVT1 bound to miR-186 and miR-186 was found to target SEMA4D. The overexpression of lncRNA PVT1 and SEMA4D, as well as the inhibition of miR-186 led to elevated CCA cell proliferation, migration and invasion. In vivo experiments confirmed the inhibitory role of lncRNA PVT1 knockdown or SEMA4D knockdown in CCA. All in all, SOX2 down-regulated miR-186 through the transcriptional activation of lncRNA PVT1, whereas elevating SEMA4D expression, thus promoting the progression of CCA.

LncRNA LINC01061 sponges miR-612 to regulate the oncogenic role of SEMA4D in cholangiocarcinoma.

Cholangiocarcinoma (CCA) is the most usual malignancy of biliary tract, possessing a relatively low overall survival rate due to limited treatment options. Recently, long non-coding RNAs (lncRNAs) have been testified to have marked regulatory impacts on human cancers. The purpose of this paper is to explore the potent regulation mechanism of LINC01061 involved in CCA. Firstly, it was observed that LINC01061 expression was heightened in CCA cell lines, whose knockdown suppressed cell proliferation, induced cell apoptosis and restrained cell migration. Besides, LINC01061 existing in the cytoplasm of CCA cells interacted with miR-612. Moreover, subsequent experiments affirmed that LINC01061 regulated SEMA4D expression by acting as a competing endogenous RNA (ceRNA) of miR-612. At last, rescue assays validated that SEMA4D overexpression restored the repression caused by LINC01061 silence on the biological activities of CCA containing cell proliferation, apoptosis and migration. To sum up, our present exploration demonstrated that LINC01061 sponges miR-612 so as to upregulate SEMA4D expression for the progression of CCA, suggesting an optional promising and effective target for the therapy of patients with CCA.

Bioinformatic analysis the expression and clinical significance of CDRT15 in cholangiocarcinoma using TCGA database.

Cholangiocarcinoma (CCA) is a common and lethal malignant tumor originating from bile duct epithelial cells. Various tumor biomarkers have been used for its clinical screening, such as carbohydrate antigen 19-9 and carcinoembryonic antigen. This study aimed to demonstrate the value of associated genes-CMT1A duplicated region transcript 15 (CDRT15) for prognosis of CCA by integrated bioinformatics analysis. We obtained CDRT15 expression data and clinical information on patients with CCA from The Cancer Genome Atlas database. Then, we processed the data by differentially expressed gene analysis, gene set enrichment analysis, statistical analysis, etc. Gene Ontology enrichment analysis was aimed to explore the function of gene-related proteins. Single-sample gene set enrichment analysis was used to analyze the correlation between CDRT15 and immune cells. Finally, we constructed the nomogram to predict the prognosis of patients with CCA. The analysis of data in The Cancer Genome Atlas database revealed that CDRT15 was overexpressed in CCA tissues. We performed the interrelation analysis of immune infiltration, showing that CDRT15 are mainly associated with the immune/inflammatory response. ROC curve showed that CDRT15 can be a diagnostic marker of CCA. Subsequently, the prognostic analysis showed that the high expression of CDRT15 was correlated with the poor OS, and patients with high CDRT15 expression may have a poor prognosis. CDRT15 is more highly expressed in CCA, thus we identified that CDRT15 could be an efficient biomarker for patients. CDRT15 expression was negatively correlated with prognosis of CCA. CDRT15 may be involved in the immune infiltration process of CCA.

Survival prognosis model for elderly women with epithelial ovarian cancer based on the SEER database.

Objectives: We aimed to analyze the risk factors of elderly women with epithelial ovarian cancer (EOC) using data on the SEER database, and to generate a nomogram model their 1-, 3-, and 5-year prognoses. The resulting nomogram model should be useful for clinical diagnoses and treatment. Methods: We collected clinical data of women older than 70 years with epithelial ovarian cancer (diagnosed on the basis of surgical pathology) from the SEER database including datasets between 2010 and 2019. We randomly grouped the data into two groups (7:3 ratio) using the R language software. We divided the independent prognostic factors obtained by univariate and multi-factor Cox regression analyses into training and validation sets, and we plotted the same independent prognostic factors in a nomogram model of overall survival (OS) at 1, 3, and 5 years. We used the C-index, calibration curve, and area under the curve to validate the nomograms. We further evaluated the model and its clinical applicability using decision curve analyses. Results: We identified age, race, marital status, histological type, AJCC staging, differentiation degree, unilateral and bilateral tumor involvement, number of positive lymph nodes, chemotherapy, surgery, sequence of systemic treatment versus surgery, and time from diagnosis to treatment as independent prognostic factors for elderly women with EOC (P < 0.5). The C-indexes were 0.749 and 0.735 in the training and validation sets, respectively; the ROC curves showed that the AUC of each prognostic factor was greater than 0.7; and, the AUC values predicted by the line plot were similar in the training and validation sets. The decision curves suggest that this line plot model has a high clinical value for predicting overall survivals at 1, 3, and 5 years in elderly women with EOC. Conclusion: The nomogram model in this study can provide an accurate assessment of the overall survival of women older than 70 years with EOC at the time of the first treatment, and it provides a basis for individualized clinical treatment.

The enhanced recovery after surgery (ERAS) protocol in elderly patients with acute cholecystitis: A retrospective study.

Enhanced recovery after surgery (ERAS) protocol is a perioperative management theory aimed at reducing the injury of surgical patients and accelerating postoperative recovery. It has been widely recognized and applied in elective surgery. This study aimed to evaluate the clinical value of the ERAS protocol during the perioperative period of laparoscopic cholecystectomy in elderly patients with acute cholecystitis. This study aimed to evaluate the clinical value of the ERAS protocol during the perioperative period of laparoscopic cholecystectomy in elderly patients with acute cholecystitis. We collected medical data from 126 elderly patients with acute cholecystitis from October 2018 to August 2021. Among the 126 patients, 70 were included in the ERAS group and 56 in the traditional group. We analyzed the clinical data and postoperative indicators of the 2 groups. No significant differences were observed regarding the general characteristics of the 2 groups (P > .05). The ERAS group had significantly earlier time to first flatus, time to first ambulation, and time to solid intake, compared with the traditional group (P < .001); additionally, the ERAS group had significantly shorter stay and gentler feeling of postoperative pain (P < .001). Furthermore, the ERAS group had significant incidences of lower postoperative lung (P = .029) and abdominal cavity infection (P = .025) compared to the traditional group. No significant difference was observed regarding the incidences of other postoperative complications between the 2 groups (P > .05). The ERAS protocol helps reduce elderly patients' stress reactions and accelerate postoperative recovery. Thus, it is effective and beneficial to implement the ERAS protocol during the perioperative period of elderly patients with acute cholecystitis.

Transcription factor HIF1α promotes proliferation, migration, and invasion of cholangiocarcinoma via long noncoding RNA H19/microRNA-612/Bcl-2 axis.

Cholangiocarcinoma, which is the most common invasive malignant tumor of the biliary tract, has poor prognosis. There is evidence suggesting that hypoxia-inducible factor 1α (HIF1α) plays an important role in cholangiocarcinoma. Also, microRNA-612 (miR-612) is another key regulator of cholangiocarcinoma. In this study, we investigate the scantly documented interaction of HIF1α and miR-612 in cholangiocarcinoma. We first undertook microarray-based cholangiocarcinoma gene expression profiles to screen out the differentially expressed long noncoding RNAs (lncRNAs) and genes. We used reverse transcription quantitative polymerase chain reaction to detect the expression of HIF1α in normal bile duct and cholangiocarcinoma tissues, and in corresponding cells lines. Cell counting kit 8, scratch, and Transwell assays were used to detect the proliferation, migration and invasion of cholangiocarcinoma cells. Cell cycle distribution and apoptosis were detected by flow cytometry. ChIP, dual luciferase reporter gene assay, RNA pull-down, and RNA immunoprecipitation were used to verify relationship between HIF1α and lncRNA H19, and lncRNA H19 and miR-612. We also monitored tumor formation in nude mice to verify the effect of HIF1α on cholangiocarcinoma. HIF1α expression was elevated in cholangiocarcinoma tissues and cells. Silencing HIF1α reduced proliferation, migration, and invasion of cholangiocarcinoma cells. HIF1α transcriptionally activated the expression of lncRNA H19. Overexpression of miR-612 could rescue the proliferation, migration and invasion of cholangiocarcinoma cells caused by lncRNA H19 overexpression. Taken together, HIF1α activated lncRNA H19-mediated miR-612/Bcl-2 pathway to promote cholangiocarcinoma, suggesting a promising therapeutic target for cholangiocarcinoma.