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Abstract Background Ankyrin repeat domain 53 (ANKRD53) plays an important role in maintaining chromosome integrity and stability, and chromosome instability is associated with cancer. Through integrative analysis, this study investigates the potential value of ANKRD53 in stomach adenocarcinoma (STAD). Methods RNA-seq and scRNA-seq data were used for integrative analysis based on online databases. Expression of ANKRD53 was confirmed by RT-PCR after bioinformatic analysis. Kaplan–Meier and Cox regression analyses were performed to evaluate the prognostic value of ANKRD53 in STAD. Gene set enrichment analysis (GSEA) was performed to evaluate ANKRD53-related signaling pathways. In addition, the interaction of ANKRD53 with immunity was also investigated. Results RT-PCR in STAD cell lines confirmed that ANKRD53 was downregulated in STAD samples compared to normal samples in the online databases. As an independent predictive biomarker, ANKRD53 was combined with other clinicopathological parameters to create a prognostic nomogram. Using GSEA, ANKRD53 was found to be involved in five pathways, including the TGF-β signaling pathway. Further investigation revealed that ANKRD53 was associated with immune checkpoint molecules, immunological pathways, and immunotherapy, in addition to MSI, TMB and neoantigens. In addition, scRNA-seq data revealed that ANKRD53 is mainly expressed in CD8+ T and dendritic cells. Conclusions ANKRD53 is an important biomarker for STAD that deserves further attention.

Abstract Background Low human epidermal growth factor receptor 2 (HER2) expression is an emerging concept in breast cancer that is defined as immunohistochemistry (IHC) 1 + or IHC 2 + and negative in situ hybridization (ISH) but has been poorly investigated. The aim of our study was to determine the frequency of low HER2 expression among HER2-negative breast cancers and compare the clinicopathological features and prognosis of HER2-low patients with those of HER2-zero patients. Methods We collected the data of 684 patients with primary HER2-negative breast cancer who underwent surgery between January 2012 and September 2021 from our self-built database. Clinicopathological features, recurrence-free interval (RFI) and breast cancer-specific survival (BCSS) were compared between HER2-low and HER2-zero (IHC 0) patients. Results Among the 684 patients, 512 (74.9%) patients had low HER2 expression, and 172 (25.1%) patients had zero HER2 expression. The average age was 57.7 ± 12.6 years, 472 (69.0%) patients were aged

Background: The occurrence and progression of lung cancer are correlated with telomeres and telomerase. Telomere length is reduced in the majority of tumors, including lung cancers. Telomere length variations have been associated with lung cancer risk and may serve as therapeutic targets as well as predictive biomarkers for lung cancer. Nevertheless, the effects of telomere-associated genes on lung cancer prognosis have not been thoroughly studied. We aim to investigate the relationship between telomere-associated genes and lung cancer prognosis. Methods: The Cancer Genome Atlas and Genotype-Tissue Expression databases were used as training sets to build a predictive model. Three integrated Gene Expression Omnibus datasets served as validation sets. Using cluster consistency analysis and regression with the least absolute shrinkage and selection operator, we developed a telomere-related gene risk signature (TMGsig) based on 11 overall survival-related genes (RBBP8, PLK1, DSG2, HOXA7, ANAPC4, CSNK1E, SYAP1, ALDOA, PHF1, MUTYH, and PGS1). Results: The results indicated a negative outcome for the high-risk score group. Immunological microenvironment and somatic mutations differed between the high- and low-risk groups. A statistically significant difference existed between the low-risk and high-risk groups in terms of the expression levels of B cells and CD4 cells, and the risk score was essentially inversely linked with immune cell expression. Conclusions: TMGsig can predict outcomes in patients with lung adenocarcinoma.

Objectives The research aimed to determine the effects of different surgical procedures on postsurgical pain and early prognosis. We reviewed the perioperative data of patients who underwent single/two-port television-assisted thoracoscopic pulmonary nodule surgery in the day surgery ward of Nanjing Drum Tower Hospital. Methods The clinical and follow-up data of 693 patients undergoing thoracoscopic for pulmonary nodules in the day surgery ward under the centralized management model of our hospital were retrospectively analyzed during the period of January 2021 to December 2022. The patients were divided into a single-port and a two-port thoracoscopy group. The propensity-matching was used to balance the baseline data and analyze the differences in postoperative pain and prognosis of the patientsin the two groups. Results After propensity score matching, the single-port group had lower intraoperative fentanyl consumption [0.5 (0.35, 0.50) mg vs. 0.5 (0.40, 0.50) mg, P = 0.034], remifentanil consumption [0.48 (0.33, 0.63) mg vs. 0.53 (0.35, 0.73) mg, P = 0.031], intraoperative hemorrhage [20 (10, 50) mL vs. 50 (20, 50) mL, P = 0.001], and Visual Analogue Scale on postoperative third day [2 (2, 4) point vs. 3 (2, 4) point, P = 0.007], which were statistically different. There were no statistically significant differences between the two groups in terms of postoperative rescue analgesia, chest drainage volume, length of hospitalization, pain on postoperative 1st, 5th, 9th, and 30th days, postoperative cough, pulmonary complications within 30 days after surgery, and unplanned hospital visits. Conclusion Compared with two-port thoracoscopy, single-port thoracoscopic day surgery for pulmonary nodules is a safe and feasible procedure that can significantly reduce the use of intraoperative opioid analgesics and the pain level of patients on postoperative 3rd day. [ABSTRACT FROM AUTHOR]

Background: The combination of anti-programmed death-1 antibodies and chemotherapy is effective; however, there are no reliable outcome prediction factors. We investigated the prognostic factors based on 18Fluorine-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT) quantitative and hematological parameters to predict progression-free survival (PFS) in relapsed/refractory classical Hodgkin lymphoma (R/R cHL) patients treated with immune checkpoint inhibitors (ICIs) and chemotherapy. Methods: This retrospective study included 31 patients who underwent 18F-FDG PET/CT before and during treatment. Pretreatment metabolic and hematological parameters were evaluated using Cox regression analysis to identify predictors of PFS. Based on the cut-off values calculated using the receiver operating characteristic (ROC) curve, patients were classified into low-, intermediate-, and high-risk groups. Kaplan–Meier curves and the log-rank test were used to compare survival differences between the groups. Results: Cox multivariable analysis indicted that the treatment response based on Lactate dehydrogenase (LDH), Lugano classification and SUVmax were independent predictors of PFS (P = 0.004, 0.007 and 0.039, respectively). The optimal cut-off values for SUVmax and LDH were 11.62 and 258.5 U/L, respectively (P < 0.01). Survival curves showed that LDH ≥ 258.5U/L and SUVmax ≥ 11.62 were correlated to shorter PFS (P < 0.001, P = 0.003, respectively). The differences in PFS between the low-, intermediate-, and high-risk groups were statistically significant (P = 0.0043). Conclusion: In R/R cHL patients treated with ICIs and chemotherapy, Lugano classification, SUVmax, and LDH were significantly correlated with PFS. The combination of metabolic and hematological parameters predicts PFS and may help to improve patient selection. [ABSTRACT FROM AUTHOR]

Background: Alterations of 11q23/KMT2A are the most prevalent cytogenetic abnormalities in acute myeloid leukemia (AML) and the prognostic significance of 11q23/KMT2A‐rearranged AML based on various translocation partners varies among different studies. However, few studies evaluated the molecular characteristics of 11q23/KMT2A‐rearranged pediatric AML. We aim to analyze the mutational landscape of 11q23/KMT2A‐rearranged AML and assess their prognostic value in outcomes. Methods: The mutational landscape and clinical prognosis of 105 children with 11q23/KMT2A‐rearranged AML in comparison with 277 children with non‐11q23/KMT2A‐rearranged AML were analyzed using publicly accessible next‐generation sequencing data from Therapeutically Applicable Research to Generate Effective Treatments (TARGET) dataset. Results: Pediatric AML patients with 11q23/KMT2A‐rearrangements harbored a low number of mutations (Median, 1 mutation/patient, range, 1‐22), 58% of which involved in RAS pathway mutations (KRAS, NRAS, and PTPN11) and 10.5% of which comprised of SETD2 mutations. Compared with non‐11q23/KMT2A‐rearranged AML, the incidence of KRAS (32.4% vs. 10.1%, P〈0.001) and SETD2 (10.5% vs. 1.4%, P=0.001) gene mutations in 11q23/KMT2A‐rearranged AML was significantly higher. Both KRAS and SETD2 mutations occurred more often in t(10;11)(p12;q23). KRAS mutations were correlated with worse 5‐year event‐free survival [EFS] (Plog‐rank = 0.001) and 5‐year overall survival [OS] (Plog‐rank = 0.009) and the presence of SETD2 mutations increases the 5‐year relapse rate (PGray = 0.004). Multivariate analyses confirmed KRAS mutations in 11q23/KMT2A‐rearranged AML as an independent predictor for poor EFS (hazard ratio [HR] = 2.10, P=0.05) and OS (HR = 2.39, P=0.054). Conclusion: Our findings show that pediatric patients with 11q23/KMT2A rearrangements have characteristic mutation patterns and varying clinical outcomes depending on different translocation partners, which could be utilized to develop more accurate risk stratification and tailored therapies. [ABSTRACT FROM AUTHOR]

Background: Anal squamous cell carcinoma (ASCC) is the main subtype of anal cancer and has great heterogeneity in prognosis. We aimed to construct a nomogram for predicting their 1‐, 3‐, and 5‐year overall survival (OS) rates. Methods: Patients with ASCC, enrolled between January 1, 2010 and December 31, 2017, were identified from the SEER database. They were divided into a training group and a validation group in a ratio of 7:3. Univariate and multivariate Cox analyses were used to identify the prognostic factors for OS. Then a prognostic nomogram was established and validated by Harrell consistency index (C‐index), area under the curve (AUC) of the receiver operating characteristic (ROC) curves, calibration plots, and decision curve analysis (DCA). Results: We identified 761 patients in training group and 326 patients in validation group. Four prognostic factors including age, sex, AJCC stage, and radiotherapy were identified and integrated to construct a prognostic nomogram. The C‐index and AUC values proved the model's effectiveness and calibration plots manifested its excellent discrimination. Furthermore, in comparison to the AJCC stage, the C‐index, AUC, and DCA proved the nomogram to be of good predictive value. Finally, we constructed a risk stratification model for dividing patients into low‐risk, medium‐risk, and high‐risk groups, and there were obvious differences in OS. Conclusions: A prognostic nomogram was firstly established for predicting the survival probability of ASCC patients and helping clinicians improve their risk management. [ABSTRACT FROM AUTHOR]

Background: This study was aimed to evaluate the value of DNA index(DI) among pediatric acute lymphoblastic leukemia (ALL) treated on Children's Oncology Group (COG) protocols between 2000 and 2015.Methods: Retrospective study were analysis among pediatric ALL patients from the TARGET dataset.Result: Totally, 1668 eligible pediatric patients were enrolled in this study. Of them, 993 are male and 675 are female with a median age of 7.6 years old. The median follow-up for those patients was 7.7 years (range 0.1-15.7 years). The probability of 15-year EFS and OS were reported to be 67.5 ± 3.1% and 78.3 ± 2.5%, respectively. BCR/ABL1 fusion gene affected the early treatment response and the survival of childhood ALL. Moreover, those patients with ETV6/RUNX1 fusion gene were also significantly associated with better EFS (HR = 0.6, 95% CI 0.4-0.8, P = 0.003) and OS (HR = 0.3, 95%CI 0.2-0.5, P < 0.001) compared to patients with no ETV6/RUNX1. On the contrary, BM NR on Day+ 29 showed a significant decrease in EFS (HR = 3.1, 95%CI 2.1-4.5, P < 0.001) and OS (HR = 1.7, 95%CI 1.1-2.8, P = 0.026). Multivariate analysis showed that DI was significantly associated with better EFS and OS. The threshold effect of DI on poor outcome was significant after adjusting for potential confounders. The adjusted regression coefficient (Log RR) was 0.7 (95%CI 0.1-3.2, P = 0.597) for DI < 1.1 while 8.8 (95%CI 1.4-56.0, P = 0.021) for DI ≥ 1.2 and 0.0 (95%CI 0.0-0.8, P = 0.041) for 1.1 ≤ DI < 1.2. Generalized additive models revealed that the lowest rates of the adverse outcomes estimated to occur among DI between 1.1 and 1.2.Conclusion: For those childhood ALL treated on COG protocols between 2000 and 2015, ETV6/RUNX1 and BM NR were closely related to the prognosis. Moreover, the DI between 1.1 and 1.2 can serve as a significant cut-point discriminating the risk group, which indicated a favourable prognostic factor. [ABSTRACT FROM AUTHOR]

Background: Mitochondrial ribosomal protein L15 (MRPL15), a member of mitochondrial ribosomal proteins whose abnormal expression is related to tumorigenesis. However, the prognostic value and regulatory mechanisms of MRPL15 in non-small-cell lung cancer (NSCLC) remain unclear. Methods: GEPIA, ONCOMINE, Gene Expression Omnibus (GEO), UALCAN, Kaplan–Meier plotter, PrognoScan, LinkedOmics and GeneMANIA database were utilized to explore the expression and prognostic value of MRPL15 in NSCLC. Additionally, immune infiltration patterns were evaluated via ESTIMATE algorithm and TISIDB database. Furthermore, the expression and prognostic value of MRPL15 in lung cancer were validated via immunohistochemistry (IHC) assays. Results: In NSCLC, multiple cohorts including GEPIA, ONCOMINE and 8 GEO series (GSE8569, GSE101929, GSE33532, GSE27262, GSE21933, GSE19804, GSE19188, GSE18842) described that MRPL15 was up-regulated. Moreover, MRPL15 was notably linked to gender, clinical stage, lymph node status and the TP53 mutation status. And patients with high MRPL15 expression showed poor overall survival (OS), progression-free survival (PFS), disease-free survival (DFS) and relapse-free survival (RFS) in NSCLC. Then, functional network analysis suggested that MRPL15 participated in metabolism-related pathways, DNA replication and cell cycle signaling via pathways involving several kinases, miRNAs and transcription factors. Additionally, it was found that MRPL15 expression was negatively related to immune infiltration, including immune scores, stromal scores and several tumor-infiltrating lymphocytes (TILs). Furthermore, IHC results further confirmed the high MRPL15 expression and its prognostic potential in lung cancer. Conclusions: These findings demonstrate that high MRPL15 expression indicates poor prognosis in NSCLC and reveal potential regulatory networks as well as the negative relationship with immune infiltration. Thus, MRPL15 may be an attractive predictor and therapeutic strategy for NSCLC. [ABSTRACT FROM AUTHOR]

The prognostic impact of Wilms tumor 1 (WT1) mutations remains controversial for patients with acute myeloid leukemia (AML). Here, we aimed to determine the clinical implication of WT1 mutations in a large cohort of pediatric AML. The clinical data of 870 pediatric patients with AML were downloaded from the therapeutically applicable research to generate effective treatment (TARGET) dataset. We analyzed the prevalence, clinical profile, and prognosis of AML patients with WT1 mutations in this cohort. Our results showed that 6.7% of total patients harbored WT1 mutations. These WT1 mutations were closely associated with normal cytogenetics (P <0.001), FMS-like tyrosine kinase 3/internal tandem duplication (FLT3 /ITD) mutations (P <0.001), and low complete remission induction rates (P <0.01). Compared to the patients without WT1 mutations, patients with WT1 mutations had a worse 5-year event-free survival (21.7 ± 5.5% vs 48.9 ± 1.8%, P <0.001) and a worse overall survival (41.4 ± 6.6% vs 64.3 ± 1.7%, P <0.001). Moreover, patients with both WT1 and FLT3 /ITD mutations had a dismal prognosis. Compared to chemotherapy alone, hematopoietic stem cell transplantation tended to improve the prognoses of WT1 -mutated patients. Multivariate analysis demonstrated that WT1 mutations conferred an independent adverse impact on event-free survival (hazard ratio 1.910, P = 0.001) and overall survival (hazard ratio 1.709, P = 0.020). In conclusion, our findings have demonstrated that WT1 mutations are independent poor prognostic factors in pediatric AML. [ABSTRACT FROM AUTHOR]

Background: Acute myeloid leukemia (AML) is a heterogeneous disease of the hematopoietic system, for which identification of novel molecular markers is potentially important for clinical prognosis and is an urgent need for treatment optimization. Methods: We selected C-type lectin domain family 11, member A (CLEC11A) for study via several public databases, comparing expression among a variety of tumors and normal samples as well as different organs and tissues. To investigated the relationship between CLEC11A expression and clinical characteristics, we derived an AML cohort from The Cancer Genome Atlas (TCGA); we also investigated the Bloodspot and HemaExplorer databases. The Kaplan-Meier method and log-rank test were used to evaluate the associations between CLEC11A mRNA expression, as well as DNA methylation, and overall survival (OS), event-free survival (EFS), and relapse-free survival (RFS). DNA methylation levels of CLEC11A from our own 28 de novo AML patients were assessed and related to chemotherapeutic outcomes. Bioinformatics analysis of CLEC11A was carried out using public databases. Results: Multiple public databases revealed that CLEC11A expression was higher in leukemia. The TCGA data revealed that high CLEC11A expression was linked with favorable prognosis (OS p -value = 2e-04; EFS p -value = 6e-04), which was validated in GSE6891 (OS p -value = 0; EFS p -value = 0; RFS p -value = 2e-03). Methylation of CLEC11A was negatively associated with CLEC11A expression, and high CLEC11A methylation level group was linked to poorer prognosis (OS p -value = 1e-02; EFS p -value = 2e-02). Meanwhile, CLEC11A hypermethylation was associated with poor induction remission rate and dismal survival. Bioinformatic analysis also showed that CLEC11A was an up-regulated gene in leukemogenesis. Conclusion: CLEC11A may be used as a prognostic biomarker, and could do benefit for AML patients by providing precise treatment indications, and its unique gene pattern should aid in further understanding the heterogeneous AML mechanisms. [ABSTRACT FROM AUTHOR]

Purpose: At the first time of metastatic breast cancer recurrence, conversion of the receptors status may occur between primary lesions and metastatic lesions, including the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Whether the decision of the treatment regimen is based on the primary receptor status or that of metastatic lesions is still unclear. Methods: This study enrolled 411 female patients with a diagnosis of metastatic breast cancer at the first time of recurrence to explore the influence of receptor conversion on prognosis prediction and treatment regimen of patients with metastatic breast cancer. Results: ER and PR changes from negative to positive are both prognostic factors for patients with breast cancer. Patients receiving endocrine therapy showed a better survival after recurrence than those using chemotherapy alone in the ER or PR Prim– Met+ subgroup. Patients in the HER2 Prim– Met+ subgroup using HER2-targeted therapy in multilines showed a post-recurrence survival advantage. In the bone re-biopsy subgroup, the PR change from positive to negative appeared to be more frequent than at other re-biopsy sites. Conclusions: Patients with metastatic breast cancer should perform re-biopsy to clarify the receptor status of the first metastatic lesions, which may provide clinicians valuable evidence to conduct treatments with higher precision. [ABSTRACT FROM AUTHOR]

Objectives. To identify risk factors associated with the prognosis of pertussis-like coughing. Methods. A retrospective study on children hospitalized with pertussis-like coughing from 2018 to 2019. We collected all the case data from medical records including age, gender, vaccination, clinical symptoms, complication, pathogens, white blood cell (WBC) count, lymphocyte ratio, application of macrolide antibiotics, usage of sulfamethoxazole, and usage of inhaled glucocorticoids. Logistic regression was used in this study. Results. A total of 213 hospitalized children with pertussis-like coughing were included in this study. About 70 children were cured within 2 weeks. One120 children were cured from 2 weeks to 3 months, including cases of initial attack and relapse. Symptoms lasting longer than 3 months accounts for 10.8%. Bordetella pertussis, WBC count >20 × 109/L and lymphocyte ratio >60% were associated with poor prognosis (P <.05). Conclusions. Bordetella pertussis, WBC count, and lymphocyte ratio are independent risk factors for poor prognosis. [ABSTRACT FROM AUTHOR]

High-grade serous ovarian cancer (HGSOC) is one of the most common and lethal gynecological cancers. Long noncoding RNAs (lncRNAs) play important roles and act as prognostic biomarkers of ovarian cancer. However, few studies have focused on the prognostic prediction of lncRNAs solely in HGSOC. In this study, we identified candidate lncRNAs for a prognostic evaluation by examining reannotated lncRNA expression profiles and clinical data of 343 patients with HGSOC from The Cancer Genome Atlas. We built a 10-lncRNA signature using Cox-LASSO regression to predict the prognosis of patients with HGSOC. Trichotomized by the 10-lncRNA signature, high-risk patients experienced significantly shorter disease-free survival and overall survival (OS). Our novel 10-lncRNA signature showed superior predictive capacity compared to the other 2 published lncRNA signature models and clinicopathological parameters. We developed a nomogram for clinical use by integrating the 10-lncRNA signature and two clinicopathological risk factors to predict 1-, 3-, and 5-year OS. In addition, gene set enrichment analysis suggested that the group of high-risk patients was associated with mitotic spindle pathways. This model was also compatible with patients with or without BRCA1/2 mutations and had the potential to predict the response to platinum-based adjuvant chemotherapy. Our findings provide a novel 10-lncRNA prognostic signature for further clinical application in patients with HGSOC and indicate the underlying mechanisms of HGSOC progression. [ABSTRACT FROM AUTHOR]

The current prognostic long noncoding RNA (lncRNA) signatures for hepatocellular carcinoma (HCC) are still controversial and need to be optimized by systematic bioinformatics analyses with suitable methods and appropriate patients. Therefore, we performed the study to establish a credible lncRNA signature for HCC outcome prediction and explore the related mechanisms. Based on the lncRNA profile and the clinical data of carefully selected HCC patients (n = 164) in TCGA, six of 12727 lncRNAs, MIR22HG, CTC‐297N7.9, CTD‐2139B15.2, RP11‐589N15.2, RP11‐343N15.5, and RP11‐479G22.8 were identified as the independent predictors of patients' overall survival in HCC by sequential univariate Cox and 1000 times Cox LASSO regression with 10‐fold CV, and multivariate Cox analysis with 1000 times bootstrapping. In the Kaplan‐Meier analysis with patients trichotomized by the six‐lncRNA signature, high‐risk patients showed significantly shorter survival than mid‐ and low‐risk patients (log‐rank test P < 0.0001). According to the ROCs, the six‐lncRNA signature showed superior predictive capacity than the two existing four‐lncRNA combinations and the traditional prognostic clinicopathological parameter TNM stage. Furthermore, low MIR22HG and CTC‐297N7.9, but high CTD‐2139B15.2, RP11‐589N15.2, RP11‐343N15.5, and RP11‐479G22.8, were, respectively, demonstrated to be related with the malignant phenotypes of HCC. Functionally, the six lncRNAs were disclosed to involve in the regulation of multiple cell cycle and stress response‐related pathways via mediating transcription regulation and chromatin modification. In conclusion, our study identified a novel six‐lncRNA signature for resectable HCC prognosis prediction and indicated the underlying mechanisms of HCC progression and the potential functions of the six lncRNAs awaiting further elucidation. By systematic bioinformatics analyses, a novel six‐lncRNA signature including MIR22HG, CTC‐297N7.9, CTD‐2139B15.2, RP11‐589N15.2, RP11‐343N15.5, and RP11‐479G22.8 was established for HCC prognosis prediction and demonstrated to have superior prediction capacity than the two established four‐lncRNA groups and the traditional prognostic TNM stage. Functionally, the six lncRNAs were disclosed to involve in the regulation of multiple cell cycle and stress response‐related pathways via mediating transcription regulation and chromatin modification. [ABSTRACT FROM AUTHOR]

Objectives:Using microarray analysis, we previously showed that many lncRNAs are differentially expressed in colorectal cancer (CRC) tissues compared with normal tissues, suggesting that lncRNAs may be involved the initiation and progression of CRC. In this study, we investigated the expression and function of lncRNA-RP11-317J10.2 in human CRC tissues and cell lines. Methods:LncRNA-RP11-317J10.2 expression level was analyzed in 52 colon cancer and cell lines. We used shRNA to knock-down the expression of RP11-317J10.2, and then proliferation assay, colony formation assay, Boyden chamber assay, FACS and Kaplan–Meier survival analysis were performed to explore the biological effect of RP11-317J10.2. Cyclin D1 protein level was detected by Western blot. Results:LncRNA-RP11-317J10.2 is downregulated in CRC and decreased expression is significantly associated with advanced tumor stage, larger tumor size and poor prognosis. RNA interference-mediated knockdown of lncRNA-RP11-317J10.2 in CRC cells promotes G1-to-S cell cycle transition, enhances invasiveness and facilitates cell growthin vitroand in mouse tumor xenograft models. Cyclin D1 was upregulated by lncRNA-RP11-317J10.2 knockdown, and co-expression of cyclin D1-targeting siRNA abrogates the pro-tumorigenic effects of lncRNA-RP11-317J10.2 knockdown. Conclusions:This study reveals a crucial role for lncRNA-RP11-317J10.2 in CRC growth and invasion via upregulation of cyclin D1 expression and suggests that expression of this lncRNA may be a potential prognostic biomarker for CRC. [ABSTRACT FROM PUBLISHER]

Purpose: Urachal carcinoma (UC) is a rare genitourinary cancer with an insidious onset, high risk of recurrence, and a poor prognosis. Surgical resection alone has difficulty in controlling the tumor. We aim to explore treatment options and prognostic risk factors for UC based on a multicenter cohort and long-term follow-up database.Materials and Methods: The clinical data, treatment and follow-up results of 163 patients with UC in 6 medical centers were analyzed retrospectively. Kaplan-Meier analysis and a Cox proportional hazards model were used to assess the treatment options and prognostic risk factors for UC.Results: Kaplan-Meier analysis showed no difference in the 5-year recurrence-free survival rate (P =0.282) or overall survival rate (P =0.673) between extended partial cystectomy (EPC) and radical cystectomy (RC) for patients at stage III and below. Whether bilateral pelvic lymph nodes were dissected was also not significantly correlated with the patient's recurrence (P =0.921) or prognosis (P =0.741). Postoperative adjuvant chemotherapy significantly reduced the recurrence rate of patients with stage Ⅲb or below (P =0.005). Combined treatment of postoperative recurrence patients prolonged the survival time of patients compared with single chemotherapy or conservative treatment (34.022±5.031 vs. 12.837±2.349 or 6.192±0.875 months, P <0.001). Kaplan-Meier and univariate Cox regression analyses showed that age >55 years, Sheldon stage, carbohydrate antigen 19-9 (CA19-9) >9.935 U/mL, carbohydrate antigen 72-4 (CA724) >6.02 U/mL, and postoperative adjuvant chemotherapy were closely related to the overall survival and recurrence-free survival of patients (P <0.05). Multivariate Cox proportional hazard regression confirmed that the Sheldon stage and CA724 >6.02 U/mL were independent recurrence risk factors.Conclusions: EPC or RC provides similar oncologic results for UC, but bilateral pelvic lymph node dissection is not necessary in early-stage patients. Postoperative adjuvant chemotherapy can significantly reduce the recurrence rate, and combination therapy may provide better survival outcomes. CA724 can predict tumor recurrence or metastasis at an early stage. [ABSTRACT FROM AUTHOR]

Most patients with epithelial ovarian cancer ( EOC) are diagnosed at an advanced stage, and therapeutic options for these patients are limited. The identification of suitable biomarkers could be helpful for patients with EOC, who might benefit from targeted therapies even in advanced stages of the disease. Trophoblast cell surface antigen 2 ( TROP2) is highly expressed in various human malignant tumours; however, this has not been demonstrated clearly in EOC. In this study, we further evaluated whether TROP2 is a promising marker for EOC, and thus also a potential target for EOC immunotherapy. Quantitative real-time polymerase chain reaction (qPCR) and fluorescence-activated cell sorting (FACS) analysis were employed to determine TROP2 mRNA and protein expression in both human EOC and normal ovarian cell lines. Additionally, TROP2 protein expression was measured by immunohistochemistry in 128 EOC tissue samples, 21 normal ovarian tissues and 18 normal fallopian tubes. The correlations between TROP2 protein expression and patients' clinicopathological features were investigated, and survival outcomes were analysed. TROP2 mRNA and protein levels were upregulated significantly in EOC cell lines compared with normal cell lines. The protein of TROP2 was expressed in the majority of EOC tissue samples (90.6%) and overexpressed in 75 (58.6%) of the 128 tumour samples. TROP2 overexpression was correlated with relevant clinicopathological characteristics and was associated with significantly shortened overall survival and disease-free survival. Furthermore, TROP2 was an independent prognostic marker for EOCs as analysed by Cox regression. TROP2 was a potential biomarker for targeted therapy in patients with TROP2-overexpressing EOC. [ABSTRACT FROM AUTHOR]

The β-catenin gene is frequently mutated in patients with hepatocellular carcinoma (HCC) and has long been thought to be one of the major oncogenes involved in the hepatocarcinogenesis. The prognostic role of β-catenin mutation in HCC remains unclear. To address this issue, a search for relevant studies was performed in the PubMed, Embase and Web of Science databases. The pooled effect was calculated from the available data to evaluate the correlation of β-catenin mutation with overall survival rate and tumor clinicopathological features in patients with HCC. The pooled odds ratio (OR) was calculated using the Mantel-Haenszel model for fixed effects. Three studies met the inclusion criteria. A total of 618 cases were included, and β-catenin mutation was identified in 104 of them. The meta-analysis revealed that the presence of β-catenin mutation (n=104), compared with the control group (n=514), was correlated with a longer overall survival rate [OR, 0.33; 95% confidence interval (CI), 0.21-0.53; P<0.00001] in patients with HCC. No significant heterogeneity was found among the eligible studies (I2=0%; P=0.72). β-catenin mutation was correlated with a relatively lower rate of hepatitis B virus infection (OR, 0.36; 95% CI, 0.21-0.61; P=0.0002), improved tumor differentiation (OR, 0.32; 95% CI, 0.19-0.56; P<0.0001) and a lower tumor-node-metastasis stage (I+II) (OR, 0.23; 95% CI, 0.14-0.38; P<0.00001). These findings suggest that β-catenin mutation may predict a favorable prognosis in patients with HCC. [ABSTRACT FROM AUTHOR]

Background: Progressive lung cancer is associated with abnormal coagulation. Platelets play a vital part in evading immune surveillance and angiogenesis in the case of tumor metastasis. The study aimed to analyze the predictive and prognostic effects of platelet count on non-small cell lung cancer (NSCLC) patients treated with epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs).Methods: This study retrospectively analyzed the prognostic effects of platelets on 52 NSCLC patients with epidermal growth factor receptor (EGFR) mutant following EGFR-TKI treatment. Related data, together with the progression-free survival (PFS) and overall survival (OS) were collected before and after 2 cycles of treatments (60 days).Results: The anti-EGFR treatment markedly reduced the platelet count in 33 (63.5%) patients after 2 cycles of treatment. Multivariate Cox analysis revealed that, the decreased platelet count was closely correlated with the longer OS (HR = 0.293; 95%CI: 0.107-0.799; p = 0.017). Besides, the median OS was 326 days in the decreased platelet count group and 241 days in the increased platelet count group (HR = 0.311; 95%CI: 0.118-0.818; P = 0.018), as obtained from the independent baseline platelet levels and other clinical features.Conclusions: The platelet count may predict the prognosis for EGFR-TKI treatment without additional costs. Besides, changes in platelet count may serve as a meaningful parameter to establish the prognostic model for NSCLC patients receiving anti-EGFR targeted therapy. [ABSTRACT FROM AUTHOR]

Background: The relationship between visceral adiposity and acute pancreatitis (AP) has not been completely elucidated. This study evaluated the significance of visceral adipose tissue (VAT) and the ratio of VAT to skeletal muscle tissue (VAT/SMT) in the prognosis of AP patients.Methods: Based on a 1:2 propensity score matching, 306 hospitalized patients were enrolled in the study analysis from 2010 to 2017. VAT, subcutaneous adipose tissue (SAT), and SMT were measured using unenhanced computed tomography (CT). Cox proportional hazards models were applied for the analysis.Results: VAT and the VAT/SMT ratio were significantly higher in the severe AP (SAP) and moderately severe AP (MSAP) groups compared to the mild AP (MAP) group (both p < 0.001). Intensive care transfer, AP severity, systemic complications, and prognostic scores (Acute Physiology and Chronic Health Evaluation II [APACHE-II] score ≥ 8, Ranson's score ≥ 3, Bedside Index of Severity in Acute Pancreatitis [BISAP] score ≥ 3, and the systemic inflammatory response syndrome [SIRS] score ≥ 2) significantly correlated with VAT and the VAT/SMT ratio in AP patients. The multivariate adjusted hazard ratios (HRs) for VAT and the VAT/SMT ratio in the relationship of body parameters and AP mortality were 1.042 (95% confidence interval (CI), 1.019-1.066) and 7.820 (95% CI, 1.978-30.917), respectively. Compared with other prognostic scores, VAT had the highest area under the curve of receiver operating characteristics (ROC) (0.943, 95% CI, 0.909-0.976).Conclusion: High VAT and VAT/SMT ratio are independent negative prognostic indicators of AP.Trial Registration: Clinical study registration number: NCT03482921 . Date of registration: 03/23/2018. [ABSTRACT FROM AUTHOR]

Chromophobe renal cell carcinoma (chRCC) is the third most common subtype of kidney cancers. In the present study, we identified 58 treatment-naïve primary chRCC patients from The Cancer Genome Atlas dataset and analyzed the genome-wide microRNA (miRNA) expression profiles, with the aim to assess the relationship of miRNA expression with the progression and prognosis of chRCC. Overall, a total of 105 miRNAs were found to be differentially expressed between tumor and the adjacent normal tissues from 22 chRCC patients. In the unpaired condition (58 chRCC vs. 22 normal tissues), 77 (96.3%) samples were distinguished correctly by the signatures. In the progression-related profiles, 27 miRNAs were selected for pathologic T and 9 for lymph node involvement. In the survival analyses, the expression levels of mir-191, mir-19a, mir-210, and mir-425 were significantly associated with both recurrence-free survival (RFS) and overall survival, while mir-210 was proven as an independent prognostic factor in terms of RFS. In summary, miRNAs are expressed differentially in chRCC, and unique expression of miRNAs is associated with the progression and prognosis of chRCC. [ABSTRACT FROM AUTHOR]

Although increasing evidence has revealed that FOXD2-AS1 overexpression exists in various solid tumors, the value of FOXD2-AS1 as a prognostic marker in such cancers remains uncertain. Accordingly, the present research aimed to assess the association of FOXD2-AS1 with cancer prognosis and predict the biological function of FOXD2-AS1. We systematically retrieved PubMed, PMC, Web of Science, EMBASE and Wiley Online Library databases for eligible articles published up to December 2018. Pooled hazard ratios (HRs) and odds ratios (ORs) with 95% confidence intervals (95%CIs) were calculated to evaluate the correlation of FOXD2-AS1 expression with overall survival (OS), disease free survival (DFS) and clinicopathological characteristics. We also used five Gene Expression Omnibus (GEO) datasets from breast cancer patients to explore the relationship between FOXD2-AS1 expression and prognosis. Finally, we validated FOXD2-AS1 expression in various carcinomas and predicted its biological function based on the public databases. A total of 13 studies with 2502 tumor patients were included. The pooled HRs demonstrated that FOXD2-AS1 overexpression was significantly associated with unfavorable OS (HR = 1.39, 95%CI: 1.23–1.57, p < 0.001) and DFS (HR = 2.24, 95%CI: 1.55–3.23, p < 0.001) in tumor patients. The pooled ORs indicated that FOXD2-AS1 upregulation was related to large tumor size (OR = 1.53, 95%CI: 1.26–1.85, p < 0.001), deep invasion depth (OR = 1.99, 95%CI: 1.53–2.58, p < 0.001), distant metastasis (OR = 2.03, 95%CI: 1.69–2.43, p < 0.001) and advanced TNM stage (OR = 1.35, 95%CI: 1.06–1.72, p = 0.0150), but not to lymph node metastasis nor differentiation. Moreover, a similar pooled result for the OS of breast cancer patients was obtained (HR = 1.55, 95%CI: 1.14–2.11, p = 0.0052) by analyzing GEO data. Finally, elevated FOXD2-AS1 expression in various solid tumor tissues was verified based on The Cancer Genome Atlas (TCGA) data. Further functional prediction demonstrated that FOXD2-AS1 may participate in some cancer-related pathways. Elevated FOXD2-AS1 expression was associated with poor survival in patients with solid tumors and may serve as a potential prognostic biomarker for a variety of cancers. [ABSTRACT FROM AUTHOR]