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PurposeThe incidence of seroma and postoperative pain after Gilbert type III inguinal hernia repair is high. To reduce postoperative complications, this study investigated the clinical efficacy of laparoscopic closed hernia ring combined with a patch repair for Gilbert type III indirect inguinal hernia.MethodsThrough a prospective randomized controlled study, a total of 193 patients with Gilbert type III indirect inguinal hernia admitted to Nanchong Central Hospital affiliated with Chuanbei Medical College from May 2020 to December 2021 were selected and randomly divided into the inner ring closed group (85 patients) and the inner ring non-closed group (95 patients). The patients in both groups underwent laparoscopic tension-free repair of their inguinal hernias. General information such as operative time, postoperative hospital stay, and hospital cost were compared between the two groups, and the patients were followed up at 1, 7, 14, 21, and 28 days and then 3, 6, and 12 months after surgery to compare complications such as incidence of seroma, volume of the seroma fluid, incidence of pain, and visual analogue scale (VAS) pain score.ResultsThere was no conversion to open procedures in any of the patients. The operation time of the closed group was significantly longer than that of the non-closed group (64.2 ± 12.2 vs. 55.3 ± 9.5 min, P 0.05). The postoperative follow-up period was 3–20 months, and no chronic pain or recurrence occurred during the postoperative follow-up period in either group.ConclusionsClosure of the hernia ring is safe and effective for laparoscopic hernia repair for Gilbert type III inguinal hernia, and it significantly reduces the incidence of postoperative seroma and further reduces the postoperative pain without increasing the risk of postoperative infection and recurrence.

Background: In the era of immunotherapy, predictive or prognostic biomarkers for head and neck squamous cell carcinoma (HNSCC) are urgently needed. Metabolic reprogramming in the tumor microenvironment (TME) is a non-negligible reason for the low therapeutic response to immune checkpoint inhibitor (ICI) therapy. We aimed to construct a metabolism-related gene prognostic index (MRGPI) for HNSCC bridging metabolic characteristics and antitumor immune cycling and identified the immunophenotype, genetic alternations, potential targeted inhibitors, and the benefit of immunotherapy in MRGPI-defined subgroups of HNSCC. Methods: Based on The Cancer Genome Atlas (TCGA) HNSCC dataset (n = 502), metabolism-related hub genes were identified by the weighted gene co-expression network analysis (WGCNA). Seven genes were identified to construct the MRGPI by using the Cox regression method and validated with an HNSCC dataset (n = 270) from the Gene Expression Omnibus (GEO) database. Afterward, the prognostic value, metabolic activities, genetic alternations, gene set enrichment analysis (GSEA), immunophenotype, Connectivity map (cMAP), and benefit of immunotherapy in MRGPI-defined subgroups were analyzed. Results: The MRGPI was constructed based on HPRT1 , AGPAT4 , AMY2B , ACADL , CKM , PLA2G2D , and ADA. Patients in the low-MRGPI group had better overall survival than those in the high-MRGPI group, consistent with the results in the GEO cohort (cutoff value = 1.01). Patients with a low MRGPI score display lower metabolic activities and an active antitumor immunity status and more benefit from immunotherapy. In contrast, a higher MRGPI score was correlated with higher metabolic activities, more TP53 mutation rate, lower antitumor immunity ability, an immunosuppressive TME, and less benefit from immunotherapy. Conclusion: The MRGPI is a promising indicator to distinguish the prognosis, the metabolic, molecular, and immune phenotype, and the benefit from immunotherapy in HNSCC. [ABSTRACT FROM AUTHOR]

The overall survival of patients with lower grade glioma (LGG) that might develop into high-grade malignant glioma shows marked heterogeneity. The currently used clinical evaluation index is not sufficient to predict precise prognostic outcomes accurately. To optimize survival risk stratification and the personalized management of patients with LGG, there is an urgent need to develop an accurate risk prediction model. The TCGA-LGG dataset, downloaded from The Cancer Genome Atlas (TCGA) portal, was used as a training cohort, and the Chinese Glioma Genome Atlas (CGGA) dataset and Rembrandt dataset were used as validation cohorts. The levels of various cancer hallmarks were quantified, which identified glycolysis as the primary overall survival-related risk factor in LGGs. Furthermore, using various bioinformatic and statistical methods, we developed a strong glycolysis-related gene signature to predict prognosis. Gene set enrichment analysis showed that in our model, high-risk glioma correlated with the chemoradiotherapy resistance and poor survival. Moreover, based on established risk model and other clinical features, a decision tree and a nomogram were built, which could serve as useful tools in the diagnosis and treatment of LGGs. This study indicates that the glycolysis-related gene signature could distinguish high-risk and low‐risk patients precisely, and thus can be used as an independent clinical feature. [ABSTRACT FROM AUTHOR]

Background: The discovery of reliable cancer biomarkers could tune a diagnosis and improve the way patients are treated. However, many cancers lack robust biomarkers. C1QTNF6 has been preliminarily elucidated for its role in some tumors. However, no pan-cancer analysis has been performed to comprehensively explore the value of C1QTNF6. Methods: Data from the TCGA database, GTEx database stored in the USUC Xena were used for analyzing the profiles of C1QTNF6 expression in normal and tumor tissues in pan-cancer. Subsequently, the gene alteration rates of C1QTNF6 were acquired on the online web cBioportal. With the aid of the TCGA data, the association between C1QTNF6 mRNA expression and copy number alterations (CNA) and methylation was determined. Survival analyses of C1QTNF6 were carried out. Moreover, the tumor biological and immunological characteristics of C1QTNF6 were clarified in the forms of the correlation between C1QTNF6 expression and hallmark Pathway scores in MsigDB database, immune cell infiltration, immune-related genes. We conducted a GSEA of C1QTNF6 to illustrate its potential biological functions. In addition, GDSC2 data with 198 drugs were adopted to explore drug sensitivity with the change of C1QTNF6 expression. Result: C1QTNF6 was overexpressed in many types of cancer, Survival analysis showed that C1QTNF6 independently served as a prognostic indicator for poor survival in many tumors. Besides, we also identified a positive correlation between C1QTNF6 and cancer hallmark pathway score, tumor microenvironment related pathways score (TMEp score), and immune characteristic. In terms of drug sensitivity analysis, we found higher expression level of C1QTNF6 predicts a high IC50 value for most of 198 drugs which predicts drug resistance. Conclusions: Our study provides a new biological marker for pan-cancer, which is beneficial to the diagnosis and treatment of cancer, which bring a new therapeutic target for tumors. [ABSTRACT FROM AUTHOR]

Randomized controlled trials have failed to report any survival advantage for WBRT combined with SRS in the management of brain metastases, despite the enhanced local and distant control in comparison to each treatment alone. Literature review have revealed important role of primary histology of the tumor when dealing with brain metastases. NSCLC responds better to combined approach even when there was only single brain metastasis present while breast cancer has registered better survival with SRS alone probably due to better response of primary tumor to advancement in surgical and chemotherapeutic agents. Furthermore, mutation status (EGFR/ALK) in lung cancer and receptor status (ER/PR/HER2) in breast cancer also exhibit diversity in their response to radiotherapy. Radioresistant tumors like renal cell carcinoma and melanoma brain metastases have achieved better results when treated with SRS alone. Secondly, single brain metastasis may benefit from local and distant brain control achieved with combined treatment. These diverse outcomes suggest a primary histology-based analysis of the radiotherapy regimens (WBRT, SRS, or their combination) would more ideally establish the role of radiotherapy in the management of brain metastases. Molecularly targeted therapeutic and immunotherapeutic agents have revealed synergism with radiation therapy particularly SRS in treating cancer patients with brain metastases. Clinical updates in this regard have also been reviewed. [ABSTRACT FROM AUTHOR]

Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied to treat nasopharyngeal carcinoma (NPC). However, the molecular changes and functions of DDP in NPC chemo-resistance remain poorly understood. In the present study, transcriptomic sequencing between 5-8F and 5-8F/DDP cells was performed to identify differential expression and alternative splicing (AS) characteristics in DDP-resistant NPC cells. Transcriptomic profiling identified 1,757 upregulated genes and 1,473 downregulated differentially expressed genes (DEGs). Bioinformatic analysis revealed that these DEGs were associated with or participated in important biological regulatory functions in NPC. Validation of 20 significant DEGs using quantitative real-time reverse transcription PCR showed that the expression patterns of 17 mRNAs were in accordance with the sequencing data. Intron retention was identified as the major AS event in chemoresistant cells. Furthermore, the expression level of matrix metalloproteinase 1 (MMP1), which was one of the most upregulated mRNAs in the chemoresistant cell lines, was significantly associated with the migration, invasion, and proliferation of NPC cells in vitro. Our study revealed that dysregulated genes and AS-mediated DDP chemoresistance might play important roles in NPC development and progression. Targeting aberrantly expressed genes might clarify the pathogenesis of NPC and contribute to developing new therapeutic strategies for NPC. [ABSTRACT FROM AUTHOR]

In humans, zinc finger protein 671 (ZNF671) is a type of transcription factor. However, the contribution of tumor heterogeneity to the functional role of ZNF671 remains unknown. The present study aimed to determine the functional states of ZNF671 in cancer single cells based on single-cell sequencing datasets (scRNA-seq). We collected cancer-related ZNF671 scRNA-seq datasets and analyzed ZNF671 in the datasets. We evaluated 14 functional states of ZNF671 in cancers and performed ZNF671 expression and function state correlation analysis. We further applied t-distributed stochastic neighbor embedding to describe the distribution of cancer cells and to explore the functional state of ZNF671 in cancer subgroups. We found that ZNF671 was downregulated in eight cancer-related ZNF671 scRNA-seq datasets. Functional analysis identified that ZNF671 might play a tumor suppressor role in cancer. The heterogeneous functional states of cell subgroups and correlation analysis showed that ZNF671 played tumor suppressor roles in heterogeneous cancer cell populations. Western blot and transwell assays identified that ZNF671 inhibited EMT, migration, and invasion of CNS cancers, lung cancer, melanoma, and breast carcinoma in vitro. These results from cancer single-cell sequencing indicated that ZNF671 played a tumor suppressor role in multiple tumors and may provide us with new insights into the role of ZNF671 for cancer treatment. [ABSTRACT FROM AUTHOR]

Zinc finger protein 671 (ZNF671) is a member of the largest transcription factor family in the human genome. However, the methylation status, expression, and prognostic role of ZNF671 in solid tumors remain unclear. The aim of this study was to explore the relationship between ZNF671 and the prognosis of patients with solid tumors. We performed a pan-cancer analysis of the methylation status and mRNA and protein expression of ZNF671 using The Cancer Genome Atlas (TCGA) database and the Human Protein Atlas. We further evaluated the prognostic value of ZNF671 expression among numerous cancer types using the "Kaplan–Meier plotter" (KM plotter) database. We found that downregulation of ZNF671 is associated with hypermethylation of its promoter. Survival analysis established that the downregulation of ZNF671 predicts poor prognosis in breast invasive carcinoma (BRCA), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), head and neck squamous cell carcinoma (HNSC), kidney renal papillary cell carcinoma (KIRP), lung adenocarcinoma (LUAD), pancreatic adenocarcinoma (PAAD), and uterine corpus endometrial carcinoma (UCEC) solid tumors. CCK-8 and Transwell functional assays showed that ZNF671 could inhibit tumor cell proliferation, migration, and invasion. These results indicate that ZNF671 is an excellent predictive factor for BRCA, CESC, HNSC, KIRP, LUAD, PAAD, SARC, and UCEC solid tumors and may play crucial roles in the development and progression of these tumors. [ABSTRACT FROM AUTHOR]

Background: Significantly better local control is achieved with combination of whole brain radiotherapy and stereotactic radiosurgery in the treatment of multiple brain metastases. However, no survival benefit was reported from this advantage in local control. Objective: The objective of this study was to review the available evidence whether better local control achieved with whole brain radiotherapy plus stereotactic radiosurgery leads to any benefit in survival in patients with favorable prognostic factors. Methods and Materials: Electronic databases (PubMed, MEDLINE, and Cochrane Library) were searched until Oct 2018 to identify studies published in English that compared efficacy of whole brain radiotherapy plus stereotactic radiosurgery vs. whole brain radiotherapy alone or stereotactic radiosurgery alone in patients with brain metastases stratified on prognostic indices (Recursive Partitioning Analysis and Diagnosis-Specific Graded Prognostic Assessment). Primary outcome was survival. Results: Five studies (n = 2728) were identified, 3 secondary analyses of the previously published RCTs and 2 retrospective studies, meeting the inclusion criteria. whole brain radiotherapy plus stereotactic radiosurgery showed improved survival in brain metastatic cancer patients with better prognostic factors particularly when compared to whole brain radiotherapy only. Its survival advantage over stereotactic radiosurgery only was limited to non-small cell lung cancer primary tumor histology. Conclusions: Whole brain radiotherapy in combination with stereotactic radiosurgery may improve survival and could be recommended selectively in patients with favorable prognostic factors particularly in comparison to whole brain radiotherapy only. [ABSTRACT FROM AUTHOR]