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Genome Divergence and also Character inside the Thin-Tailed Wilderness Sheep Through Sudan.
Purpose Prostate cancer (PCa) is a widespread urinary neoplasm and one of the most prevalent and second most frequent malignancies diagnosed in males worldwide. This study aimed to identify a candidate marker and explore its molecular mechanism in PCa. Methods Gene expression datasets, GSE55945 (n=21) and GSE46602 (n=50), were downloaded from the Gene Expression Omnibus database. Bioinformatic approaches were applied to identify potential markers. Effects of the candidate marker on proliferation, migration, invasion, and ferroptosis (ferrous iron and malondialdehyde (MDA)) in PCa cells and its mechanism were assessed after performing cell transfection. Setanaxib Results A total of 1435 common differentially expressed genes were identified in GSE55945 and GSE46602. Five key gene modules were listed based on a protein-protein interaction network, containing five hub genes. Pannexin 2 (PANX2), a candidate marker was identified, and findings revealed substantial upregulation of its expression levels in PCa cell lines. Blocking expression of PANX2 resulted in suppression of proliferation, migration, and invasion in PCa cells, while increasing ferrous iron and MDA levels. However, these effects were rescued by Nrf2 activator, oltipraz. The Nrf2 signaling pathway was consequently applied to determine underlying mechanism of PANX2 in PCa cells. We established that silencing PANX2 remarkably reduced protein expression levels in members of Nrf2 signaling pathway (Nrf2, HO-1, and FTH1). Conclusion Our study demonstrated that PANX2 is implicated in the pathogenesis of PCa, which regulates malignant phenotypes and ferroptosis through Nrf2 signaling pathway, and maybe a potential therapeutic target for PCa.Objective Patients with HER2-positive metastatic breast cancer (MBC) benefit from trastuzumab-based therapy but eventually develop intrinsic or acquired resistance. Whether plasma HER2 gene copy number (GCN) could predict survival after trastuzumab treatment remained controversial. We evaluated the prognostic value of plasma HER2 GCN using low-coverage whole-genome sequencing (LC-WGS). Methods The plasma was collected from HER2-positive MBC patients whose pre-therapeutic samples were available before first-line trastuzumab-based treatment. Plasma DNA was extracted and assessed by LC-WGS for HER2 GCN. The optimal cut-off point for HER2 GCN to shorter survival was determined by receiver operating characteristic (ROC) curve analysis. Results A total of 49 patients were retrieved from 2013 to 2017, among whom 21 had multiple organ involvement (≥3 sites). Variations of HER2 GCN in pre-therapeutic plasma ranged from 1.89 to 23.86 (median = 2.59). ROC analysis identified the optimal cut-off point for HER2 GCN as 2.82 (P = 0.005), with 23 patients had high-level HER2 GCN and 26 in the low-level group. Both progression-free survival (PFS, P = 0.032) and overall survival (OS, P = 0.006) were adversely associated with high-level HER2 GCN. In multivariate analyses, high HER2 GCN was independently associated with shorter PFS [hazard ratio (HR) = 2.042, P = 0.037], while both high HER2 GCN (HR = 4.909, P = 0.004) and more metastatic organs (HR = 4.019, P = 0.011) were negative prognostic factors for OS. Conclusion In this population of patients with HER2-positive MBC, individuals with high HER2 GCNs in plasma had worse prognosis after trastuzumab-based therapy. Plasma HER2 GCN may be a prognostic marker in these patients.Purpose FAM110B is a member of the FAM110 family (family with sequence similarity 110), which is a component of the centrosome associated proteins. Previous studies have shown that FAM110B may be involved in the process of cell cycle and may play a role in carcinogenesis and tumor progression. Using an online database, we found that FAM110B may predict favorable prognosis in non-small cell lung cancer (NSCLC). Therefore, the role of FAM110B playing in NSCLC needs to be further investigated. Patients and methods Online databases and immunohistochemistry were used to predict the expression and prognostic value of FAM110B in NSCLC samples. Immunofluorescence staining was used to investigate the subcellular distribution of FAM110B. Western blot, MTT, colony formation, and matrigel invasion assay were used to detect the expression and the effect of FAM110B on mediating proliferation and invasion in NSCLC cell lines. Results In this study, immunohistochemistry results showed that FAM110B expression significantly coon of NSCLC cells by inhibiting Wnt/β-catenin signaling. Our study reveals the antitumor function of FAM110B in NSCLC and indicates that FAM110B is a potential therapeutic target.Background and aim Circular RNAs (circRNAs) have been highlighted to exert essential biological functions in papillary thyroid cancer (PTC). The purpose of this study was explore diagnostic utility of circRNAs in PTC patients. Patients and methods The distinctive expression profile of serum circRNAs was determined by individual quantitative real-time PCR (qRT-PCR) in two independent cohorts of 113 PTC patients, 80 thyroid nodules, and 111 healthy controls (HCs). A combination of circRNAs (circRNA-based combination index) was constructed by logistic regression. Results Individual qRT-PCR identification showed that two circRNAs (circRAPGEF5 and hsa_circ_0058124) were significantly up-regulated in PTC patients compared with HCs and thyroid nodules. Receiver-operating characteristic (ROC) curve analysis suggested that a combination of circRNAs was superior to individual circRNA in distinguishing PTC patients from HCs and thyroid nodules with area under ROC curve of more than 0.80. Furthermore, the combination of circRNAs increased significantly after systematic treatment, suggesting that it could monitor PTC dynamics. Additionally, the combination of circRNAs was independently correlated with PTC presence. Conclusion The combination of these altered circRNAs was correlated with PTC and may serve as a novel diagnostic approach.Hepatoid adenocarcinoma of the lung (HAL) is extremely rare and standardized treatment strategy for HAL has not been established. Patients with unresectable HAL have a shorter survival time ranges from 1 to 36 months. Here, we reported a 65-year-old female patient with unresectable alpha-fetoprotein-producing HAL harboring KRAS-G12V and no other targetable driver mutations. The patient was treated with multiple lines of chemotherapies followed by PD-1 inhibitor, sintilimab, due to positive staining of PD-L1, and achieved an overall survival of 52 months. Although the disease was under control, the patient experienced fifth-grade pneumonia and died after 6 months of anti-PD-1 treatment. This is the first case of KRAS-positive HAL patient achieved stable disease by PD-1 inhibitor, which may provide valuable information for the treatment strategy development of advanced HAL patients, and highlights the importance of molecular diagnosis in treatment decision-making.
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