PSMD14 is a 19S-proteasome-associated deubiquitinating enzyme that facilitates protein degradation by the 20S proteasome core particle Although accumulating evidence indicates that PSMD14 has emerged as a critical oncogenic factor by promoting tumor growth, the expression and function of PSMD14 in non-small cell lung cancer NSCLC remain largely unknown In this study, we assessed PSMD14 expression and correlated it with clinical-pathological features and patient survival in NSCLC We also determined the roles of PSMD14 in the regulation of lung adenocarcinoma LUAD cell growth The results showed that PSMD14 expression was significantly upregulated in human NSCLC tissues compared with adjacent non-cancerous tissues The PSMD14 level was associated with tumor size, lymph node invasion, and TNM stage in LUAD patients Importantly, high PSMD14 expression was associated with poor overall survival OS and disease-free survival DFS in LUAD patients Further, knockdown of PSMD14 significantly inhibited cell growth and caused G1 arrest and cellular senescence by increasing p21 stability in LUAD cells PSMD14 knockdown also promoted cell apoptosis by increasing cleaved caspase-3 levels in H1299 cells PSMD14 may serve as a potential prognostic marker and therapeutic target for LUAD patients © The authorsTrend analysis is the analysis using statistical models to estimate and predict potential trends over time, space or any independent continuous-variable It has been widely used in epidemiology and public health, but much less so in clinical oncology and basic cancer research  https//wwwselleckchemcom/products/serotonin-hclhtml  Methodological imitations of the chosen statistical package also appear to result in biased or less rigorous interrogation of cancer-related data We thus review the basic statistics of trend analysis, commonly used commands of statistical packages and the common pitfalls of conducting trend analysis Four free and 3 commercial statistical-packages were discussed in depth, including Joinpoint, Epi info, R package, Python, SAS, Stata and SPSS We hope that this review could serve as a practical yet concise guide for using statistical packages for trend analysis in translational and clinical oncology, and help improve the scientific rigor of trend analyses in these fields The guide, however, may also be applied to other research fields © The authorsPurpose Polymorphisms of genes in the platelet-derived growth factor PDGF signaling pathway have been found to predict cutaneous melanoma CM survival, but their clinical effects in acral melanoma AM patients have not been explored The aim of this study was to characterize the functional effect of the tag single-nucleotide polymorphism SNP rs2228230Cgt;T and assess its association with clinical outcomes in AM patients Methods The effect of rs2228230Cgt;T on mRNA structures and codon usage values were evaluated using in silico analyses PDGF receptor alpha PDGFRA expression vectors with the rs2228230C or rs2228230T allele were constructed to evaluate the expression and signaling activity of PDGFRA The expression of PDGFRA in AM samples was measured using in situ RNAscope hybridization and immunohistochemical staining The association of the rs2228230 genotype with survival was analyzed in two independent AM cohorts Results In silico analyses indicated that the rs2228230T allele increases the minimum free energy and reduces synonymous codon usage The rs2228230T allele decreased the expression of PDGFRA by reducing the stability of its mRNA and protein as well as the signaling activity of the MAPK and PI3K/AKT pathways PDGFRA mRNA and protein expression was significantly reduced in AM tissues with the rs2228230T allele The progression-free survival and overall survival of AM patients with the rs2228230T allele were significantly longer than those of patients with the CC genotype Conclusion Our study indicated that rs2228230T can reduce the expression of PDGFRA and downstream signaling activity and is associated with better survival in AM patients © The authorsPurpose This study aimed to investigate whether long noncoding RNA lncRNA LINC00467 could regulate proliferative and invasive abilities of glioma cells via p53 and DNA methyltransferase 1 DNMT1, so as to participate in the occurrence and progression of glioma Methods LINC00467 expression in glioma was analyzed by GEPIA database and LINC00467 expression in glioma cell lines was detected by qRT-PCR The regulatory effects of LINC00467 and p53 on proliferative, invasive capacities and cell cycle were conducted by CCK-8 and EdU assays, transwell assay and flow cytometry, respectively The binding conditions between LINC00467, DNMT1 and p53 were determined by RNA immunoprecipitation RIP and Chromatin immunoprecipitation ChIP assays Western blot was conducted to determine whether LINC00467 could regulate p53 in glioma cells Finally, rescue experiments were carried out to evaluate whether LINC00467 regulates proliferative and invasive abilities of glioma cells through p53 Results The expression of LINC00467 was significantly up-regulated in tumor samples than that in normal samples, which was not correlated with patient survival time Besides, expression of LINC00467 was higher in glioma cells than that of negative control cells Upregulation of LINC00467 promoted proliferative and invasive abilities, and accelerated cell cycle in G0/G1 phase of U87 and LN229 cells The results of RIP and ChIP assays demonstrated that LINC00467 could bind to DNMT1 and inhibit p53 expression Overexpression of p53 partially reversed the enhancement of LINC00467 on proliferative and invasive abilities of glioma cells Conclusion These results indicated that high expression of LINC00467 could promote proliferative and invasive abilities of glioma cells through targeting inhibition of p53 expression by binding to DNMT1 © The authorsBackground Lung cancer is the most common cancer worldwide, both in terms of the incidence and mortality NDC80 complex comprising of NDC80, NUF2, SPC24, and SPC25 is a heterotetrameric protein complex located in the outer layer of the kinetochore and plays a critical role in mitosis This study focuses on the effects of NDC80 complex genes on clinical features and prognosis in lung adenocarcinoma LUAD Materials and methods Expression of NDC80 complex in LUAD and related clinical information was extracted from the TCGA website NDC80 complex gene functional analysis and correlation analysis was conducted by using DAVID, BiNGO, Gene MANIA, STRING and GSEA Survival probability was predicted by nomogram Statistical analysis was used to predict NDC80 complex gene expression on clinical features and prognosis in patients with LUAD Results Expression of NDC80, NUF2, SPC24 and SPC25 was significantly elevated in LUAD tumors compared with normal tissues P 0600 for each Higher expression of NDC80, NUF2, SPC24 and SPC25 was associated with low overall survival OS in univariate analysis Higher expression of NDC80 and SPC25 was associated with low OS in multivariate analysis High expression of NDC80 combined with high expression of SPC25 was predictive of poor OS in LUAD in joint analysis link2 Conclusion NDC80 complex gene might be an early indicator of diagnosis and prognosis of LUAD The combined detection of NDC80, NUF2, SPC24 and SPC25 may become a new research direction in LUAD diagnosis and a new target for tumor targeted gene therapy © The authorsModern research into carcinogenesis has undergone three phases Surgeons and pathologists started the first phase roughly 250 years ago, establishing morphological traits of tumors for pathologic diagnosis, and setting immortality and autonomy as indispensable criteria for neoplasms A century ago, medical doctors, biologists and chemists started to enhance "experimental cancer research" by establishing many animal models of chemical-induced carcinogenesis for studies of cellular mechanisms In this second phase, the two-hit theory and stepwise carcinogenesis of "initiation-promotion" or "initiation-promotion-progression" were established, with an illustrious finding that outgrowths induced in animals depend on the inducers, and thus are not authentically neoplastic, until late stages The last 40 years are the third incarnation, molecular biologists have gradually dominated the carcinogenesis research fraternity and have established numerous genetically-modified animal models of carcinogenesis However, evidence has not been provided for immortality and autonomy of the lesions from most of these models Probably, many lesions had already been collected from animals for analyses of molecular mechanisms of "cancer" before the lesions became autonomous We herein review the monumental work of many predecessors to reinforce that evidence for immortality and autonomy is essential for confirming a neoplastic nature We extrapolate that immortality and autonomy are established early during sporadic human carcinogenesis, unlike the late establishment in most animal models It is imperative to resume many forerunners' work by determining the genetic bases for initiation, promotion and progression, the genetic bases for immortality and autonomy, and which animal models are, in fact, good for identifying such genetic bases © The authorsAims Aberrant hypermethylation of CpG islands is an important hallmark of colorectal cancer CRC We previously utilized methyl-DNA immunoprecipitation assays to identify a novel methylated gene, chondrolectin CHODL, preferentially methylated in human CRC In this study, we examined the epigenetic inactivation, biological effects and prognostic significance of CHODL in CRC Main methods The methylation status of CHODL in CRC was evaluated by bisulfite genomic sequencing BGS The functions of CHODL in CRC were determined by proliferation, apoptosis, cell migration and invasion assays The impact and underlying mechanisms of CHODL in CRC were characterized by western blot and RNA-Seq analyses The association between CHODL and CRC clinical features was examined using The Cancer Genome Atlas TCGA database and immunohistochemical staining Key findings CHODL was downregulated in 10 CRC cell lines and CRC tissues, and promoter hypermethylation contributed to its inactivation Ectopic expression of CHODL inhibited colony formation, suppressed cell viability, induced apoptosis, and restrained cell migration and invasion in vitro and in vivo 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 authorsBackground 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 link3 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