method have become a research trend. The ultimate biomarkers must be easily detectable with fine sensitivity and specificity and also must discriminate PC from other benign pancreatic diseases 9. Blood is a simply reachable and rather steady sample to find alerting biomarkers. Technological advances in the recent years have provided possibilities to detect circulating biomarkers based on "omics" research, relying on proteins, cell-free DNAs, non-coding RNAs, circulating tumor cells (CTCs), and exosomes molecular contents 10. MicroRNAs (miRs) are small (~22 nucleotides) non-coding RNAs that have gene regulatory roles via targeting the 3′-untranslated region (3′-UTR) of their target mRNA and finally cause either translational repression or mRNA degradation 11,12. Up to now, a number of biomarkers have been introduced as PC biomarkers such CEA, CA19-9, CA125 and CA72-4. Nonetheless, none of these tumor markers has shown efficient sensitivity or specificity for diagnosing PC at primary stages and have been used for post resection monitoring rather than earlier detection purposes. MiRNAs seem to be truly stable in blood and several authors reported that miRNAs show dysregulation in pancreatic diseases being able to differentiate PC from pancreatitis, pancreatic benign masses as well as normal subjects 13. Furthermore, owing to advanced technologies in high-throughput molecular methods the understanding of the pathophysiology of pancreatic cancer have been improved. Various genome-wide mRNA and miRNA expression profiling studies using microarray-based and NGS approaches have provided important insights into the phenotypic characteristics of pancreatic cancer 14. In this study, using multiple bioinformatics tools, we integrated various serum expression profiles of miRNAs to find the most significant potential miRNA signatures helpful in the diagnosis of PC and constructed a novel miRNA-mRNA regulatory network in PC using bioinformatics approaches. Next, we investigated the molecular mechanisms downstream of the captured miRNA signatures and their predicted target genes correlated to PC progression and analyzed them in a logistic model. Material and method Microarray datasets search. In order to find proper miRNA expression profiles in microarray datasets, we conducted a systematic search in Gene Expression Omnibus (GEO) database (https://www.ncbi.nlm.nih.gov/ geo/) 15. Using the keywords "Pancreatic cancer" and "Serum", at the first step we reached 900 datasets. Then, we limited the results using 'Homo sapiens' and 'Non-coding RNA profiling by array' filters, so we reached to 16 datasets. Finally, by setting the sample count on more than 200 samples, 4 final datasets were achieved. Differentially expressed miRNAs (DEMs) detection. The DEMs were obtained using the online tool GEO2R in the GEO database 15 , which makes evaluations using the GEOquery and limma R packages from the Bioconductor project to compare two or more groups of samples in a GEO dataset. Normalization has been carried out using the RMA algorithm. To ke...

BackgroundNon-small cell lung cancer (NSCLC) as the most frequent type of lung cancer is associated with extensive mortality. Researchers have studied the suitability of several molecules as biomarkers for early detection of this cancer. Long non-coding RNAs (lncRNAs) as the main regulators of gene expression have also been assessed in this regard.MethodsIn the present study, we compared expression level of Fas-antisense 1 (FAS-AS1), Growth Arrest Specific 5 (GAS5), PVT1, Nuclear Paraspeckle Assembly Transcript 1 (NEAT1), HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1), taurine upregulated gene 1 (TUG1) and TNFα and hnRNPL related immunoregulatory LincRNA (THRIL) in 32 NSCLC samples and their corresponding adjacent non-cancerous tissues (ANCTs).ResultsNEAT1 has been significantly over-expressed in NSCLC tissues obtained from male subjects compared with the corresponding ANCTs (Relative expression (REx) = 3.022, P = 0.019) but not in female subjects (P = 0.975). FAS-AS1 was significantly down-regulated in NSCLC tissues obtained from both males and females subjects compared with the corresponding ANCTs (REx = − 4.12 and − 3.14, P = 0.015 and 0.033 respectively). TUG1, GAS5, THRIL and HOTAIRM1 were significantly down-regulated in tumoral tissues obtained from male subjects compared with the corresponding ANCTs.ConclusionsThe observed dysregulation of these lncRNAs in NSCLC tissues compared with the corresponding ANCTs warrants future studies to confirm the results of the current study in larger sample sizes to elaborate their role as cancer biomarkers.

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Cancer-testis (CT) antigens are tumor-associated antigens attracting immunologists for their possible application in the immunotherapy of cancer. Several clinical trials have assessed their therapeutic potentials in cancer patients. Breast cancers, especially triple-negative cancers are among those with significant expression of CT genes. Identification of CT genes with high expression in cancer patients is the prerequisite for any immunotherapeutic approach. CT genes have gained attention not only for immunotherapy of cancer patients, but also for immunoprevention in high-risk individuals. Many CT genes have proved to be immunogenic in breast cancer patients suggesting the basis for the development of polyvalent vaccines.

Breast cancer accounts for one third of new cancer cases among women. The need for biomarkers for early detection is the stimulus to researchers to evaluate altered expression of genes in tumours. Cancer-testis (CT) genes are a group with limited expression in normal tissues except testis but up-regulation in a wide variety of cancers. We here evaluated expression of two CT genes named FBXO39 and TDRD4 in 32 invasive ductal carcinoma samples, 10 fibroadenomas and 6 normal breast tissue samples, in addition to two breast cancer cell lines, MCF-7 and MDA-MB-231, by the means of quantitative real time RT-PCR. FBXO39 showed significant up-regulation in invasive ductal carcinoma samples in comparison with normal samples. It also was expressed in both cell lines and after RHOXF1 gene knock down it was down-regulated in MCF-7 but up-regulated in the MDA-MB-231 cell line. TDRD4 was not expressed in the MCF-7 cell line and any of the tissue samples except testis. However, it was expressed in MDA-MB-231 and was up-regulated after RHOXF1 gene knock down. Our results show that FBXO39 but not TDRD4 can be used for cancer detection and if proved to be immunogenic, might be a putative candidate for breast cancer immunotherapy.

PurposeNeuropilin-1 (NRP1) as an isoform-specific receptor for vascular endothelial growth factor and placenta growth factor in endothelial cells has been demonstrated to be expressed in breast cancer cells where it plays functional roles in cell survival, invasion, and migration. We hypothesized that an expression of NRP1 in breast cancer tissues is associated with clinicopathological data of patients and expression of the tumor suppressor miR-206.Patients and methodsWe evaluated the expression of NRP1 in 48 invasive ductal carcinomas of the breast and their corresponding adjacent noncancerous tissues (ANCTs) by means of real-time polymerase chain reaction. We also extracted data on miR-206 gene expression from the same cohort of patients to evaluate the correlation between expression levels of miR-206 and NRP1. In addition, we quantified NRP1 protein levels using the enzyme-linked immunosorbent assay technique.ResultsNo significant difference was found in NRP1 expression between tumoral tissues and ANCTs. We also assessed the associations between expression levels of NRP1 and clinicopathological data of patients and found no significant associations between NRP1 transcript levels and any characteristic. However, NRP1 protein concentrations were significantly higher in patients with lymph node involvement compared with those without lymph node involvement. No correlation was found between NRP1 and miR-206 expression levels.ConclusionNRP1 protein levels might be an indicator of metastasis potential in breast cancer. Future studies are needed to confirm these results in larger cohorts of patients.

Background: Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest malignancies and a major health problem worldwide. There were no major advances in conventional treatments in inhibiting tumor progression and increasing patient survival time. In order to suppress mechanisms responsible for tumor cell development such as those with oncogenic roles, more advanced therapeutic strategies should be sought. One of the most important oncogenes of pancreatic cancer is the MYC gene. The overexpression of MYC can activate many tumorigenic processes such as cell proliferation and pancreatic cancer cell invasion. MiRNAs are important molecules that are confirmed by targeting mRNA transcripts to regulate the expression of the MYC gene. Therefore, restoring MYC-repressing miRNAs expression tends to be an effective method of treating MYC-driven cancers. Objective: The purpose of this study was to identify all validated microRNAs targeting C-MYC expression to inhibit PDAC progression by conducting a systematic review. Methods: In this systematic review study, the papers published between 2000 and 2020 in major online scientific databases including PubMed, Scopus, and Web of Science were screened, following inclusion and exclusion criteria. We extracted all the experimental studies that showed miRNAs could target the expression of the MYC gene in PDAC. Results: Eight papers were selected from a total of 89 papers. We found that six miRNAs (Let-7a, miR-145, miR-34a, miR-375, miR-494, and miR-148a) among the selected studies were validated for targeting MYC gene and three of them confirmed Let-7a as a direct MYC expression regulator in PC cells. Finally, we summarized the latest shreds of evidence of experimentally validated miRNAs targeting the MYC gene with respect to PDAC's therapeutic potential. Conclusion: Restoring the expression of MYC-repressing miRNAs tends to be an effective way to treat MYC-driven cancers such as PDAC. Several miRNAs have been proposed to target this oncogene via bioinformatics tools, but only a few have been experimentally validated for pancreatic cancer cells and models. Further studies should be conducted to find the interaction network of miRNA-MYC to develop more successful therapeutic strategies for PC, using the synergistic effects of these miRNAs.

Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED), also named as autoimmune polyglandular syndrome (APS) type 1, is a rare autosomal recessive disorder caused by mutations in autoimmune regulator (