Head and neck paragangliomas (HNPGLs) are rare neuroendocrine tumors that have a high degree of heritability and are predominantly associated with mutations in ten genes, such as SDHx, SDHAF2, VHL, RET, NF1, TMEM127, MAX, FH, MEN2, and SLC25A11. Elucidating the mutation prevalence is crucial for the development of genetic testing. In this study, we identified pathogenic/likely pathogenic variants in the main susceptibility genes in 102 Russian patients with HNPGLs (82 carotid and 23 vagal paragangliomas) using whole exome sequencing. Pathogenic/likely pathogenic variants were detected in 43% (44/102) of patients. PY-60 ic50 We identified the following variant distribution of the tested genes SDHA (1%), SDHB (10%), SDHC (5%), SDHD (24.5%), and RET (5%). SDHD variants were observed in the majority of the patients with bilateral/multiple paragangliomas. Thus, among Russian patients with HNPGLs the most frequently mutated gene was SDHD followed by SDHB, SDHC, RET, and SDHA. Hepatocellular carcinoma (HCC) is a common malignant tumor with high mortality and poor prognoses around the world. Ferroptosis is a new form of cell death, and some studies have found that it is related to cancer immunotherapy. The aim of our research was to find immunity- and ferroptosis-related biomarkers to improve the treatment and prognosis of HCC by bioinformatics analysis. First, we obtained the original RNA sequencing (RNA-seq) expression data and corresponding clinical data of HCC from The Cancer Genome Atlas (TGCA) database and performed differential analysis. Second, we used immunity- and ferroptosis-related differentially expressed genes (DEGs) to perform a computational difference algorithm and Cox regression analysis. Third, we explored the potential molecular mechanisms and properties of immunity- and ferroptosis-related DEGs by computational biology and performed a new prognostic index based on immunity- and ferroptosis-related DEGs by multivariable Cox analysis. Finally, we used HCC dataHCC prognoses beyond conventional clinicopathological factors. Moreover, it also brings us new insights into the molecular mechanisms of HCC.Our results suggest that this specific seven-biomarker signature may be clinically useful in the prediction of HCC prognoses beyond conventional clinicopathological factors. Moreover, it also brings us new insights into the molecular mechanisms of HCC. The tumor immune microenvironment is closely related to the malignant progression and treatment resistance of glioma. Long non-coding RNA (lncRNA) plays a regulatory role in this process. We investigated the pathological mechanisms within the glioma microenvironment and potential immunotherapy resistance related to lncRNAs. We downloaded datasets derived from glioma patients and analyzed them by hierarchical clustering. Next, we analyzed the immune microenvironment of glioma, related gene expression, and patient survival. Coexpressed lncRNAs were analyzed to generate a model of lncRNAs and immune-related genes. We analyzed the model using survival and Cox regression. Then, univariate, multivariate, receiver operating characteristic (ROC), and principle component analysis (PCA) methods were used to verify the accuracy of the model. Finally, GSEA was used to evaluate which functions and pathways were associated with the differential genes. Normal brain tissue maintains a low-medium immune state, and gliom expression of immune-related lncRNAs and the relationship between risk scores and immune-related indicators (PDL1, CTLA4, CD3, CD8, iNOS) were verified by q-PCR and immunohistochemistry (IHC). For the first time, we constructed immune gene-related lncRNA risk models. The risk score may be a new biomarker for tumor immune subtypes and provide molecular targets for glioma immunotherapy.For the first time, we constructed immune gene-related lncRNA risk models. The risk score may be a new biomarker for tumor immune subtypes and provide molecular targets for glioma immunotherapy. Bladder cancer (BLCA) is the 11th most common malignancy worldwide. Although significant improvements have been made in screening, diagnosis, and precise management in recent years, the prognosis of BLCA remains bleak. This study aimed to investigate the prognostic significance of tumor-infiltrating immune cells and construct ceRNA networks in BLCA patients. The expression data of BLCA patients were obtained from The Cancer Genome Atlas (TCGA) database. A competing endogenous RNA (ceRNA) network was constructed to identify the hub genes involved in the prognosis of BLCA. The CIBERSORT algorithm was utilized to investigate the infiltration levels of 22 subsets of immune cells. Ultimately, the nomogram was generated to visualize the survival probability of each patient, with the calibration curve being performed to assess its performance. Furthermore, the Pearson correlation test was used to explore the correlation between the identified hub genes in the ceRNA network and the prognostic-related immune cells. A total of eight elements in the ceRNA network were considered as key members and correlated with the prognosis of BLCA, including , , , , , , , and . T cells CD8, T cells follicular helper (Tfh), and neutrophils were identified as independent prognostic factors in BLCA. The co-expression analysis showed that there was a significant correlation between the identified hub genes and immune cells. Our results suggest that the mechanism of regulates the expression of and , and the infiltration of Tfh and neutrophils might play pivotal roles in the progression of BLCA.Our results suggest that the mechanism of hsa-miR-29c-3p regulates the expression of ELN and DSC2, and the infiltration of Tfh and neutrophils might play pivotal roles in the progression of BLCA.We take advantage of synteny blocks, the analytical construct enabled at the evolutionary moment of speciation or polyploidization, to follow the independent loss of duplicate genes in two sister species or the loss through fractionation of syntenic paralogs in a doubled genome. By examining how much sequence remains after a contiguous series of genes is deleted, we find that this residue remains at a constant low level independent of how many genes are lost-there are few if any relics of the missing sequence. Pseudogenes are rare or extremely transient in this context. The potential exceptions lie exclusively with a few examples of speciation, where the synteny blocks in some larger genomes tolerate degenerate sequence during genomic divergence of two species, but not after whole genome doubling in the same species where fractionation pressure eliminates virtually all non-coding sequence.