Clear cell renal cell carcinoma (ccRCC) is the most common and lethal renal malignant tumor in adults. The aim of the present study was to identify the key genes involved in ccRCC metastasis. Expression profiling data for ccRCC patients with metastasis and without metastasis were obtained from The Cancer Genome Atlas database. The datasets were used to identify differentially expressed genes (DEGs) between the metastasis group and the non-metastasis group using the DESeq2 package. Function enrichment analyses of DEGs were performed. The protein-protein interaction (PPI) network was constructed and analyzed using the Search Tool for the Retrieval of Interacting Genes and Cytoscape for further analysis of the identified hub genes. A total of 472 DEGs were identified, including 247 that were upregulated and 225 that were downregulated in the metastasis group. Gene Ontology enrichment analysis revealed that DEGs were mainly enriched in cell transmembrane movement and mitotic cell cycle process. Kyoto Encyclopedia of Genes Genomes pathway analysis revealed that the DEGs were mainly involved in the ‘cell cycle’ (hsa04110), ‘collecting duct acid secretion’ (hsa04966), ‘complement and coagulation cascades’ (hsa04610) and ‘aldosterone-regulated sodium reabsorption’ (hsa04960) pathways. Using the PPI network, 35 hub genes were identified, and the majority of them were upregulated in ccRCC tissue compared with normal kidney tissue. The expression levels of certain hub genes (CDKN3, TPX2, BUB1B, CDCA8, UBE2C, NDC80, RRM2, NCAPG, NCAPH, PTTG1, FAM64A, ANLN, KIF4A, CEP55, CENPF, KIF20A, ASPM and HJURP) were significantly associated with overall survival and recurrence-free survival in ccRCC. The present study has identified key genes associated with the metastasis of ccRCC.

The expression profile of seven lncRNAs can effectively predict ER after surgical resection for HCC.

Background: MicroRNAs (miRs) have been shown to play important roles in various cancers and may be a reliable prognostic marker. However, its prognostic value in endometrial carcinoma (UCEC) needs to be further explored. Objectives: The aim of this study was to create a miR-based signature to effectively predict the prognosis for patients with uterine corpus endometrial carcinoma (UCEC). Method: Using UCEC data set in TCGA, we identified differentially expressed miRs between UCEC and healthy endometrial tissues. The LASSO method was used to construct a miR-based signature prognosis index for predicting prognosis in the training cohort. The miR-based signature prognosis index was validated in an independent test cohort. MiRNet tool was applied to performed functional enrichment analysis of this miR-based signature. Results: A total of 208 miRs were differentially expressed between UCEC and healthy endometrial tissues. Five miRs (miR-652, miR-3170, miR-195, miR-34a, and miR-934) were identified to generate a prognosis index (PI). The five-miR signature is a promising biomarker for predicting 5-year-survival rate of UCEC with AUC = 0.730. The PI remained an independent prognostic factor adjusted by routine clinicopathologic factors. Using the PI, we could successfully identify the high-risk individuals, furthermore, it still worked in an independent test cohort. The five miRs involved in various pathways associated with cancer. Conclusions: We proposed and validated a five-miR signature that could serve as an independent prognostic predictor of UCECs.

Abstract. Chronic myelogenous leukemia (CML) is a condition characterized by a balanced genetic translocation, t (9;22) (q34;q11.2), which leads to a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This rearrangement is referred to as the Philadelphia chromosome. At a molecular level, this translocation results in the formation of the BCR-ABL fusion oncogene, which translates into a BCR-ABL oncoprotein. Imatinib, nilotinib and dasatinib are three tyrosine kinase inhibitors that have been approved by the US Food and Drug Administration for the treatment of patients diagnosed with CML in the chronic phase (CML-CP). The present study describes the case of a patient with imatinib-resistant CML who, following two months of treatment with nilotinib, no longer exhibited detectable BCR-ABL fusion genes or M244V mutations. This suggests that nilotinib may be effective for treating CML cases in which the BCR-ABL fusion protein has an M244V mutation. IntroductionChronic myelogenous leukemia (CML) is a cancer of the white blood cells characterized by a balanced genetic translocation, t (9;22) (q34;q11.2), which leads to a fusion of the Abelson oncogene (ABL) from chromosome 9q34 with the breakpoint cluster region (BCR) gene on chromosome 22q11.2. This chromosomal translocation is known as the Philadelphia chromosome. At a molecular level, the rearrangement results in the formation of the BCR-ABL fusion oncogene, which translates into a BCR-ABL oncoprotein (1).The US Food and Drug Administration has approved three tyrosine kinase inhibitors (TKIs), imatinib, nilotinib and dasatinib, as first-line treatments for patients diagnosed with CML in the chronic phase (CML-CP) (2-5). Imatinib mesylate, otherwise known as Gleevec ® (Novartis Pharmaceuticals Corp., East Hanover, NJ, USA), was the first of the TKIs to receive approval; however, 20-40% of patients receiving imatinib as a first-line therapy are likely to eventually require an alternative treatment, due to intolerance or resistance to imatinib (5). It is recommended that, upon failure of imatinib treatment, patients with CML should be assessed for BCR-ABL kinase domain mutations, as this can indicate which TKI should be selected for continued therapy. Dasatinib and nilotinib have been demonstrated to retain efficacy against several of the mutations known to confer resistance to imatinib (6). Notably, a number of distinct mutations leading to decreased sensitivity to dasatinib and nilotinib have been found in in vitro and in vivo studies (7,8). Dasatinib is favored when patients have Y253H, E255K/V or F359C/V mutations in BCR-ABL. By contrast, nilotinib is more effective when V299L or F317L mutations are present (2). Despite this evidence, it remains unclear how the M244V mutation to the BCR-ABL fusion protein should affect the choice of treatment. The present study describes the effect of nilotinib therapy in a patient with imatinib-resistant CML. Case reportThis study was conducted in accordanc...

Skin cancer is a typical cancer tumor, which occurs all over the world and has a relatively high recurrence rate, including metastatic tumors that occur in other tissues and metastases to the skin, thus jeopardizing the personal life satisfaction and soundness of patients. Due to individual differences, the traditional treatment methods cannot adapt to every patient accurately, so it is difficult to achieve the desired treatment effect for each individual. Nowadays, with the development of gene chip, many new therapies based on gene are more targeted and flexible for the treatment of skin cancer patients. Therefore, it is necessary to mine and analyze appropriate gene biomarkers according to patients' genes. Because of the high cost of gene chip technology and the large number of human genes, there are few samples of gene data and high dimensions. It is a key problem to mine effective genetic biomarkers from the sample data. In this paper, we firstly performed the preliminary analysis using the difference expression analysis and proportional hazards model, then used the elastic network method to reduce the range of genetic data selection, and screened 26 gene prognostic markers closely related to the recurrence of metastatic skin cancer. Finally, the 26 gene biomarkers were analyzed by functional analysis and verified using a test sample. Research findings have shown that the obtained genetic markers have certain value in the clinical prognostic treatment of metastatic skin cancer.