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Background Mixed cell ovarian adenocarcinoma (MCOA) is a malignant gynecologic tumor consisting of serous, mucous, and papillary tumor cells. However, the clinical features and prognosis of MCOA patients are unclear. Methods In this study, univariate and multivariate Cox proportional risk models were performed to identify independent prognostic factors. The Kaplan–Meier method was used to assess the relationship between clinical characteristics and patient survival. Finally, a nomogram was constructed and validated to predict patient survival time, and the C-index was used to evaluate the efficacy of the nomogram. Results A total of 2,818 patients diagnosed with MCOA were identified, and the 5-year survival rate was 62%. Univariate and multivariate Cox models suggested that age (HR=1.28, 95% CI[1.15,1.44]), grade (HR=1.26, 95% CI[1.12,1.41]), SEER stage (HR=1.63, 95% CI[1.25,2.13]) and AJCC (American Joint Committee on Cancer) stage (HR=1.59, 95% CI[1.36,1.86]) were independent prognostic factors for MCOA patients. After propensity score matching for age, grade, SEER stage, and AJCC stage, the 5-year survival rate was 69.7% for ovarian serous cystadenocarcinoma and 62.9% for ovarian papillary serous cystadenocarcinoma. These results mean that serous adenocarcinoma had the best prognosis of the three pathologic types of ovarian carcinoma (pp=0.712). Finally, a nomogram consisting of age, grade, SEER stage, and AJCC stage was established and validated to predict the survival time, with C-indices of 0.743 and 0.731, respectively. Conclusions In summary, MCOA is uncommon, and age, grade, SEER stage, and AJCC stage are independent prognostic factors. Compared with other common malignant ovarian tumors, MCOA has a poor prognosis.

Hepatic angiosarcoma(HAS) is rare and is the primary vascular-derived malignancy of the liver. Its clinical characteristics, therapeutic strategy management, and the outcome are unclear.This is a retrospective study of patients from the SEER database. Survival analysis was performed by the Kaplan-Meier method. Univariate and multivariate Cox models were used to identify risk factors. Propensity Score Matching(PSM) analysis was used to remove confounding bias. The nomogram was constructed, and the performance was measured using the C-index.A total of 300 HAS patients diagnosed between 1975 and 2016 were identified for this study, with an estimated median cancer-specific survival(CSS) of 1 month. The median CSS was 6 months in both the surgery and chemotherapy groups. Age(HR = 1.5206, p = 0.0058), sex(HR = 1.3906, p = 0.0391), SEER stage(HR = 1.4426, p 0.0001), surgery(HR = 0.4493, p = 0.0001) and chemotherapy(HR = 0.28161, p 0.0001) are potential independent prognostic factors. Of these HAS patients, 29 received surgical treatment without chemotherapy, and 63 received chemotherapy without surgery. A 1:1 PSM was performed to select candidates from the surgery-only group and the chemotherapy-only group. The survival analysis showed that the median survival time was 3 months in the surgery-only cohort and 5 months in the chemotherapy-only cohort, and there was no statistical difference between the two groups. Finally, a nomogram was constructed, with a C-index of 0.754.HAS is uncommon and has a poor prognosis. It was found that age, sex, SEER stage, surgery, and chemotherapy were independent prognostic factors for patients. Both surgery and chemotherapy could significantly prolong the survival of patients, and there was no statistical difference between the prognosis of patients treated with chemotherapy alone and those treated with surgery alone.

Background Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and the third leading cause of cancer-related death. MicroRNAs and transcription factors (TFs) cooperate to regulate the same target gene, thus affecting the progression of HCC. Methods Differentially expressed miRNAs and mRNAs were screened. Functional enrichment analysis of these HCC-related mRNAs was performed, and a protein-protein interaction network was constructed. TFs that regulate these miRNAs and hub genes were also screened. Results Ten differentially upregulated miRNAs and 5 differentially downregulated miRNAs were screened. Additionally, 183 downregulated mRNAs and 303 upregulated mRNAs that are potentially bound to these differentially expressed miRNAs were identified. The Kyoto Encyclopedia of Genes and Genomes (KEGG) results showed that the differentially expressed mRNAs were significantly enriched in pathways in cancer, the Wnt signaling pathway, and the Rap1 signaling pathway. Then, 220 TFs were identified for 5 candidate genes of the downregulated mRNAs, and 258 TFs were identified for 9 candidate genes of the upregulated mRNAs. Finally, the 9 upregulated hub genes were related to higher overall survival (OS) in the low-expression group, and 4/5 downregulated hub genes were related to higher OS in the high-expression group. Conclusions This study constructed a potential regulatory network between candidate molecules and that need to be further verified. These regulatory relationships are expected to clarify the new molecular mechanisms of the occurrence and development of HCC.

Background Chaperonin containing TCP1 subunits (CCTs) are important components in the folding of newly synthesized proteins and are involved in cell growth, proliferation, and apoptosis in eukaryotes. Accumulating evidence indicates that dysregulation of CCTs is involved in tumorigenesis. However, the roles of distinct CCTs in the occurrence and development of hepatocellular carcinoma (HCC) are largely unknown. To address this issue, the mRNA expression and the prognostic value of different CCTs in HCC patients were analyzed. Methods The mRNA expression levels of CCTs in tumors and the relationship between clinical parameters and CCTs in patients with HCC were analyzed by using ONCOMINE and Gene Expression Profiling Interactive Analysis (GEPIA) databases. The prognostic values of CCTs in HCC patients were determined by using the Kaplan-Meier plotter. The genetic alteration, coexpression, and interaction of CCTs and their frequently altered neighboring genes in HCC patients were analyzed by c-BioPortal. Gene functional enrichment and signaling pathways affected by CCTs in patients with HCC were investigated by using R software. Results The mRNA expression levels of CCTs were significantly upregulated in HCC tissues. Upregulated expression of CCTs was found to be significantly associated with alpha-fetoprotein (AFP), pathological grade, and macro- and microvascular invasion, but there was no correlation with the Child-Pugh classification. Moreover, survival analysis showed that the upregulated expression of CCTs correlated with shorter overall survival (OS) and disease-free survival (DFS) in patients with HCC. The observed genetic alteration rate of CCTs was as high as 51.39% in HCC and was associated with a poorer prognosis in HCC patients. Pathway analysis confirmed that the expression levels of PI3K/AKT pathway genes were affected by CCT genetic alterations. Conclusions Our results suggest that CCTs could be promising prognostic biomarkers and potential therapeutic targets for HCC patients. However, further studies are required to validate our findings and promote the clinical utility of CCTs in HCC patients.

Lenvatinib is a long-awaited alternative to sorafenib for the first-line targeted therapy of patients with advanced hepatocellular carcinoma (HCC). However, resistance to lenvatinib has also become a major obstacle to improving the prognosis of HCC patients. The underlying molecular mechanisms contributing to lenvatinib resistance in HCC are largely unknown. HGF/c-MET axis activation is related to tumor progression and several hallmarks of cancer and is considered as the key contributor to drug resistance. In the present study, we focused on the role of the HGF/c-MET axis in mediating lenvatinib resistance in HCC cells. We showed that HGF reduced the antiproliferative, proapoptotic, and anti-invasive effects of lenvatinib on HCC cells with high c-MET expression but did not significantly affect HCC cells with low c-MET expression. The c-MET inhibitor PHA-665752 rescued HCC cells from HGF-induced lenvatinib resistance. Furthermore, HGF/c-MET activated the downstream PI3K/AKT and MAPK/ERK pathways and promoted epithelial-mesenchymal transition (EMT) in HCC cells. Collectively, our results suggested that combining lenvatinib treatment with a c-MET inhibitor may improve its systemic therapeutic efficacy in HCC patients with high c-MET expression.