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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.

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.