Identification and Validation of Autophagy-Related Gene Nomograms to Predict the Prognostic Value of Patients with Cervical Cancer

Autophagy is a process of engulfing one’s own cytoplasmic proteins or organelles and coating them into vesicles, fusing with lysosomes to form autophagic lysosomes, and degrading the contents it encapsulates. Increasing studies have shown that autophagy disorders are closely related to the occurrence of tumors. However, the prognostic role of autophagy genes in cervical cancer is still unclear. In this study, we constructed risk signatures of autophagy-related genes (ARGs) to predict the prognosis of cervical cancer. The expression profiles and clinical information of autophagy gene sets were downloaded from TCGA and GSE52903 queues as training and validation sets. The normal cervical tissue expression profile data from the UCSC XENA website (obtained from GTEx) were used as a supplement to the TCGA normal cervical tissue. Univariate COX regression analysis of 17 different autophagy genes was performed with the consensus approach. Tumor samples from TCGA were divided into six subtypes, and the clinical traits of the six subtypes had different distributions. Further absolute shrinkage and selection operator (LASSO) and multivariable COX regression yielded an autophagy genetic risk model consisting of eight genes. In the training set, the survival rate of the high-risk group was lower than that of the low-risk group ( p < 0.0001). In the validation set, the AUC area of the receiver operating characteristic (ROC) curve was 0.772 for the training set and 0.889 for the verification set. We found that high and low risk scores were closely related to TNM stage ( p < 0.05). The nomogram shows that the risk score combined with other indicators, such as G, T, M, and N, better predicts 1-, 3-, and 5-year survival rates. Decline curve analysis (DCA) shows that the risk model combined with other indicators produces better clinical efficacy. Immune cells with an enrichment score of 28 showed statistically significant differences related to high and low risk. GSEA enrichment analysis showed the main enrichment being in KRAS activation, genes defining epithelial and mesenchymal transition (EMT), raised in response to the low oxygen level (hypoxia) gene and NF-kB in response to TNF. These pathways are closely related to the occurrence of tumors. Our constructed autophagy risk signature may be a prognostic tool for cervical cancer.

A comparative study of four diffusion-weighted imaging models in the diagnosis of cervical cancer

Background Most commonly used diffusion-weighted imaging (DWI) models include intravoxel incoherent motion (IVIM), diffusion kurtosis imaging (DKI), stretched exponential model (SEM), and mono-exponential model (MEM). Previous studies of the four models were inconsistent on which model was more effective in distinguishing cervical cancer from normal cervical tissue. Purpose To assess the performance of four DWI models in characterizing cervical cancer and normal cervical tissue. Material and Methods Forty-seven women with suspected cervical carcinoma underwent DWI using eight b-values before treatment. Imaging parameters, calculated using IVIM, SEM, DKI, and MEM, were compared between cervical cancer and normal cervical tissue. The diagnostic performance of the models was evaluated using independent t-test, Mann–Whitney U test, receiver operating characteristic (ROC) curve analysis, and multivariate logistic regression analysis. Results All parameters except pseudo-diffusion coefficient (D*) differed significantly between cervical cancer and normal cervical tissue ( P < 0.001). Through logistic regression analysis, all combined models showed a significant improvement in area under the ROC curve (AUC) compared to individual DWI parameters. The model with combined IVIM parameters had a larger AUC value compared to those of other combined models ( P < 0.05). Conclusion All four DWI models are useful for differentiating cervical cancer from normal cervical tissue and IVIM may be the optimal model.