Construction and Validation of a Potent Epigenetic Modification-Related Prognostic Signature for Osteosarcoma Patients. (22nd November 2021)

• Record Type: Journal Article
• Authors: Liu, Siyu; Wu, Bing; Li, Xiaomin; Zhao, Lulu; Wu, Wen; Ai, Songtao
• Other Names: Cao Song Academic Editor.
• Is Part Of: Journal of oncology. Volume 2021(2021)
• Publication Date: 2021-11-22
• Subjects: Oncology -- Research -- Periodicals; Tumors -- Periodicals; Neoplasms; Oncology -- Research; Tumors; Periodicals; Periodicals; 616.994
• DOI: 10.1155/2021/2719172
• Languages: English
• ISSNs: 1687-8450

Abstract

Abstract : Background . Increasing evidence has shown that tumorigenesis correlates with aberrant epigenetic factors, such as DNA methylation, histone modification, RNA m6A modification, RNA binding proteins, and transcription factors. However, it is unclear that how epigenetic genes linked with alteration contribute to osteosarcoma's incidence and clinical prognosis. We developed an epigenetic modification-related prognostic model that may improve the diagnosis and prognosis of osteosarcoma. Methods . We investigated the epigenetic modification-associated genes and their clinical significance in osteosarcoma in this research. Our gene transcriptome data were obtained from the TARGET database and the GEO database. Bioinformatics techniques were used to investigate their functionalities. The diagnostic and prognostic models were constructed using univariate and multivariate Cox regression. In addition, we developed a nomogram indicating the practicability of the prognostic model described above. Results . A risk score model constructed based on four epigenetic modification-related genes (MYC, TERT, EIF4E3, and RBM34) can effectively predict the prognosis of patients with osteosarcoma. Based on the risk score and clinical features, we constructed a nomogram. Conclusion . Epigenetic modification-related genes have been identified as important prognostic markers that may assist in osteosarcoma therapy therapeutic decision-making.