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Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer
Abnormal lipid metabolism is closely related to the malignant biological behavior of tumor cells. Such abnormal lipid metabolism provides energy for rapid proliferation, and certain genes related to lipid metabolism encode important components of tumor signaling pathways. In this study, we analyzed...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8564347/ https://www.ncbi.nlm.nih.gov/pubmed/33386701 http://dx.doi.org/10.1002/2211-5463.13074 |
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author | Ye, Yanrong Chen, Zhe Shen, Yun Qin, Yan Wang, Hao |
author_facet | Ye, Yanrong Chen, Zhe Shen, Yun Qin, Yan Wang, Hao |
author_sort | Ye, Yanrong |
collection | PubMed |
description | Abnormal lipid metabolism is closely related to the malignant biological behavior of tumor cells. Such abnormal lipid metabolism provides energy for rapid proliferation, and certain genes related to lipid metabolism encode important components of tumor signaling pathways. In this study, we analyzed pancreatic cancer datasets from The Cancer Genome Atlas and searched for prognostic genes related to lipid metabolism in the Molecular Signature Database. A risk score model was built and verified using the GSE57495 dataset and International Cancer Genome Consortium dataset. Four molecular subtypes and 4249 differentially expressed genes (DEGs) were identified. The DEGs obtained by Weighted Gene Coexpression Network Construction analysis were intersected with 4249 DEGs to obtain a total of 1340 DEGs. The final prognosis model included CA8, CEP55, GNB3 and SGSM2, and these had a significant effect on overall survival. The area under the curve at 1, 3 and 5 years was 0.72, 0.79 and 0.87, respectively. These same results were obtained using the validation cohort. Survival analysis data showed that the model could stratify the prognosis of patients with different clinical characteristics, and the model has clinical independence. Functional analysis indicated that the model is associated with multiple cancer‐related pathways. Compared with published models, our model has a higher C‐index and greater risk value. In summary, this four‐gene signature is an independent risk factor for pancreatic cancer survival and may be an effective prognostic indicator. |
format | Online Article Text |
id | pubmed-8564347 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85643472021-11-09 Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer Ye, Yanrong Chen, Zhe Shen, Yun Qin, Yan Wang, Hao FEBS Open Bio Research Articles Abnormal lipid metabolism is closely related to the malignant biological behavior of tumor cells. Such abnormal lipid metabolism provides energy for rapid proliferation, and certain genes related to lipid metabolism encode important components of tumor signaling pathways. In this study, we analyzed pancreatic cancer datasets from The Cancer Genome Atlas and searched for prognostic genes related to lipid metabolism in the Molecular Signature Database. A risk score model was built and verified using the GSE57495 dataset and International Cancer Genome Consortium dataset. Four molecular subtypes and 4249 differentially expressed genes (DEGs) were identified. The DEGs obtained by Weighted Gene Coexpression Network Construction analysis were intersected with 4249 DEGs to obtain a total of 1340 DEGs. The final prognosis model included CA8, CEP55, GNB3 and SGSM2, and these had a significant effect on overall survival. The area under the curve at 1, 3 and 5 years was 0.72, 0.79 and 0.87, respectively. These same results were obtained using the validation cohort. Survival analysis data showed that the model could stratify the prognosis of patients with different clinical characteristics, and the model has clinical independence. Functional analysis indicated that the model is associated with multiple cancer‐related pathways. Compared with published models, our model has a higher C‐index and greater risk value. In summary, this four‐gene signature is an independent risk factor for pancreatic cancer survival and may be an effective prognostic indicator. John Wiley and Sons Inc. 2021-09-20 /pmc/articles/PMC8564347/ /pubmed/33386701 http://dx.doi.org/10.1002/2211-5463.13074 Text en © 2021 The Authors. FEBS Open Bio published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Ye, Yanrong Chen, Zhe Shen, Yun Qin, Yan Wang, Hao Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
title | Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
title_full | Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
title_fullStr | Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
title_full_unstemmed | Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
title_short | Development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
title_sort | development and validation of a four‐lipid metabolism gene signature for diagnosis of pancreatic cancer |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8564347/ https://www.ncbi.nlm.nih.gov/pubmed/33386701 http://dx.doi.org/10.1002/2211-5463.13074 |
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