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Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases

BACKGROUND: Lung adenocarcinoma (LUAD) accounts for approximately 40% of all lung cancer patients. There is an urgent need to understand the mechanisms of cancer progression in LUAD and to identify useful biomarkers to predict prognosis. METHODS: In this study, Oncomine database was used to identify...

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Autores principales: Liu, Wei, Ouyang, Songyun, Zhou, Zhigang, Wang, Meng, Wang, Tingting, Qi, Yu, Zhao, Chunling, Chen, Kuisheng, Dai, Liping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393652/
https://www.ncbi.nlm.nih.gov/pubmed/30556321
http://dx.doi.org/10.1002/mgg3.528
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author Liu, Wei
Ouyang, Songyun
Zhou, Zhigang
Wang, Meng
Wang, Tingting
Qi, Yu
Zhao, Chunling
Chen, Kuisheng
Dai, Liping
author_facet Liu, Wei
Ouyang, Songyun
Zhou, Zhigang
Wang, Meng
Wang, Tingting
Qi, Yu
Zhao, Chunling
Chen, Kuisheng
Dai, Liping
author_sort Liu, Wei
collection PubMed
description BACKGROUND: Lung adenocarcinoma (LUAD) accounts for approximately 40% of all lung cancer patients. There is an urgent need to understand the mechanisms of cancer progression in LUAD and to identify useful biomarkers to predict prognosis. METHODS: In this study, Oncomine database was used to identify potential genes contributed to cancer progression. Bioinformatics analysis including pathway enrichment and text mining was used to explain the potential roles of identified genes in LUAD. The Cancer Genome Atlas database was used to analyze the association of gene expression with survival result. RESULTS: Our results indicated that 80 genes were significantly dysregulated in LUAD according to four microarrays covering 356 cases of LUAD and 164 cases of normal lung tissues. Twenty genes were consistently and stably dysregulated by more than twofold. Ten of 20 genes had a relationship with overall survival or disease‐free survival in a cohort of 516 LUAD patients, and 19 genes were associated with tumor stage, gender, age, lymph node, or smoking. Low expression of AGER and high expression of CCNB1 were specifically associated with poor survival. CONCLUSION: Our findings implicate AGER and CCNB1 might be potential biomarkers for diagnosis and prognosis targets for LUAD.
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spelling pubmed-63936522019-03-08 Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases Liu, Wei Ouyang, Songyun Zhou, Zhigang Wang, Meng Wang, Tingting Qi, Yu Zhao, Chunling Chen, Kuisheng Dai, Liping Mol Genet Genomic Med Original Articles BACKGROUND: Lung adenocarcinoma (LUAD) accounts for approximately 40% of all lung cancer patients. There is an urgent need to understand the mechanisms of cancer progression in LUAD and to identify useful biomarkers to predict prognosis. METHODS: In this study, Oncomine database was used to identify potential genes contributed to cancer progression. Bioinformatics analysis including pathway enrichment and text mining was used to explain the potential roles of identified genes in LUAD. The Cancer Genome Atlas database was used to analyze the association of gene expression with survival result. RESULTS: Our results indicated that 80 genes were significantly dysregulated in LUAD according to four microarrays covering 356 cases of LUAD and 164 cases of normal lung tissues. Twenty genes were consistently and stably dysregulated by more than twofold. Ten of 20 genes had a relationship with overall survival or disease‐free survival in a cohort of 516 LUAD patients, and 19 genes were associated with tumor stage, gender, age, lymph node, or smoking. Low expression of AGER and high expression of CCNB1 were specifically associated with poor survival. CONCLUSION: Our findings implicate AGER and CCNB1 might be potential biomarkers for diagnosis and prognosis targets for LUAD. John Wiley and Sons Inc. 2018-12-16 /pmc/articles/PMC6393652/ /pubmed/30556321 http://dx.doi.org/10.1002/mgg3.528 Text en © 2018 The Authors. Molecular Genetics & Genomic Medicine published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Liu, Wei
Ouyang, Songyun
Zhou, Zhigang
Wang, Meng
Wang, Tingting
Qi, Yu
Zhao, Chunling
Chen, Kuisheng
Dai, Liping
Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases
title Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases
title_full Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases
title_fullStr Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases
title_full_unstemmed Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases
title_short Identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: Analyses based on microarray from Oncomine and The Cancer Genome Atlas databases
title_sort identification of genes associated with cancer progression and prognosis in lung adenocarcinoma: analyses based on microarray from oncomine and the cancer genome atlas databases
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6393652/
https://www.ncbi.nlm.nih.gov/pubmed/30556321
http://dx.doi.org/10.1002/mgg3.528
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