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Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis

BACKGROUND: To investigate the gene expression profile of a set of candidate genes for a better understanding of the molecular mechanism underlying the pathogenesis of thymoma with or without myasthenia gravis. METHODS: Thymoma patients and thymoma patients with myasthenia gravis were analyzed using...

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Detalles Bibliográficos
Autores principales: Guo, Feng, Wang, Chun‐Yang, Wang, Shuo, Zhang, Jun, Yan, Yi‐Jie, Guan, Zhi‐Yu, Meng, Fan‐Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397909/
https://www.ncbi.nlm.nih.gov/pubmed/30734484
http://dx.doi.org/10.1111/1759-7714.12980
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author Guo, Feng
Wang, Chun‐Yang
Wang, Shuo
Zhang, Jun
Yan, Yi‐Jie
Guan, Zhi‐Yu
Meng, Fan‐Jie
author_facet Guo, Feng
Wang, Chun‐Yang
Wang, Shuo
Zhang, Jun
Yan, Yi‐Jie
Guan, Zhi‐Yu
Meng, Fan‐Jie
author_sort Guo, Feng
collection PubMed
description BACKGROUND: To investigate the gene expression profile of a set of candidate genes for a better understanding of the molecular mechanism underlying the pathogenesis of thymoma with or without myasthenia gravis. METHODS: Thymoma patients and thymoma patients with myasthenia gravis were analyzed using microarray profiling to identify significant changes in gene expression of autoimmune regulator pathway genes including AIRE, IL‐7R, CHRNA3, SYMD1, THRA, and CAV3. RESULTS: Across all of our samples, we found that 1484 mRNAs were upregulated and 770 were downregulated in thymoma patients compared with thymoma with myasthenia gravis patients. Gene ontology and pathway analysis revealed that a large number of genes participated in cellular functions for humoral immune response, sequence‐specific DNA binding RNA polymerase II transcription factor activity, positive regulation of gene expression, regulation of neuron projection development, extracellular ligand‐gated ion channel activity, positive regulation of striated muscle cell differentiation, and regulation of nuclear factor‐kappaB import into the nucleus. CONCLUSION: Our results revealed genetic differences between thymomas and myasthenia gravis, and identified the key candidate genes/pathways for molecular mechanism.
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spelling pubmed-63979092019-03-04 Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis Guo, Feng Wang, Chun‐Yang Wang, Shuo Zhang, Jun Yan, Yi‐Jie Guan, Zhi‐Yu Meng, Fan‐Jie Thorac Cancer Original Articles BACKGROUND: To investigate the gene expression profile of a set of candidate genes for a better understanding of the molecular mechanism underlying the pathogenesis of thymoma with or without myasthenia gravis. METHODS: Thymoma patients and thymoma patients with myasthenia gravis were analyzed using microarray profiling to identify significant changes in gene expression of autoimmune regulator pathway genes including AIRE, IL‐7R, CHRNA3, SYMD1, THRA, and CAV3. RESULTS: Across all of our samples, we found that 1484 mRNAs were upregulated and 770 were downregulated in thymoma patients compared with thymoma with myasthenia gravis patients. Gene ontology and pathway analysis revealed that a large number of genes participated in cellular functions for humoral immune response, sequence‐specific DNA binding RNA polymerase II transcription factor activity, positive regulation of gene expression, regulation of neuron projection development, extracellular ligand‐gated ion channel activity, positive regulation of striated muscle cell differentiation, and regulation of nuclear factor‐kappaB import into the nucleus. CONCLUSION: Our results revealed genetic differences between thymomas and myasthenia gravis, and identified the key candidate genes/pathways for molecular mechanism. John Wiley & Sons Australia, Ltd 2019-02-07 2019-03 /pmc/articles/PMC6397909/ /pubmed/30734484 http://dx.doi.org/10.1111/1759-7714.12980 Text en © 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Original Articles
Guo, Feng
Wang, Chun‐Yang
Wang, Shuo
Zhang, Jun
Yan, Yi‐Jie
Guan, Zhi‐Yu
Meng, Fan‐Jie
Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis
title Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis
title_full Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis
title_fullStr Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis
title_full_unstemmed Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis
title_short Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis
title_sort alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor‐kappab/autoimmune regulator pathway to myasthenia gravis pathogenesis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6397909/
https://www.ncbi.nlm.nih.gov/pubmed/30734484
http://dx.doi.org/10.1111/1759-7714.12980
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