A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer
Abstract Epidemiological studies indicate that patients suffering from Alzheimer’s disease have a lower risk of developing lung cancer, and suggest a higher risk of developing glioblastoma. Here we explore the molecular scenarios that might underlie direct and inverse co-morbidities between these di...
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Nature Portfolio
2017
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oai:doaj.org-article:aeb2aaf4301c4094ad5facefc5016e2b2021-12-02T11:52:29ZA molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer10.1038/s41598-017-04400-62045-2322https://doaj.org/article/aeb2aaf4301c4094ad5facefc5016e2b2017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04400-6https://doaj.org/toc/2045-2322Abstract Epidemiological studies indicate that patients suffering from Alzheimer’s disease have a lower risk of developing lung cancer, and suggest a higher risk of developing glioblastoma. Here we explore the molecular scenarios that might underlie direct and inverse co-morbidities between these diseases. Transcriptomic meta-analyses reveal significant numbers of genes with inverse patterns of expression in Alzheimer’s disease and lung cancer, and with similar patterns of expression in Alzheimer’s disease and glioblastoma. These observations support the existence of molecular substrates that could at least partially account for these direct and inverse co-morbidity relationships. A functional analysis of the sets of deregulated genes points to the immune system, up-regulated in both Alzheimer’s disease and glioblastoma, as a potential link between these two diseases. Mitochondrial metabolism is regulated oppositely in Alzheimer’s disease and lung cancer, indicating that it may be involved in the inverse co-morbidity between these diseases. Finally, oxidative phosphorylation is a good candidate to play a dual role by decreasing or increasing the risk of lung cancer and glioblastoma in Alzheimer’s disease.Jon Sánchez-ValleHéctor TejeroKristina IbáñezJosé Luis PorteroMartin KrallingerFátima Al-ShahrourRafael Tabarés-SeisdedosAnaïs BaudotAlfonso ValenciaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017) |
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Medicine R Science Q Jon Sánchez-Valle Héctor Tejero Kristina Ibáñez José Luis Portero Martin Krallinger Fátima Al-Shahrour Rafael Tabarés-Seisdedos Anaïs Baudot Alfonso Valencia A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer |
| description |
Abstract Epidemiological studies indicate that patients suffering from Alzheimer’s disease have a lower risk of developing lung cancer, and suggest a higher risk of developing glioblastoma. Here we explore the molecular scenarios that might underlie direct and inverse co-morbidities between these diseases. Transcriptomic meta-analyses reveal significant numbers of genes with inverse patterns of expression in Alzheimer’s disease and lung cancer, and with similar patterns of expression in Alzheimer’s disease and glioblastoma. These observations support the existence of molecular substrates that could at least partially account for these direct and inverse co-morbidity relationships. A functional analysis of the sets of deregulated genes points to the immune system, up-regulated in both Alzheimer’s disease and glioblastoma, as a potential link between these two diseases. Mitochondrial metabolism is regulated oppositely in Alzheimer’s disease and lung cancer, indicating that it may be involved in the inverse co-morbidity between these diseases. Finally, oxidative phosphorylation is a good candidate to play a dual role by decreasing or increasing the risk of lung cancer and glioblastoma in Alzheimer’s disease. |
| format |
article |
| author |
Jon Sánchez-Valle Héctor Tejero Kristina Ibáñez José Luis Portero Martin Krallinger Fátima Al-Shahrour Rafael Tabarés-Seisdedos Anaïs Baudot Alfonso Valencia |
| author_facet |
Jon Sánchez-Valle Héctor Tejero Kristina Ibáñez José Luis Portero Martin Krallinger Fátima Al-Shahrour Rafael Tabarés-Seisdedos Anaïs Baudot Alfonso Valencia |
| author_sort |
Jon Sánchez-Valle |
| title |
A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer |
| title_short |
A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer |
| title_full |
A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer |
| title_fullStr |
A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer |
| title_full_unstemmed |
A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer’s Disease, Glioblastoma and Lung cancer |
| title_sort |
molecular hypothesis to explain direct and inverse co-morbidities between alzheimer’s disease, glioblastoma and lung cancer |
| publisher |
Nature Portfolio |
| publishDate |
2017 |
| url |
https://doaj.org/article/aeb2aaf4301c4094ad5facefc5016e2b |
| work_keys_str_mv |
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