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A molecular hypothesis to explain direct and inverse co-morbidities between alzheimer's disease, glioblastoma and lung cancer

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A molecular hypothesis to explain direct and inverse co-morbidities between alzheimer's disease, glioblastoma and lung cancer

dc.contributor.author	Sánchez Valle, Jon
dc.contributor.author	Tejero, Hector
dc.contributor.author	Ibáñez, Kristina
dc.contributor.author	Portero, Jose Luis
dc.contributor.author	Krallinger, Martin
dc.contributor.author	Al-Shahrour, Fátima
dc.contributor.author	Tabarés Seisdedos, Rafael
dc.contributor.author	Baudot, Anaïs
dc.contributor.author	Valencia, Alfonso
dc.date.accessioned	2018-09-04T08:26:26Z
dc.date.available	2018-09-04T08:26:26Z
dc.date.issued	2017
dc.identifier.citation	Sánchez Valle, Jon Tejero, Hector Ibáñez, Kristina Portero, Jose Luis Krallinger, Martin Al-Shahrour, Fátima Tabarés Seisdedos, Rafael Baudot, Anaïs Valencia, Alfonso 2017 A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer's Disease, Glioblastoma and Lung cancer Scientific Reports 7 1 4400
dc.identifier.uri	http://hdl.handle.net/10550/67387
dc.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.
dc.language.iso	eng
dc.relation.ispartof	Scientific Reports, 2017, vol. 7, num. 1, p. 4400
dc.subject	cáncer
dc.title	A molecular hypothesis to explain direct and inverse co-morbidities between alzheimer's disease, glioblastoma and lung cancer
dc.type	journal article	es_ES
dc.date.updated	2018-09-04T08:26:27Z
dc.identifier.doi	10.1038/s41598-017-04400-6
dc.identifier.idgrec	126535
dc.rights.accessRights	open access	es_ES