Molecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses.
Identifieur interne : 000590 ( PubMed/Curation ); précédent : 000589; suivant : 000591Molecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses.
Auteurs : Kristina Ibá Ez [Espagne] ; César Boullosa [Espagne] ; Rafael Tabarés-Seisdedos [Espagne] ; Anaïs Baudot [France] ; Alfonso Valencia [Espagne]Source :
- PLoS genetics [ 1553-7404 ] ; 2014.
English descriptors
- KwdEn :
- Alzheimer Disease (epidemiology), Alzheimer Disease (genetics), Alzheimer Disease (pathology), Central Nervous System (pathology), Comorbidity, Gene Expression Profiling, Gene Expression Regulation, Humans, NIMA-Interacting Peptidylprolyl Isomerase, Neoplasms (epidemiology), Neoplasms (genetics), Neoplasms (pathology), Parkinson Disease (epidemiology), Parkinson Disease (genetics), Parkinson Disease (pathology), Peptidylprolyl Isomerase (genetics), Schizophrenia (epidemiology), Schizophrenia (genetics), Schizophrenia (pathology), Signal Transduction.
- MESH :
- chemical , genetics : Peptidylprolyl Isomerase.
- chemical : NIMA-Interacting Peptidylprolyl Isomerase.
- epidemiology : Alzheimer Disease, Neoplasms, Parkinson Disease, Schizophrenia.
- genetics : Alzheimer Disease, Neoplasms, Parkinson Disease, Schizophrenia.
- pathology : Alzheimer Disease, Central Nervous System, Neoplasms, Parkinson Disease, Schizophrenia.
- Comorbidity, Gene Expression Profiling, Gene Expression Regulation, Humans, Signal Transduction.
Abstract
There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.
DOI: 10.1371/journal.pgen.1004173
PubMed: 24586201
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pubmed:24586201Le document en format XML
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<term>Central Nervous System (pathology)</term>
<term>Comorbidity</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>NIMA-Interacting Peptidylprolyl Isomerase</term>
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<term>Neoplasms (genetics)</term>
<term>Neoplasms (pathology)</term>
<term>Parkinson Disease (epidemiology)</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (pathology)</term>
<term>Peptidylprolyl Isomerase (genetics)</term>
<term>Schizophrenia (epidemiology)</term>
<term>Schizophrenia (genetics)</term>
<term>Schizophrenia (pathology)</term>
<term>Signal Transduction</term>
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<term>Neoplasms</term>
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<front><div type="abstract" xml:lang="en">There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.</div>
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<Abstract><AbstractText>There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.</AbstractText>
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