Evidence map›Paper›PMID 28667284›Full record

ArticleScientific reports2017

A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer's Disease, Glioblastoma and Lung cancer.

Jon Sánchez-Valle, Héctor Tejero, Kristina Ibáñez, José Luis Portero, Martin Krallinger, Fátima Al-Shahrour, Rafael Tabarés-Seisdedos, Anaïs Baudot, Alfonso Valencia

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 2 pooled it
8.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 2 syntheses or guidelines pooled it, 105 citations in OpenAlex.

  1. Pooled it
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  3. Accumulation of amyloid beta in human glioblastomas.Clinical and experimental immunology · 2020
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1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 2 countries.

Jon Sánchez-ValleStructural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Madrid, 28029, Spain.
Héctor TejeroClinical Research Programme, Spanish National Cancer Research Centre (CNIO), Madrid, 28029, Spain.
Kristina IbáñezBioinformatics section, Institute of Medical and Molecular Genetics (INGEMM), Hospital Universitario La Paz, Madrid, 28046, Spain.
José Luis PorteroDepartment of Medicine, Hospital HM Sanchinarro, Madrid, 28050, Spain.
Martin KrallingerStructural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Madrid, 28029, Spain.
Fátima Al-ShahrourClinical Research Programme, Spanish National Cancer Research Centre (CNIO), Madrid, 28029, Spain.
Rafael Tabarés-SeisdedosDepartment of Medicine, University of Valencia, CIBERSAM, INCLIVA, Valencia, 46010, Spain.
Anaïs BaudotAix-Marseille Université, CNRS, Centrale Marseille, I2M UMR7373, Marseille, France. anais.baudot@univ-amu.fr.ORCID 0000-0003-0885-7933
Alfonso ValenciaStructural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), Madrid, 28029, Spain. valencia@cnio.es.
Spanish National Cancer Research Centre · ESCentre National de la Recherche Scientifique · FRHospital Universitario HM Sanchinarro · ESHospital Universitario La Paz · ESInstitució Catalana de Recerca i Estudis Avançats · ESUniversitat de València · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Alzheimer DiseaseBiomarkersComorbidityDisease SusceptibilityGene ExpressionGenetic VariationGlioblastomaHumansLung NeoplasmsModels, BiologicalReactive Oxygen SpeciesSignal TransductionBiomarkersReactive Oxygen Species

Identifiers

PMID28667284
PMCPMC5493619
OpenAlexW2655375924

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.