ArticleOncogene2010
High sensitivity to carcinogens in the brain of a mouse model of Alzheimer's disease.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Genetic Polymorphisms in Oxidative Stress and Inflammatory Pathways as Potential Biomarkers in Alzheimer's Disease and Dementia.Antioxidants (Basel, Switzerland) · 2023Article
- Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Tomatidine Represses Invasion and Migration of Human Osteosarcoma U2OS and HOS Cells by Suppression of Presenilin 1 and c-Raf-MEK-ERK Pathway.Molecules (Basel, Switzerland) · 2020Article
- p110δ PI3-Kinase Inhibition Perturbs APP and TNFα Trafficking, Reduces Plaque Burden, Dampens Neuroinflammation, and Prevents Cognitive Decline in an Alzheimer's Disease Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Novel Functions of the Neurodegenerative-Related Gene Tau in Cancer.Frontiers in aging neuroscience · 2019Article
- A molecular hypothesis to explain direct and inverse co-morbidities between Alzheimer's Disease, Glioblastoma and Lung cancer.Scientific reports · 2017Article
- Plasma Amyloid-Beta Levels in Patients with Different Types of Cancer.Neurotoxicity research · 2017Article
- Presenilin Mutation Suppresses Lung Tumorigenesis via Inhibition of Peroxiredoxin 6 Activity and Expression.Theranostics · 2017Article
- Loss of presenilin 2 is associated with increased iPLA2 activity and lung tumor development.Oncogene · 2014Article
- Conformational altered p53 affects neuronal function: relevance for the response to toxic insult and growth-associated protein 43 expression.Cell death & disease · 2013Article
- Conformational altered p53 as an early marker of oxidative stress in Alzheimer's disease.PloS one · 2012Article
- Is neurodegenerative disease a long-latency response to early-life genotoxin exposure?International journal of environmental research and public health · 2011Review
- Article
- Histone deacetylase inhibitor valproic acid inhibits cancer cell proliferation via down-regulation of the alzheimer amyloid precursor protein.The Journal of biological chemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer and Alzheimer's disease (AD) are commonly found among elderly patients. Chronic inflammation is the characteristic of both diseases. Amyloid-beta peptide is the main inducer of inflammation in AD. Moreover, chronic inflammation promotes cancer, suggesting that AD patients may be more prone to develop cancer than non-demented people. To test this hypothesis, we injected the carcinogen 20-methylcholanthrene in the brain of transgenic mice overexpressing the mutant forms of amyloid precursor protein (APP) and presenilin 1 (PS1), as a model of AD, and their wild-type (WT) littermates. Mutant mice developed tumors faster and with higher incidence than their WT counterparts. Expression of the inflammatory markers interleukin (IL)-1alpha, IL-1beta, IL-6, IP-10 and tumor necrosis factor-alpha (TNF-alpha) was measured in AD and WT mice of 3 and 12 months of age that had not been exposed to the carcinogen. These cytokines were elevated in older AD mice, indicating the existence of a highly inflammatory milieu in these animals. We also found elevated expression of a mutated form of p53 in older AD mice, suggesting an alternative mechanism for the predisposition of AD brains to develop brain tumors. Clinical studies reporting comorbidity of AD and brain cancer are needed to understand whether our observations hold true for humans.
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Registered trials
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.