ReviewJournal of Huntington's disease2018
Cancer: From Wild-Type to Mutant Huntingtin.
Review in Journal of Huntington's disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Concomitant pathologies and their impact on Huntington's disease. A brief review of current evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Docetaxel response in BRCA1,p53-deficient mammary tumor cells is affected by Huntingtin and BAP1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A Specific Mini-Intrabody Mediates Lysosome Degradation of Mutant Huntingtin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases.Biomolecules · 2022Review
- Reboot: a straightforward approach to identify genes and splicing isoforms associated with cancer patient prognosis.NAR cancer · 2021Article
- Who and Why? Requests for Presymptomatic Genetic Testing for Amyotrophic Lateral Sclerosis/Frontotemporal Dementia vs Huntington Disease.Neurology. Genetics · 2021Article
- Htt is a repressor of Abl activity required for APP-induced axonal growth.PLoS genetics · 2021Article
- Investigational Assay for Haplotype Phasing of the Huntingtin Gene.Molecular therapy. Methods & clinical development · 2020Article
- Uncovering cancer gene regulation by accurate regulatory network inference from uninformative data.NPJ systems biology and applications · 2020Article
- R-loops promote trinucleotide repeat deletion through DNA base excision repair enzymatic activities.The Journal of biological chemistry · 2020Article
- Prion-like mechanisms in neurodegenerative disease: Implications for Huntington's disease therapy.Stem cells translational medicine · 2020Review
- Article
- miR-146a Overexpression in Oral Squamous Cell Carcinoma Potentiates Cancer Cell Migration and Invasion PossiblyFrontiers in oncology · 2020Article
- Possible Role of the Polyglutamine Elongation in Evolution of Amyloid-Related Evolvability.Journal of Huntington's disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntingtin (HTT) is a scaffold protein mostly known because it gives rise to the severe and incurable inherited neurological disorder Huntington's disease (HD) when mutated. The Huntingtin gene (HTT) carries a polymorphic trinucleotide expansion of CAGs in exon 1 that ranges from 9 to 35 in the non-HD affected population. However, if it exceeds 35 CAG repeats, the altered protein is referred to as mutant HTT and leads to the development of HD. Given the wide spectrum of severe symptoms developed by HD individuals, wild-type and mutant HTT have been mostly studied in the context of this disorder. However, HTT expression is ubiquitous and several peripheral symptoms in HD have been described, suggesting that HTT is of importance, not only in the central nervous system (CNS), but also in peripheral organs. Accordingly, HTT and mutant HTT may interfere with non-brain-related diseases. Correlative studies have highlighted a decreased cancer incidence in the HD population and both wild-type and mutant HTT have been implicated in tumor progression. In this review, we describe the current evidence linking wild-type and mutant HTT to cancer and discuss how CAG polymorphism, HTT function, and partners may influence carcinogenesis and metastatic progression.
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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.