ArticleCancers2014
Replicative Stress and the FHIT Gene: Roles in Tumor Suppression, Genome Stability and Prevention of Carcinogenesis.
Article in Cancers, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- An Analysis of Two Genome-wide Association Meta-analyses Identifies a New Locus for Broad Depression Phenotype.Biological psychiatry · 2017Pooled it
- Inflammation and Oxidative-Stress Pathways Are Associated with Idiopathic Sudden Hearing Loss: A Genome-Wide Association Study in 15,494 Japanese Individuals.International journal of molecular sciences · 2026Article
- Single-cell and Mendelian analyses reveal shared mechanisms between head and neck neoplasms and aging.Discover oncology · 2026Article
- Altered intersubject functional variability of brain white-matter in major depressive disorder and its association with gene expression profiles.Human brain mapping · 2024Article
- Unveiling the relationship between WWOX and BRCA1 in mammary tumorigenicity and in DNA repair pathway selection.Cell death discovery · 2024Article
- The risk status, signatures of adaptation, and environmental suitability of village-based indigenous chickens from certain regions of Limpopo and KwaZulu-Natal provinces of South Africa.Frontiers in genetics · 2024Article
- Review
- Genome-wide association analysis identifies new candidate risk loci for familial intracranial aneurysm in the French-Canadian population.Scientific reports · 2018Article
- Fhit loss-associated initiation and progression of neoplasia in vitro.Cancer science · 2016Article
- Targetable genetic features of primary testicular and primary central nervous system lymphomas.Blood · 2016Article
- Association of activated Gαq to the tumor suppressor Fhit is enhanced by phospholipase Cβ.BMC cancer · 2015Article
- Genetic and Chromosomal Aberrations and Their Clinical Significance in Renal Neoplasms.BioMed research international · 2015Review
- Tumor Suppressor WWOX Contributes to the Elimination of Tumorigenic Cells in Drosophila melanogaster.PloS one · 2015Article
- Comprehensive exploration of novel chimeric transcripts in clear cell renal cell carcinomas using whole transcriptome analysis.Genes, chromosomes & cancer · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The fragile FHIT gene, encompassing the chromosomal fragile site FRA3B, is an early target of DNA damage in precancerous cells. While vulnerable to DNA damage itself, FHIT protein expression is essential to protect from DNA damage-induced cancer initiation and progression by modulating genome stability, oxidative stress and levels of accumulating DNA damage. Thus, FHIT, whose expression is lost or reduced in many human cancers, is a tumor suppressor and genome caretaker whose loss initiates genome instability in preneoplastic lesions. Ongoing studies are seeking more detailed understanding of the role of FHIT in the cellular response to oxidative damage. This review discusses the relationship between FHIT, reactive oxygen species production, and DNA damage in the context of cancer initiation and progression.
Identifiers
What OpenQuestion holds
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.