ReviewCellular and molecular life sciences : CMLS2014
The FHIT gene product: tumor suppressor and genome "caretaker".
Review in Cellular and molecular life sciences : CMLS, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
61 citing papers in PubMed, 100 citations in OpenAlex.
- Single-cell and Mendelian analyses reveal shared mechanisms between head and neck neoplasms and aging.Discover oncology · 2026Article
- Tracing the Genetic Heritage of the Kirgiz People: Dual-Wave Admixture and Ancestry-Biased Adaptation.Molecular biology and evolution · 2025Article
- Integrating SNP data to reveal the adaptive selection features of goat populations in extreme environments.BMC genomics · 2025Article
- Interstitial Lung Diseases and Lung Cancer: A Review on Similarities, Common Pathogenesis and Therapeutic Approach.Journal of personalized medicine · 2025Review
- Association of FHIT gene variant and salty food preference with the incidence of metabolic syndrome.Genes & nutrition · 2025Article
- Article
- Detection of a novel DNA methylation marker panel for esophageal cancer diagnosis using circulating tumor DNA.BMC cancer · 2024Article
- Unveiling the relationship between WWOX and BRCA1 in mammary tumorigenicity and in DNA repair pathway selection.Cell death discovery · 2024Article
- Evolving copy number gains promote tumor expansion and bolster mutational diversification.Nature communications · 2024Article
- Proteogenomic characterization of primary colorectal cancer and metastatic progression identifies proteome-based subtypes and signatures.Cell reports · 2024Article
- Lack of imbalance between the master regulators TTF1/NKX2-1 and ΔNp63/p40 implies adverse prognosis in non-small cell lung cancer.Scientific reports · 2024Article
- Expression of Tumor SuppressorInternational journal of molecular sciences · 2023Article
- Loss of fragile WWOX gene leads to senescence escape and genome instability.Cellular and molecular life sciences : CMLS · 2023Article
- Deciphering complex breakage-fusion-bridge genome rearrangements with Ambigram.Nature communications · 2023Article
- Evidence of cancer-linked rodent zoonoses from biophysical genomic variations.Scientific reports · 2023Article
- Review
- MicroRNAs as Potential Biomarkers in Gynecological Cancers.Biomedicines · 2023Review
- The oncogenic and immunological roles of histidine triad nucleotide-binding protein 1 in human cancers and their experimental validation in the MCF-7 cell line.Annals of translational medicine · 2023Article
- Review
- Epigenetics of Thymic Epithelial Tumors.Cancers · 2023Review
1 more citing papers are in PubMed but not listed here.
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 4 institutions in 1 country.
Funding
Abstract
The FHIT gene at FRA3B is one of the earliest and most frequently altered genes in the majority of human cancers. It was recently discovered that the FHIT gene is not the most fragile locus in epithelial cells, the cell of origin for most Fhit-negative cancers, eroding support for past claims that deletions at this locus are simply passenger events that are carried along in expanding cancer clones, due to extreme vulnerability to DNA damage rather than to loss of FHIT function. Indeed, recent reports have reconfirmed FHIT as a tumor suppressor gene with roles in apoptosis and prevention of the epithelial-mesenchymal transition. Other recent works have identified a novel role for the FHIT gene product, Fhit, as a genome "caretaker." Loss of this caretaker function leads to nucleotide imbalance, spontaneous replication stress, and DNA breaks. Because Fhit loss-induced DNA damage is "checkpoint blind," cells accumulate further DNA damage during subsequent cell cycles, accruing global genome instability that could facilitate oncogenic mutation acquisition and expedite clonal expansion. Loss of Fhit activity therefore induces a mutator phenotype. Evidence for FHIT as a mutator gene is discussed in light of these recent investigations of Fhit loss and subsequent genome instability.
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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.