ArticleBritish journal of cancer2004
Fhit-deficient normal and cancer cells are mitomycin C and UVC resistant.
Article in British journal of cancer, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 53 citations in OpenAlex.
- Inhibition of GSK3β is synthetic lethal with FHIT loss in lung cancer by blocking homologous recombination repair.Experimental & molecular medicine · 2025Article
- Tanshinones induce tumor cell apoptosis via directly targeting FHIT.Scientific reports · 2021Article
- Fhit-Fdxr interaction in the mitochondria: modulation of reactive oxygen species generation and apoptosis in cancer cells.Cell death & disease · 2019Article
- Impact of FHIT loss on the translation of cancer-associated mRNAs.Molecular cancer · 2017Article
- Fhit loss-associated initiation and progression of neoplasia in vitro.Cancer science · 2016Article
- Fragile histidine triad (FHIT) suppresses proliferation and promotes apoptosis in cholangiocarcinoma cells by blocking PI3K-Akt pathway.TheScientificWorldJournal · 2014Article
- A knockdown with smoke model reveals FHIT as a repressor of Heme oxygenase 1.Cell cycle (Georgetown, Tex.) · 2014Article
- Initiation of genome instability and preneoplastic processes through loss of Fhit expression.PLoS genetics · 2012Article
- Common fragile site tumor suppressor genes and corresponding mouse models of cancer.Journal of biomedicine & biotechnology · 2011Review
- Fragile histidine triad protein: structure, function, and its association with tumorogenesis.Journal of cancer research and clinical oncology · 2010Review
- The effects of Fhit on tumorigenesis after multi-exposure to low-dose radiation.International journal of clinical and experimental medicine · 2009Article
- Article
- Nit1 and Fhit tumor suppressor activities are additive.Journal of cellular biochemistry · 2009Article
- Fragile gene product, Fhit, in oxidative and replicative stress responses.Cancer science · 2009Review
- Fhit tumor suppressor: guardian of the preneoplastic genome.Future oncology (London, England) · 2008Review
- Fhit interaction with ferredoxin reductase triggers generation of reactive oxygen species and apoptosis of cancer cells.The Journal of biological chemistry · 2008Article
- Restoration of fragile histidine triad expression restores Chk2 activity in response to ionizing radiation in oral squamous cell carcinoma cells.Cancer science · 2008Article
- Fhit modulation of the Akt-survivin pathway in lung cancer cells: Fhit-tyrosine 114 (Y114) is essential.Oncogene · 2006Article
- Development of spontaneous tumours and intestinal lesions in Fhit gene knockout mice.British journal of cancer · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
To identify functions of the fragile tumour suppressor gene, FHIT, matched pairs of Fhit-negative and -positive human cancer cell clones, and normal cell lines established from Fhit -/- and +/+ mice, were stressed and examined for differences in cell cycle kinetics and survival. A larger fraction of Fhit-negative human cancer cells and murine kidney cells survived treatment with mitomycin C or UVC light compared to matched Fhit-positive cells; approximately 10-fold more colonies of Fhit-deficient cells survived high UVC doses in clonigenic assays. The human cancer cells were synchronised in G1, released into S and treated with UVC or mitomycin C. At 18 h post mitomycin C treatment approximately 6-fold more Fhit-positive than -negative cells had died, and 18 h post UVC treatment 3.5-fold more Fhit-positive cells were dead. Similar results were obtained for the murine -/- cells. After low UVC doses, the rate of DNA synthesis in -/- cells decreased more rapidly and steeply than in +/+ cells, although the Atr-Chk1 pathway appeared intact in both cell types. UVC surviving Fhit -/- cells appear transformed and exhibit >5-fold increased mutation frequency. This increased mutation burden could explain the susceptibility of Fhit-deficient cells in vivo to malignant transformation.
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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.