ArticleBritish journal of cancer2004
Development of spontaneous tumours and intestinal lesions in Fhit gene knockout mice.
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 9 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
9 citing papers in PubMed, 24 citations in OpenAlex.
- Integrated analysis ofCell cycle (Georgetown, Tex.) · 2024Review
- FHIT down-regulation was inversely linked to aggressive behaviors and adverse prognosis of gastric cancer: a meta- and bioinformatics analysis.Oncotarget · 2017Article
- Genetic and Chromosomal Aberrations and Their Clinical Significance in Renal Neoplasms.BioMed research international · 2015Review
- A dual radiologic contrast agent protocol for 18F-FDG and 18F-FLT PET/CT imaging of mice bearing abdominal tumors.Molecular imaging and biology · 2011Article
- Chromosomal abnormalities and novel disease-related regions in progression from Barrett's esophagus to esophageal adenocarcinoma.International journal of cancer · 2009Article
- Chromosomal imbalances and partial uniparental disomies in primary central nervous system lymphoma.Leukemia · 2009Article
- Mammalian nitrilase 1 homologue Nit1 is a negative regulator in T cells.International immunology · 2009Article
- A hybrid machine learning-based method for classifying the Cushing's Syndrome with comorbid adrenocortical lesions.BMC genomics · 2008Article
- Fhit modulation of the Akt-survivin pathway in lung cancer cells: Fhit-tyrosine 114 (Y114) is essential.Oncogene · 2006Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The fragile histidine triad (FHIT) gene is frequently inactivated in various types of tumours. However, the system-wide pathology caused by FHIT inactivation has not been examined in detail. Here we demonstrate that Fhit gene knockout mice develop tumours in the lymphoid tissue, liver, uterus, testis, forestomach and small intestine, together with structural abnormalities in the small intestinal mucosa. These results suggest that Fhit plays important roles in systemic tumour suppression and in the integrity of mucosal structure of the intestines.
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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.