FHITFragile Histidine Triad (gene)
FHITFlexx Hockey Institute of Training (est. 2005; Mendota Heights, MN)
FHITFarndon House Information Trust
FHITFort Hare Institute of Technology (Alice, South Africa)
FHITFoundation for the Harmonization of Information Technology
References in periodicals archive ?
Perfil de metilacion de genes supresores de tumores APAF, ASSP1, p73, FHIT en pacientes con leucemia linfoblastica aguda infantil.
Keywords: Hepatocellular carcinoma, Fragile histidine triad, FHIT, Proteomics, Bioinformatics.
Quantitative detection of methylation of FHIT and BRCA1 promoters in the serum of ductal breast cancer patients.
Listado de genes susceptibles a hipermetilacion en su region promotora en cancer de pulmon Gen Locus CDKN2A/ 9p21 NSCLC60% p16INK4a SCLC 10 % FHIT 3p14.
50 CpG island methylation of the FHIT gene is correlated with loss of gene expression in lung and breast cancer.
There were no statistically significant differences between the expression of gastric cancer cell proteins: FHIT, p-catenin, y-catenin, cathepsin B, EGF, HER-2, MMP-9, MCM-2, Bak, Bax, BclXL, p53, FasL and Procaspase 3, depending on the classification according to Lauren (Table 2).
Methods: Truncated structures of FHIT were screened to reveal critical sections engaging in FHIT interaction.
4] Genes: E6, E6 transforming protein [human papillomavirus 18]; E2, E2 regulatory protein [human papillomavirus]; E7, E7 transforming protein [human papillomavirus]; TP53, tumor protein p53; IFNG, interferon, gamma; TMC6 (previously known as EVER1), transmembrane channel-like 6; TMC8 (previously known as EVER2), transmembrane channel-like 8; DAPK, death-associated protein kinase 1; CDH1, cadherin 1, type 1, E-cadherin (epithelial); RASSF1, Ras association (RalGDS/AF-6) domain family member 1; CDKN2A, cyclin-dependent kinase inhibitor 2A; FHIT, fragile histidine triad; MGMT, O-6-methylguanine-DNA methyltransferase; RARB, retinoic acid receptor, beta.
Other topics considered are cell cycle control proteins in human breast cancer, primary roles of the retinoblast protein family in cell cycle regulation, and FHIT and cancer initiating cells.
They analyzed the behavior of two tumor-suppressing genes, p16 and FHIT, that are silenced or damaged in the early stages of cancer development, and tracked whether the genes were silenced by methylation, the attachment of a chemical methyl group to an atom or molecule, which in this case, eventually leads to the function of a gene shutting down.
For example, they found strong correlations in the inhibition (promoter methylation) of tumor suppressor genes pl6 and FHIT in 1,774 tissue samples.