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FHIT, a member of the histidine triad gene family, encodes a diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. Additionally we are shipping FHIT Antibodies (131) and FHIT Proteins (30) and many more products for this protein.
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the expression profile of miRNAs that may be associated with expression of the FHIT gene in breast cancer, was examined.
FHIT hypermethylation, which induces the inactivation of FHIT gene, plays an important role in the carcinogenesis and clinical outcome and may serve as a potential drug target of non-small cell lung cancer.
FHIT hypermethylation, which induces the inactivation of FHIT gene, plays an important role in the carcinogenesis and clinical outcome and may serve as a potential diagnostic marker and drug target of non-small-cell lung carcinoma
Low FHIT Gene Expression is associated with Acute Lymphoblastic Leukemia.
In 22 lung cancer patients with negative histology and cytology at initial bronchoscopy, FHIT and p16 mRNA loss was detected in 40.9% (9/22) and 36.4% (8/22) cases, respectively.
The results showed that the methylation levels of both BRCA1 and FHIT promoters were higher in the serum of the breast ductal carcinoma group than those of the breast fibroadenoma group.
Review/Meta-analysis: FHIT methylation could be a diagnostic biomarker of breast carcinogenesis.
Mutations of the FHIT gene are not major cause of Peutz-Jeghers syndrome.
Adenylylsulfate-ammonia adenylyltransferase activity is another inherent property of Fhit proteins.
APOBEC3B overexpression and Fhit-loss induced DNA damage are independent events that, when occurring together, result in a significantly increased frequency of APOBEC-induced mutations that drive cancer progression.
Fhit-deficiency mutation signature also resembles a C>T and T>C mutation signature reported for human papillary kidney cancers and a similar signature recently reported for esophageal and bladder cancers, cancers that are frequently Fhit deficient.
Fhit deficiency-induced global genome instability promotes mutation and clonal expansion
Fhit delocalizes annexin A4 (show ANXA4 ELISA Kits) from plasma membrane to cytosol and sensitizes lung cancer cells to paclitaxel.
FHIT gene is a "caretaker gene" necessary for maintenance of genome stability.
Loss of Fhit expression contributes to cell transformation.
Defects in Fhit expression may promote MHC-I down-regulation in cancer cells and allow escape from immunosurveillance.
Human and mouse orthologous genes, FHIT and Fhit, are more highly conserved through evolution than PTPRG/Ptprg (show PTPRG ELISA Kits) and yet contain more sequence elements that are exquisitely sensitive to genomic rearrangements
Association of Fhit gene inactivation with increased survival after DNA damage, related to over-active checkpoints regulated by ATR/CHK1 pathway. Potential effects of Fhit-dependent DNA damage response on tumor progression.
Fhit has a role in bladder cancer development
UV-induced alterations of the FHIT and WWOX (show WWOX ELISA Kits) fragile site gene expression are involved at least partially in the checkpoint function of DNA damage
the same mRNA isoforms of FHIT were detected in bladder tumors and in healthy tissues, including a novel isoform that was found in this study, suggesting that epigenetic modifications and altered expression profiles are not a hallmark of vesical tumors
This gene, a member of the histidine triad gene family, encodes a diadenosine 5',5'''-P1,P3-triphosphate hydrolase involved in purine metabolism. The gene encompasses the common fragile site FRA3B on chromosome 3, where carcinogen-induced damage can lead to translocations and aberrant transcripts of this gene. In fact, aberrant transcripts from this gene have been found in about half of all esophageal, stomach, and colon carcinomas. Alternatively spliced transcript variants have been found for this gene.
, diadenosine 5',5'''-P1,P3-triphosphate hydrolase
, tumor suppressor protein
, fragile histidine triad protein
, diadenosine triphosphate hydrolase