scholarly journals FHIT Gene

2020 ◽  
Author(s):  
Keyword(s):  
Fhit Gene

Deletion of the FHIT gene in neoplastic and invasive cervical lesions is related to high-risk HPV infection but is independent of histopathological features

2000 ◽  
Vol 192 (4) ◽  
pp. 502-510 ◽  
Author(s):  
David Butler ◽  
Claire Collins ◽  
Mohamed Mabruk ◽  
Caitriona Barry Walsh ◽  
Mary B. Leader ◽  
...  
Keyword(s):  
High Risk ◽  
Hpv Infection ◽  
Cervical Lesions ◽  
Fhit Gene ◽  
Histopathological Features ◽  
High Risk Hpv

scholarly journals FHIT gene transfection inhibits the proliferation and invasiveness of human cholangiocarcinoma QBC939 cells

2009 ◽  
Vol 17 (33) ◽  
pp. 3437
Author(s):  
Fang Xie ◽  
Qiang Huang
Keyword(s):  
Gene Transfection ◽  
Fhit Gene

A homozygous deletion at FRA3B in a lung adenocarcinoma cell line with normal expression of the FHIT gene

1996 ◽  
Vol 91 (2) ◽  
pp. 170 ◽  
Author(s):  
Tineke G. Draaijers ◽  
Anke van den Berg ◽  
Klaas Kokl ◽  
Tineke Timmer ◽  
Anneke Y. van der Veen ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Cell Line ◽  
Homozygous Deletion ◽  
Adenocarcinoma Cell Line ◽  
Fhit Gene ◽  
Adenocarcinoma Cell ◽  
Lung Adenocarcinoma Cell Line ◽  
Normal Expression

Methylation status of fragile histidine triad (FHIT) gene and its clinical impact on prognosis of patients with myelodysplastic syndrome

2008 ◽  
Vol 32 (10) ◽  
pp. 1541-1545 ◽  
Author(s):  
Jiang Lin ◽  
Dong-ming Yao ◽  
Jun Qian ◽  
Ya-li Wang ◽  
Lan-xiu Han ◽  
...  
Keyword(s):  
Myelodysplastic Syndrome ◽  
Methylation Status ◽  
Clinical Impact ◽  
Fhit Gene ◽  
Fragile Histidine Triad

scholarly journals Regulation of DNA methylation on the expression of the FHIT gene contributes to cervical carcinoma cell tumorigenesis

2006 ◽  
Author(s):  
Ying Wu ◽  
Li Meng ◽  
Hui Wang ◽  
Qian Xu ◽  
Shixuan Wang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Cervical Carcinoma ◽  
Carcinoma Cell ◽  
Fhit Gene

Homozygous Deletion of the Fhit Gene, p21WAF1 Protein Expression and Apoptosis in Bilharzial Bladder Cancer

2011 ◽  
Vol 14 (3) ◽  
pp. 212-218 ◽  
Author(s):  
Khaled Ismail Ghaleb ◽  
Ali Alkaladi
Keyword(s):  
Bladder Cancer ◽  
Protein Expression ◽  
Homozygous Deletion ◽  
Fhit Gene

scholarly journals P828 DNA methylation profile defines epigenetic characteristics and molecular targets of Crohn’s disease

2020 ◽  
Vol 14 (Supplement_1) ◽  
pp. S643-S643
Author(s):  
T O Kim ◽  
J Yi ◽  
S H Jung ◽  
D H Baek ◽  
H S Lee
Keyword(s):  
Dna Methylation ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Methylation Level ◽  
Methylation Profile ◽  
Fhit Gene ◽  
Body Regions ◽  
Dna Methylation Profile ◽  
Hypermethylated Genes

Abstract Background Inflammatory bowel disease(IBD) is known to be caused by a genetic predisposition involving multiple genes; however, there is growing evidence that abnormal interaction with environmental, particularly epigenetic, factors can have a significant contribution during the development of IBD. Although many studies, particularly genome-wide association studies (GWAS), have been performed to identify the genetic changes underlying the pathogenesis of Crohn’s disease (CD), the role of epigenetic changes in the development of complications arising from CD is poorly understood. Methods Here, we employed an unbiased approach to define DNA methylation alteration in CD patients using the Human Methylation 450K Bead Chip platform. Compared to normal controls, the majority of differential DNA methylation in CD patient samples was in the promoter, intergenic, and gene body regions. Results The DNA methylation profile in CD revealed 134 probes (23 hypermethylated and 111 hypomethylated probes) that were differentially methylated. We validated the methylation levels of 19 genes that showed hypermethylation in CD patients compared with normal control. Technical validation was performed using quantitative MSP analysis and we finally identified that the Fragile Histidine Triad (FHIT) genes were hypermethylated in a disease-specific manner. Using a large cohort for CD patients samples (n = 207), we found that FHIT is frequently methylated in CD patients (71%) by MSP and significantly increasing methylation level in CD patient samples. In addition, we confirmed the methylation level of FHIT gene between normal colon and CD patients. Due to hypermethylation of FHIT gene promoter in CD patients, we observed that the level of FHIT protein is downregulated in CD patient samples compared with normal by IHC analysis. Gene network analysis by GO and metascape for hypermethylated genes in CD patients suggested putative cellular and molecular interactions relevant to IBD pathology. Conclusion Overall, our DNA methylation profile identifies newly hypermethylated genes in CD, as well as paves the way to a better understanding of the role of epigenetics in the pathogenesis of CD, and provides direction for future research in the diagnosis/prognosis or therapeutic treatments for CD.

The FHIT gene, a multiple tumor suppressor gene encompassing the carcinogen sensitive chromosome fragile site, FRA3B

1997 ◽  
Vol 1332 (3) ◽  
pp. M65-M70 ◽  
Author(s):  
Kay Huebner ◽  
Piotr Hadaczek ◽  
Zurab Siprashvili ◽  
Teresa Druck ◽  
Carlo M. Croce
Keyword(s):  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Fragile Site ◽  
Suppressor Gene ◽  
Fhit Gene ◽  
Multiple Tumor ◽  
Chromosome Fragile Site

scholarly journals Intramitochondrial calcium regulation by the FHIT gene product sensitizes to apoptosis

2009 ◽  
Vol 106 (31) ◽  
pp. 12753-12758 ◽  
Author(s):  
A. Rimessi ◽  
S. Marchi ◽  
C. Fotino ◽  
A. Romagnoli ◽  
K. Huebner ◽  
...  
Keyword(s):  
Gene Product ◽  
Calcium Regulation ◽  
Fhit Gene
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