The FHIT gene, recently cloned and mapped on chromosome 3p14.2, has frequently been found to be abnormal in several established cancer cell lines and primary tumours. As alterations of chromosome 3p are common events in ovarian cancers with breakpoint sites at 3p14.2, we decided to investigate the role of FHIT in human ovarian tumorigenesis. Fifty-four primary ovarian carcinomas were studied by reverse transcription of FHIT mRNA followed by polymerase chain reaction (PCR) amplification and sequencing of products. The same tumours and matched normal tissues were also investigated for loss of heterozygosity using three microsatellite markers located inside the gene. We found an abnormal transcript of the FHIT gene in two cases (4%) and allelic losses in eight cases (15%). Twelve (22%) of the 54 tumours investigated belonged to young patients with a family history of breast/ovarian cancer. In none of these cases was the FHITgene found to be altered. Our results indicate that FHITplays a role in a small proportion of ovarian carcinomas.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2150139 | PMC |
http://dx.doi.org/10.1038/bjc.1998.175 | DOI Listing |
Ann Clin Lab Sci
November 2024
Department of Laboratory Medicine, Linyi People's Hospital, Linyi, Shandong, China
Objective: C-X-C motif chemokine receptor 2 (CXCR2) plays a crucial role in inflammation and immunity, and the involvement of chemokine receptors in the tumor microenvironment is extensively documented. However, the impact of CXCR2 deficiency on the complete transcriptome, including mRNA and ncRNAs, in tumor cells remains unclear.
Methods: In this study, we aimed to identify differentially expressed (DE) messenger RNA (mRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) in CXCR2 knockout HeLa cells through transcriptome sequencing and to construct regulatory networks.
Neoplasma
December 2024
Department of Clinical and Molecular Pathology and Medical Genetics, Faculty of Medicine, University of Ostrava, Ostrava, Czech Republic.
DNA methylation is recognized as an early event in cancer initiation and progression. This review aimed to compare the methylation status of promoter regions in selected genes across different histological subtypes of non-small cell lung cancer (NSCLC), including adenocarcinoma, squamous cell carcinoma, large cell carcinoma, and the rare but highly aggressive large-cell neuroendocrine carcinoma (LCNEC). A comprehensive literature search was conducted in the PubMed database until August 17, 2024, using standardized keywords to identify reports on promoter methylation in NSCLC.
View Article and Find Full Text PDFEur J Cell Biol
March 2025
Université de Reims Champagne-Ardenne, INSERM, P3Cell, UMR-S 1250, Reims, France. Electronic address:
The tumor suppressor fragile histidine triad (FHIT) is frequently lost in non-small cell lung cancer (NSCLC). We previously showed that a down-regulation of FHIT causes an up-regulation of the activity of HER2 associated to an epithelial-mesenchymal transition (EMT) and that lung tumor cells harboring a FHIT/pHER2 phenotype are sensitive to anti-HER2 drugs. Here, we sought to decipher the FHIT-regulated HER2 signaling pathway in NSCLC.
View Article and Find Full Text PDFBMC Cancer
December 2024
Department of Molecular Pathology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, No 127, Dongming Road, Zhengzhou, 450008, Henan, China.
Background: Esophageal cancer (ECa) is one of the most deadly cancers, with increasing incidence worldwide and poor prognosis. While endoscopy is recommended for the detection of ECa in high-risk individuals, it is not suitable for large-scale screening due to its invasiveness and inconvenience.
Methods: In this study, a novel gene methylation panel was developed for a blood-based test, and its diagnostic efficacy was evaluated using a cohort of 304 participants (203 cases, 101 controls).
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!