The identification of allelic loss in approximately half of the tumors analyzed supports the hypothesis that inactivation of p53 is involved in the pathogenesis of esophageal cancer.
Thus, changes in gene copy number or level of expression of HER-I or c-myc DNA sequences may play an important role in the pathogenesis of esophageal cancer in this high-risk region.
Our results suggest that enhanced transcription of the epidermal growth factor receptor gene is associated with the development of some esophageal cancers.
These results suggest that several putative tumor suppressor genes, in addition to the cyclin D and TP53 genes that are sometimes mutated in esophageal carcinomas, may be associated with development and/or progression of esophageal cancer.
We report a highly frequent homozygous deletion of the p16/CDKN2 gene in the esophageal cancer cell line and a relatively high frequency of homozygous deletion in gastric cancer cell lines.
We report a highly frequent homozygous deletion of the p16/CDKN2 gene in the esophageal cancer cell line and a relatively high frequency of homozygous deletion in gastric cancer cell lines.
To further address the roles of cyclin D1 in growth control and tumorigenesis, we have overexpressed an antisense cyclin D1 cDNA construct, either constitutively or inducibly, in the HCE7 human esophageal cancer cell line in which cyclin D1 is amplified and expressed at high levels.
The prognostic significance of the cytophotometric DNA content and its relationship with the argyrophilic nucleolar organizer regions (AgNOR) and proliferating cell nuclear antigen (PCNA) in oesophageal cancer.
DNA-damaging agents alter levels of p53 protein in several cell types and it has been speculated that regulation of p53 can be involved in the resistance or sensitivity of cancer cells to some chemotherapeutic drugs, depending on whether cells have mutant or wild-type p53; however, little is known about the relationship of p53 to drug sensitivity in gastric/esophageal cancers.
If these preliminary observations are confirmed in larger prospective studies, p53 may prove to be a clinically useful molecular marker in future clinical trials of esophageal cancer.
Epidemiological studies have shown an increased incidence of lung cancer, bladder cancer, and esophageal cancer in chimney sweeps, probably due to their exposure to PAH in soot.
These results suggest that cyclin D1 may play an important role in carcinogenesis and that cyclin D1 overexpression may be a useful prognostic factor in esophageal cancer.
The finding that sevenfold or greater amplification of the hst-1 gene seems to be associated with haematogenous recurrence of oesophageal cancer after resection may serve to assess the clinical outcome.
Esophageal cancer is one primary human tumor in which MTS1 constitutes an apparent target of heterozygous or homozygous deletions occurring at chromosome 9p21.
Esophageal cancer is one primary human tumor in which MTS1 constitutes an apparent target of heterozygous or homozygous deletions occurring at chromosome 9p21.
Esophageal cancer is one primary human tumor in which MTS1 constitutes an apparent target of heterozygous or homozygous deletions occurring at chromosome 9p21.