Gene alteration of the c-myc locus, as well as overexpression of the c-myc oncogene, appeared to be limited, and analysis of the c-myc gene yielded limited prognostic value in human esophageal carcinomas.
In a total of 42 xenografted lung carcinomas studied, 45% amplification and 77% overexpression of one of the myc genes were detected with a high prevalence of L-myc overexpression in NE carcinomas (50%) and of c-myc overexpression in non-small cell lung carcinomas (66%).
Amplification of the c-myc gene was observed in 5 cell lines derived from well-differentiated carcinomas and all of them were accompanied by co-amplification of other examined oncogenes.
Consecutive tissue sections were investigated for expression of the major histocompatibility complex class I (MHC-I) and c-myc using immunohistochemical double staining procedures, since a role has been suggested for the c-myc protein in MHC-I down-regulation and c-myc overexpression has been described in cervical carcinomas.
The overall frequency of gene amplification among the gastric carcinomas rose to 19.4% when MYC, ERBB2, and INT2 were included in the analysis, with significant association with advanced tumor stage.
Although the c-myc gene is overexpressed in approximately 70% of human colonic cancers, previous studies have not detected frequent gene amplification or rearrangement of c-myc in these tumors, although such amplification has been reported in chemically induced rodent colon cancer and quantitative analysis of gene copy number has shown the gene to be amplified at a low level in mucinous and poorly differentiated human colon carcinomas.
To evaluate both the incidence of c-myc gene mutation and the relationship of this finding to the clinico-pathologic characteristics of patients with cervical cancer, a polymerase chain reaction (PCR)-based heteroduplex gel electrophoresis method was used to screen DNA extracted from 102 cervical invasive carcinomas referred to the Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong.
The UG/MYC transgenics will be useful to investigate the biochemical mechanisms underlying the development of carcinomas and the oncogenic properties of c-MYC in epithelial cells of various tissues.
We investigated genomic amplification on chromosomes 7 and 8 by comparative genomic hybridization (CGH) and protein expression of relevant oncogenes (EGFR, HGF, MET, CTSB, MYC) by immunohistochemistry (IHC) in 22 esophageal and 22 gastric cardia carcinomas.
The TRPS1 and MYC expression levels were similar in all prostate tumour groups, whereas EIF3S3 expression was higher (P=0.029) in prostate carcinomas compared to BPH.