High MYC amplification was seen in grade III carcinomas (MYC: CEP8 = 2.42), pre-menopausal women (MYC: CEP8 = 2.49), PR-negative status (MYC: CEP8 = 2.42), and ER-positive status (MYC: CEP8 = 2.4).
Head and neck carcinomas show frequent activation of c-MYC function and SIRT6 down-regulation, which contributes to a strong dependence on glucose and glutamine availability.
The rs6983267 SNP may contribute to the increased MYC expression as well as the spread and rapid growth of cervical SCC as compared to lower grade carcinomas.
Notably, switching off the oncogene in advanced carcinomas revealed that MYC was required for the continuous activation and repression of distinct sets of genes, constituting no more than half of all genes deregulated during tumor progression and an even smaller subset of all MYC-bound genes.
On the other hand, the expression of MYC and p53 was more frequent in gallbladder carcinomas than in control samples (p = 0.002, p = 0.046, respectively).
In addition, the expression levels of Mina53 and c-Myc protein in gastric carcinomas were higher when compared with levels in the adjacent normal epithelium. mina53 expression was significantly increased during gastric carcinogenesis and was correlated with different clinicopathological factors in IGC and DGC.
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.
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 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.
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.
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.