To determine if mutations of the E-cadherin gene (on chromosome 16q22) contribute to epithelial tumorigenesis, 135 carcinomas of the endometrium and ovary were examined for alterations in the E-cadherin coding region.
Single-strand conformation polymorphism (SSCP) analysis and direct sequencing demonstrated a G-->A transition at the second position of Ha-ras codon 12, with the resultant substitution of glutamic acid for glycine, in two of 10 carcinomas induced by 100 ppm PhIP and in one of seven induced by the 400 ppm dose.
Our data indicate that a subset of penile carcinomas are etiologically related to HPV and that an overlapping subset may arise from mutational events in the p53 gene.
In addition, carcinomas from animals on the high-fat diet showed on average a 5-fold higher expression of beta-casein and transferrin than carcinomas from animals on the low-fat diet.
Of the carcinomas analyzed, 81% expressed increased bcl-2 (54/67), 78% expressed increased bcl-X(L) (52/67) and 69% expressed increased levels of both bcl-2 and bcl-X(L) (46/67).
The level of COX-2 mRNA was found to be elevated in carcinomas, relative to histologically normal pancreas from a healthy individual, as assessed by reverse transcription-PCR.
Normal Sprague-Dawley rat mammary gland epithelial cells and mammary gland carcinomas induced by 2-amino-1-methyl-6-phenylimidazo[4, 5-b]pyridine, a carcinogen found in the diet, were examined for the expression of peroxisome proliferator-activated receptor alpha (PPAR alpha).
In humans, silencing of GST pi(GSTP1) through CpG island hypermethylation is found in nearly all prostate carcinomas and is believed to be an early event in prostate carcinogenesis.
These data suggested that PhIP-induced mammary carcinomas could model human breast cancers that show reduced BRCA1 immunoreactivity without promoter hypermethylation and with normal mRNA expression.
Copper-transporting P-type adenosine triphosphatase (ATP7B) as a cisplatin based chemoresistance marker in ovarian carcinoma: comparative analysis with expression of MDR1, MRP1, MRP2, LRP and BCRP.