Ethanol and the tobacco-specific carcinogen, NNK, contribute to signaling in immortalized human pancreatic duct epithelial cells.

Objectives: Smoking is a well-documented risk factor for pancreatic cancer. The tobacco-specific nitrosamine, NNK (4-[methylnitrosamino]-1-[3-pyridyl]-1-butanone), significantly induces pancreatic ductal adenocarcinomas in laboratory rodents. Recent observations suggest that ethanol enhances the tumorigenic effects of smoking.

The tobacco-specific carcinogen, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone stimulates proliferation of immortalized human pancreatic duct epithelia through beta-adrenergic transactivation of EGF receptors.

Purpose: Pancreatic ductal adenocarcinoma is an aggressive smoking-associated human cancer in both men and women. The nicotine-derived 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is thought to contribute to the development of these neoplasms in smokers through genotoxic effects. However, NNK has been recently identified as an agonist for both beta(1)- and beta(2)-adrenergic receptors.

Implication of mitochondrial involvement in apoptotic activity of fragile histidine triad gene: application of synchronous luminescence spectroscopy.

The fragile histidine triad (FHIT) tumor suppressor gene incorporates the common human chromosomal fragile site at 3p14.2. The structure and expression of the FHIT gene are frequently altered in many cancers.

Simultaneous detection of the tumor suppressor FHIT gene and protein using the multi-functional biochip.

The tumor suppressor gene, fragile histidine triad (FHIT), encompasses the most common human chromosomal fragile site, at 3pl4.2. Detection of FHIT gene is important in cancer diagnostics since its alterations have been associated with several human cancers.