AACR 102nd Annual Meeting 2011

AACR 102nd Annual Meeting 2011
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The study provides insights into epigenetic mechanisms underlying nickel carcinogenesis. Monday, April 4, , 1: In the study combinations of non-toxic nutraceuticals, dietary components providing health benefits, were administered at or near physiological levels. Several combinations of nutraceuticals were tested for their abilities to inhibit mutagenesis in these cell lines at 1x concentrations.


December , • San Antonio, Texas AACR-NCI-EORTC International Conference on Molecular Targets and nd AACR Annual Meeting: Proceedings: AACR nd Annual Meeting April 2–6 Abstracts: AACR International Conference on the Science of Cancer Health Disparities.

These results indicate these combinations can inhibit mutagenesis and suggests a role for fibroblast cells in the bioactivation of carcinogens. Tuesday, April 5, , 8: Hardee, house staff, Radiation Oncology; Ariel E. Glioblastomas are routinely treated with radiation and have a poor prognosis with a median survival of only Tuesday, April 5, , 1: However, the accumulation, nuclear translocation and phosphorylation of p53 are not affected. Moreover, ablation of p53 acetylation at Lys by site-directed mutagenesis dramatically suppresses UVB-induced expression of the specific presponsive gene as well as cell apoptosis.

Guttenplan, PhD, research associate professor, Environmental Medicine and Basic Science Butyl-hydroxybutyl-N-nitrosamine BBN is a powerful carcinogen that specifically causes bladder cancer in rodents, the reason for such a high degree of organ specificity is unclear. BBN is a primary metabolite of the environmental carcinogen, dibutylnitrosamine and hence a potential human carcinogen.

Mutagenesis induced by BBN in a chromosomally incorporated mutagenesis reporter gene was measured in bladder urothelial cells and smooth muscle cells of mice or rats and compared with mutagenesis in liver, kidney, ureter and forestomach.

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Since mutagenesis in the reporter gene is a surrogate for mutagenesis in general, researchers hypothesized mutations also induced in critical growth control genes would contribute to the tumor formation induced by BBN. Researchers found mutagenesis correlated with the organ specificity for cancer induction by BBN. The study results provide molecular explanations to the puzzling organ and species specificity of BBN, and indicate that BBN-induced mutagenesis in the urinary bladder represents a model for initiation of bladder cancer, and combined with other models can help explain distinct steps in bladder carcinogenesis.

Stefan Feske, MD, assistant professor, Pathology Melanoma, the deadliest form of skin cancer, has a poor prognosis because of its strong metastatic ability controlled by its cell migration. However, little is known about the role of SOCE in melanoma.

Peregrine Announces Four Abstracts Accepted for Presentation at AACR Annual Meeting

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