The BESCT (Biology, Education, Screening, Chemoprevention and Treatment) Lung Cancer Program
Abstract
Our long-term objectives are to define the molecular processes contributing to lung cancer development and progression to recognize genetic and phenotypic changes early enough to be reversed with molecular targeted therapy and to develop innovative therapeutic approaches to lung cancer. Thus, the specific aims are to understand molecular alterations, develop prevention strategies, and implement experimental molecular approaches to lung cancer. In the past year, we identified that hypermethylation of p16(INK4a) and RASSF1A was associated with clinical outcomes in patients with respectable NSCLC; hypermethylated DAP kinase attenuated TRAIL-induced apoptosis of NSCLC cells; tumor-dominant DNMT3B variants was strongly associated with methylation status of p16(INK4a) and RASSF1A, and clinical outcomes. Also growth inhibition and apoptosis induction by the combination of Celecoxib and 4HPR were mediated by both pathway and inhibited P13K/Akt survival pathway activated. We demonstrated that SCH66336 inhibited angiognic activities of NSCLC and HNSCC cells Partly by inhibiting hypoxia- or IGF-stimulated HIF-1a and thus VEGF production via blocking the interaction HIF-1 and Hsp90 and inducing protessomal degradation of HIF-1. Moreover, a mouse lung cancer model that develops lung carcinomas has been successfully developed and will be used for various studies including drug test and mechanistic studies of lung carcinogenesis.
Document Details
- Document Type
- Technical Report
- Publication Date
- Apr 01, 2006
- Accession Number
- ADA469406
Entities
People
- Waun Hong
Organizations
- The University of Texas MD Anderson Cancer Center