A paragraph describing the group
Melanoma Research at TGen is focused in three areas:
1. Genetics of familial melanoma: In collaboration with members of the Melanoma Genetics Consortium, we have performed a whole-genome linkage scan on a collection of familial melanoma pedigrees, and have identified a novel melanoma susceptibility locus on chromosome 1. We are actively pursuing the identification of this gene using both traditional mutation screening methods and high-throughput genomic methods, including focused SNP association studies and array-based gene expression, CGH, and loss-of-heterozygosity (LOH) methods. We are also performing genome-wide scanning on additional families contributed by Consortium members with the aim of identifying additional novel melanoma susceptibility genes.
2. Genomic characterization of somatic events in early through late stage melanoma: We are applying several genomic technologies to identify somatic lesions that characterize specific stages of melanoma development as well as the transitions from early to advanced tumor. We are utilizing several microarray-based platforms aimed at characterizing gene expression, DNA-copy number, and LOH, coupled with candidate gene resequencing.
3. Clinical Therapeutic Development: Lastly, we are working to validate novel molecular targets on the pre-clinical level, develop and optimize novel therapies for clinical use, and define mediators of response to therapy at the clinical level. Potential molecular targets are being validated both alone and in combination using small molecule inhibitors and RNAi in TGens Cancer Drug Development Laboratory using highly parallel, miniaturized cell-based microassays. Towards defining response to therapy, we are applying microarray-based methods on clinical specimens to define gene expression patterns, somatic alterations, and germline sequence variation that correlate with response to specific therapies. Using expression microarrays, we have already defined a core set of genes that distinguish patients who respond to IL-2 therapy from non responders.
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