National Cancer Institute researchers and their colleagues report online in BMC Cancer that they used a comprehensive gene candidate approach to find genetic variants associated with osteosarcoma. The researchers hypothesized that DNA repair and ribosomal function-related genes could be involved in osteosarcoma pathogenesis, and, as such, they set about to determin whether variants in genes in bone formation, DNA repair, growth/hormone, and ribosomal pathways had a role in the disease. The researchers found 12 SNPs in growth or DNA repair genes that were significantly associated with osteosarcoma while four SNPs in a DNA repair gene and two SNPs downstream of a growth hormone gene were significantly associated. "Our results suggest that several SNPs in biologically plausible pathways are associated with OS. Larger studies are required to confirm our findings," the researchers conclude.
Peter Hersey and his colleagues at the University of Newcastle in Australia say that an aberrant function of P53 may contribute to melanoma. Hersey and his team used whole genome bead arrays to determine the expression levels of P53 target genes in 82 melanoma metastases, six melanoma cell lines, and extracts from diploid human melanocytes and fibroblasts. The authors write that their results show that "P53 target transcripts involved in apoptosis were under-expressed in melanoma metastases and melanoma cell lines, while those involved in the cell cycle were over-expressed in melanoma cell lines."