an immunohistochemical evaluation with an antibody to the cell proliferation marker Ki67 unmasked obvious differences between WM983 B MGP melanoma xenografts from mice that were treated with a mix of the inhibitor and paclitaxel and WM983 B MGP melanoma xenografts from mice that didn’t receive treatment. But, we still find it impossible that amplification or re-arrangement of the genetic loci is the reason because neither 2, the locus of Aurora kinase A, or 17p13. 1, where Aurora kinase B exists, is reported to be altered in advanced stage melanomas. Taking care of, however, that Docetaxel Taxotere could be of relevance to melanoma and that partly may help unravel why VGP and MGP melanomas are refractory to radiotherapy is the recently published finding that Aurora kinase An overexpression inhibits the recruitment of RAD51 to DNA double strand breaks and decreases DSB repair by homologous recombination. Given the findings of this Aurora kinase targeting study, it’s not astonishing that in vitro, melanomas, like other malignant cells, are inhibited in their growth, undergo cell cycle arrest, and thereupon, enter apoptosis in the presence of Aurora kinase An or Aurora kinase W siRNAs or when treated with the Aurora kinase inhibitor. But, in light of the fact that Meristem this disease in its advanced stages is refractory to practically all standard therapies, it is very encouraging that, as we report here, systemic therapy with an Aurora kinase chemical demonstrates efficiency for individual MGP melanoma xenografts when used alone and a lot more effectively, as also shown in other cases, when combined with paclitaxel. Unlike in the case of malignancies such as breast or lung cancer, there’s not a single gene that to date has demonstrated to be the driver of advanced melanoma, which in part is among the factors that phase I/II studies concentrating upon molecular targeted therapy for patients with advanced melanoma are lacking behind that for other malignancies. Next, despite ubiquitin conjugation the actual fact that recently, high throughput studies have identified many genes that are upregulated to high levels in advanced melanoma, maybe not all of them has turned out to be described as a useful target for molecular therapy. As an example, whilst the result of entire genome expression profiling studies of nevus and melanoma muscle types, osteopontin was found to be one of the absolute most abundantly expressed genes in advanced melanoma and, as recent studies have suggested, a prognostic marker and predictor of reduced relapse free survival of melanoma. Nevertheless, none of our molecular targeting approaches have provided a signal that osteopontin will be a of good use target for molecular therapy of advanced cancer. Still another instance is the Ataxia Telangiectasia Mutated gene, which like the Aurora kinases is expressed at high levels in high level stage melanomas, yet, our molecular targeting studies of this pivotal DNA damage sensor did not sensitize VGP or MGP melanomas to the effects of radiation treatment.