A limit of this study is the use of different cell lines between human and NHP. PERV-A infection conducted in parallel using the same primary human and NHP cells such as PBMC could provide more information on the suitability of AGM as animal model in xenotransplantation. Here, infection of human-tropic, recombinant PERV-A/C in NHP cells has been examined, and several steps have been identified which are responsible for the lower efficiency of infection compared to that of human cells. PERV entry is inefficient in rhesus macaque cells because of the defect in PAR-1 PERV-A receptor function. The same is predicted for baboon and cynomolgus monkey cells, which have the same defective mutation. A genotypic analysis of the PAR sequences in the candidate species to be employed in pig-to-NHP transplantation will provide useful information on the likelihood that an animal may be as susceptible as humans to PERV infection. Indeed, AGM has no such defect in the PAR-1 gene, suggesting possible advantage for the use of this species. Melanoma is a highly aggressive human cancer refractory to most treatments. Progression from benign hyperplastic melanocytes to more aggressive disease occurs when tumor cells begin to break down and invade through the basement membrane, and subsequently migrate into the collagen-rich dermis. It has become clear that cancer cells have multiple modes of cell migration during tissue invasion: collective, individual elongated or “mesenchymal-type,” and individual rounded or “Vorinostat amoeboidtype”. The latter two modes of individual cell migration are determined in large part by the balance of Rho and Rac small GTPase signalling. The mesenchymal mode is driven by Rac activation, and involves extensive protrusions and proteolytic activity. The rounded “amoeboid-type” on the other hand is associated with a high degree of actomyosin contractility, membrane blebbing and squeezing through matrices. The amoeboid mode is favored by high Rho/ROCK signalling to elevate actomyosin contractility and is not dependent on extracellular protease activity. Importantly, there is negative feedback between these two signalling pathways, with Rho-kinase inhibiting the mesenchymal mode and Rac inhibiting the rounded form of migration. This interplay allows for dynamic signalling and survival pathway dependence, and plasticity or switching between different morphologies allows cancer cells to invade using distinct pathways to adapt to different environments. Cancer cell morphology can be modulated by microRNA activity. MicroRNAs are 20–24 nucleotide non-coding RNAs that regulate gene expression by targeting the 39 untranslated region of target mRNA transcripts for degradation and/or translation inhibition. Target specificity is directed by sequence complementarity to the microRNA particularly in the 29-89 seed region – and families have been identified based on miRs that have highly similar or identical seed sequences. Of particular interest in the field of metastasis.