Genomics and Melanoma: A case study

The swine melanoma model is a well established spontaneous melanoma model and one of the best developed for genomic approaches. The Sinclair melanoma and Melanoma-bearing Libechov Minipig (MeLiM) have been studied in detail using immune analyses, focusing on the role of tumor infiltrating lymphocytes, the potential effects of natural killer (NK) and ?d T cells in tumor regression. Imaging and sentinel lymph node (SLN) mapping will enhance these studies 54. Comparative studies of normal melanocytes with localized tumor cells should reveal tumor specific regulatory pathways 78; indeed laser capture microdissection studies revealed loss of the 13q36-49 chromosomal region in nodular melanoma cells 79.
Early mapping studies in the Sinclair swine melanoma model determined that a single dose of a specific “B” swine leukocyte antigen (SLA) haplotype on SSC7 was required for tumor initiator 80; complex segregation analysis identified a second locus 81. These were followed by more detailed QTL studies using the MeLiM model which identified numerous melanoma candidate loci 40; interestingly human candidate genes CDK4 and BRAF were not susceptibility genes in this model. Zhi-Qiang 41 continued these studies identifying QTL for the synthetic trait, development of melanoma on SSC1, 2, 13, 15 and 17. Their detailed phenotyping of 331 pigs revealed highly significant QTLs (p < 0.001/p < 0.05 respectively, chromosome-/genome-wide levels) for precise disease traits. These included SSC10 42.0 cM for ulceration; SSC12 95.6 cM for presence of melanoma at birth; SSC13 81.0 cM for lesion type; SSC16 45.3 cM and SSC17 44.8 cM for number of aggressive melanomas; and the SSC1 MeLiM MC1R*2 allele for black coat color predisposing to melanoma. As outlined in Table Table33 these studies affirmed that more exact mapping of complex traits such as tumor growth and regression are improved when very detailed phenotypic information is collected on a large group of animals.

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