Oral Presentation ASPCR-ASDR Conference 2013

Pervasive and intrinsic evolutionary potential in human melanoma cells (#24)

M Shackleton 1 2 , E Quintana 2 , M L Yang 3 , J Li 3 , S J Morrison 2 4
  1. Melanoma Research Laboratory, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia
  2. Howard Hughes Medical Institute, Life Sciences Institute, Center for Stem Cell Biology, Department of Internal Medicine, Ann Arbor, USA
  3. Department of Human Genetics, University of Michigan, Ann Arbor, USA
  4. Howard Hughes Medical Institute, Children's Medical Center Research Institute, University of Texas Southwestern , Dallas, USA

 Malignant tumors are frequently incurable because of their evolutionary nature. However, revealing the extent of heritable molecular variation in cancer has been difficult, as it has not been possible to study genetic and epigenetic change in individual cells from the same tumor. In overcoming this, we have found that genetic and epigenetic changes are remarkably dynamic in human melanoma.


Using melanomas from four separate patients, we performed serial in vivo xenotransplantation of single cells isolated from each tumor, creating multi-generational clonal tumor families. SNP genotyping and DNA methylation arrays were performed on each clonal tumor. Inter-clonal comparisons of CNVs and DNA methylomes revealed widespread and rapidly emergent changes in a high proportion of tumorigenic clones; a majority of clones in each family were genetically and epigenetically distinct from one other. Importantly, some of the changes were found to affect genes known to be functionally relevant in melanoma, such as N-RAS and BRAF. This indicates that potentially targetable molecular changes may evolve in melanoma after tumors are already established.

These data reveal pervasive and profound instability of the human melanoma genome and epigenome that helps to explain the rapid emergence of resistance commonly seen against anti-melanoma therapies.