Converging lines of evidence suggest that melanoma comprises biologically distinct subtypes arising through multiple causal pathways. The distribution of melanoma subtypes differs by age, anatomical location of the cancer, and sun exposure. Somatic mutation patterns vary across melanoma subtypes, though the large majority of studies suggesting this phenomenon were based on metastatic melanoma alone, due to the difficulty in obtaining sufficient genetic material from thin primary melanomas once they are used for diagnostic review.
To further our understanding of the heterogeneity of melanoma, and to determine a predictive pattern of progression for dysplastic nevi, a melanoma precursor and risk factor, we are conducting tissue-based analyses of precursors, melanoma tumors and metastases within existing study populations. These cases are well annotated with detailed clinical and epidemiological data, and sufficient biological samples.
We are undertaking genetic analyses as well as targeted sequencing of previously identified driver genes for a more comprehensive classification of primary melanomas and the molecular changes associated with metastatic potential. In addition, with the extensive pathology data, particularly on lymphocyte infiltration and presence of other inflammatory cells, we can examine the link between molecular changes and tissue microenvironment.
For more information, contact Maria Teresa Landi.