Powerful evidence exists that deregulation of cell type-specific gene
expression is a major feature of the genesis of several cancers, with
many oncogenic proteins known to possess transcription regulation prop
erties. As a consequence of this deregulation, melanomas may ectopical
ly express HLA-DR and also fail to express enzymes required for melani
n synthesis, resulting in amelanotic melanoma. Recent work has demonst
rated that these phenomena may be accounted for by the expression of a
transcription factor called Brn-2, now known to be involved with the
development of neural crest-derived tissues. Brn-2 is normally express
ed at high levels in melanoblasts and melanomas but only at low levels
in normal melanocytes. Brn-2 may act by competing with another transc
ription factor, mi, necessary for normal melanocyte development.