melanoma, the stage of the disease, and especially with the amount of sun exposure.36–38 Strikingly, our ﬁndings indicate that a core of genes is expressed in both in situ and invasive melanoma and in lesions of various histologies, including those associated (i.e. lentigo maligna) or not associated (i.e. superﬁcial spreading) with chronic sun exposure. Among 142 upregulated genes in melanoma, many are known to be expressed speciﬁcally in melanocytes, including KIT, Melan-A, TYR, TRPM1, EDNRB, DCT, SOX10 and SILV (Fig. 2). In addition, the biological functions of these upregulated genes are also involved in melanocyte biology, skin ⁄ hair pigmenta- tion, cellular growth ⁄ proliferation and cancer (Fig. 2, Table 2), thereby suggesting that many are biologically rele- vant to processes occurring within the underlying epidermal tissue. Thus, it is possible that these genes represent a com- mon thread of genetic progression for melanoma develop- ment that occurs at the earliest stage of disease – and may provide a target or group of targets for therapeutic interven- tion. Lastly, the histopathological differentiation of lentigo maligna and lentigo maligna melanoma from solar lentigo can often be extremely difﬁcult. This 17-gene classiﬁer sepa- rates this form of melanoma from the benign process, pro- viding a potential tool for the accurate diagnosis of these difﬁcult pigmented lesions. Preliminary qRT-PCR results for expression of the 17-gene classiﬁer from 10 melanomas and 10 naevi showed very simi- lar results to the data from the GeneChip microarray, with all 10 melanomas and nine of 10 naevi being discerned correctly (Data S2; see Supporting Information). This preliminary ﬁnd- ing strongly suggests that the classiﬁer, discovered by micro- array analyses of EGIR specimens, will translate well on to a qRT-PCR platform that should be cost-effective for use in the clinical setting. Should these ﬁndings be recapitulated in an expanded clinical validation study, such an assay may be sub- stantially more accurate and certainly more objective than the visual and optical means currently available for melanoma detection. Such a test would also permit clinicians to be vastly more selective in their choice of pigmented skin lesions that need to be biopsied and further evaluated. What’s already known about this topic? • Adhesive tape stripping of skin yields RNA from stratum corneum that can be assayed for gene expression to assess allergic and irritant skin reactions and psoriasis. What does this study add? • RNA from tape-stripped skin identiﬁed genes present in stratum corneum that are differentially expressed between melanoma, naevus and normal skin specimens. • A 17-gene genomic biomarker was characterized that accurately discriminates in situ and invasive melanomas from naevi. 2011 The Authors BJD 2011 British Association of Dermatologists 2011 164, pp797–806 Genomic detection of melanoma, W. Wachsman et al. 805 Acknowledgments We express our great appreciation to B. Bastian (University of California, San Francisco), for his expertise and service as the central dermatopathologist for this study. We thank R. Owsley (Saltzer Medical Group, Nampa, ID), A. Fernandez- Obregon (Hudson Dermatology and Skin Cancer Center, Hoboken, NJ), S. Smith (Dermatology & Advanced Aesthet- ics, Lake Charles, LA), R. Geronemus (Laser Skin Surgery, New York, NY), D. Pariser (Virginia Clinical Research, Nor- folk, VA), P. Rich (Oregon Dermatology & Research Center, Portland, OR), A. Balin (Sally Balin Medical Center, Media, PA), J. Spencer (Spencer Dermatology & Skin Surgery Center, St Petersburg, FL), B. Goff (Dermatology Associates, Seattle, WA) and J. Raoof (Raoof Laser & Dermatology Center, Encino, CA) for their efforts on subject enrolment and sub- mission of specimens and clinical data for the study. We thank C. Peters (DermTech International, Inc.), K. Peters (DermTech International, Inc.) and C. Gall (Gall Clinical Consulting) for their assistance with clinical study coordina- tion and monitoring. We thank M. Golovnya (Salford Systems, Inc.) for his advice on the TreeNet. We thank H. Rashidi (University of California San Diego and the Veter- ans Affairs San Diego Healthcare System) for his assistance with preparation of photomicrographs provided as part of the Supporting Information. Lastly, we thank S. Menzies (Sydney Melanoma Diagnostic Centre), A. 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