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In Response

Requena, Luis MD*; LeBoit, Philip E. MD†,‡

The American Journal of Dermatopathology: August 2017 - Volume 39 - Issue 8 - p 635
doi: 10.1097/DAD.0000000000000733
Letters to the Editor
Free

*Department of Dermatology, Fundación Jiménez Díaz, Universidad Autónoma, Madrid, Spain

Departments of Dermatology

Pathology, The UCSF Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA

The authors declare no conflicts of interest.

In Response:

We really appreciate the comments of Salgado et al to our article. In our case, however, neither a specimen from the atypical proliferation in the congenital melanocytic nevus nor one from the metastasis showed amplification of n-ras. The software that we use to analyze comparative genomic hybridization results (Nexus 6.1; Biodiscovery, Hawthorne, CA) permits a “high power” view with a look up by gene. There is adequate probe coverage in the area of n-ras that amplification should be detectable. Regarding whether the congenital melanocytic nevus had an n-ras mutation, we attempted immunostaining with a new antibody that recognizes the codon 61R mutation (clone SP174, catalog number, M4742; Spring Bioscience, Pleasanton, CA), but the degree of background staining did not allow for a meaningful result. In the absence of amplification, given the frequency of n-ras mutations in large congenital nevi, we did not believe that the new knowledge acquired would justify the cost in performing Sanger sequencing for n-ras.

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