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Comparison of the Inflammatory Infiltrates in Tumoral Melanosis, Regressing Nevi, and Regressing Melanoma

George, Eva Vertes MD*; Kalen, Jessica E. MD*; Kapil, Jyoti P. MD; Motaparthi, Kiran MD*

The American Journal of Dermatopathology: July 2019 - Volume 41 - Issue 7 - p 480–487
doi: 10.1097/DAD.0000000000001346
Original Study
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Background: Tumoral melanosis (TM) is a histologic diagnosis characterized by abundant pigment-laden macrophages in the dermis. It is generally thought to represent a regressed melanoma, although it has also been reported after benign pigmented lesions as well. Determining the antecedent lesion in cases of TM is of clinical importance to accurately guide therapy and prognostication. Comparing the histopathologic and immunohistochemical (IHC) characteristics of TM, halo nevi (HN), and regressing melanoma (RM) may help predict the antecedent lesion in cases of TM.

Methods: Cases of TM, HN, and RM were selected and assessed for histopathologic (preservation of junctional melanocytic component, depth and width, solar elastosis, fibrosis, and preservation of rete ridge architecture) and IHC (SOX-10, CD138, and PD-1) parameters. PD-L1 immunostaining was also evaluated in cases of HN and RM.

Results: Severe solar elastosis, fibrosis, and marked rete ridge effacement were more frequent in RM than in HN. By contrast, numerous plasma cells, clusters of lymphocytes expressing PD-1, and >50% PD-L1 expression in melanocytes were more common in HN than in RM. However, the association of these variables did not reach statistical significance.

Discussion: Although studies with higher statistical power are needed, this study serves as an initial investigation to characterize the histopathologic and IHC characteristics, which may help better understand TM and its precursor lesions.

*Department of Dermatology, University of Florida College of Medicine, Gainesville, FL; and

Inform Diagnostics Research Institute, Irving, TX.

Correspondence: Kiran Motaparthi, MD, Assistant Professor, Department of Dermatology, University of Florida College of Medicine, 4037 NW 86 Terrace, 4th Floor, Room 4130 Springhill, Gainesville, FL 32606 (e-mail: kmotaparthi@dermatology.med.ufl.edu).

Financial support for this research was generously provided by the Franklin Flowers Melanoma Research Fund, University of Florida College of Medicine. Biostatistical analysis was performed in the Department of Biostatistics, University of Florida by Drs Susmita Datta, Alejandro Riveras Walker, and Dr Heather Lauritano.

The authors declare no conflicts of interest.

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