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J Cutan Pathol 2008: 35: 89 Blackwell Munksgaard. Printed in Singapore Copyright # Blackwell Munksgaard 2007 Journal of Cutaneous Pathology Letter to the Editor Reply To the Editor , I believe that Dr Francois Milette has completely missed the purpose of the paper by Doctors Davis and Zembowicz (1). The main gist of Dr Milette’s argument, as summarized in his concluding remarks, is that the authors misdiagnosed melanoma in situ as a junctional nevus and that the authors have concocted new diagnostic terminology to hide their diagnoses or cover them up. This reductionist position is simplistic at best and anti-progressive at worst. Dr. Milette’s view that all these cases outlined in the paper are diagnostically straightforward and easily diagnosed as melanoma in situ, completely nullifies the reality of the field of melanocytic lesions in which atypical lentiginous melanocytic proliferations are difficult to classify. If one were to simply classify all these lesions as melanoma, I believe that we truly would have an epidemiological explosion of case reports of melanomas. Doctors Davis and Zembowicz have attempted to generate criteria for a subset of atypical lentiginous melanocytic prolifer- ations which if left alone, will continue to persist and progress, thus behaving in a malignant fashion. Dr Milette disagrees with the criteria proposed in table 2 as negative and irrelevant. The criteria generated in the table reflect an attempt to reproduce reliable criteria for diagnosing these problematic lesions. I do agree with Dr Milette’s query of the use of the term Ôfloating’ above the basal layer of the epidermis. However, the remainder of the criteria does provide a framework around which to analyze similar lesions. Dr Milette’s contention that the images in fig. 1 are all diagnostic of melanoma in situ is puzzling. Firstly, fig. 1 is divided into three time periods over which the proliferation appears to increase in cellularity, how- ever, the overall picture is that of an atypical lentiginous junctional proliferation. There is no solar elastosis or effacement of the retiform epidermis, changes seen in lentigo maligna, or the typical shotgun appearance of malignant melanoma of the superficial spreading type. I therefore, think that these are not diagnostically straightforward or typical of melanoma in situ as previously classified. Dr Milette’s point that only high magnifications are shown is well taken and the authors perhaps would have been better served to submit more low-power fields. In fig. 2, the caption does state that it is a Level 2 melanoma, which is in agreement with what Dr Milette has ascertained. With regards to the biological behavior, it is precisely this fact that has led the authors to maintain that these lesions do indeed behave in a malignant fashion. The time course of 12 years for their index to develop into invasive melanoma, is precisely what lead the authors to conclude that these were indeed a melanoma, and most probably a variant of a lentigo maligna. Our experience was indeed similar with three of our index cases being initially diagnosed as atypical lentiginous nevi and the lesions persisting and progressing over long periods of time (2). In summary, the well-recognized patterns of cutane- ous melanoma, namely, lentigo maligna type, superficial spreading type and acral lentiginous type, are well- defined in the literature, and for the most part are readily recognized as malignant melanoma. However, there exist a substantial number of cases in which atypical lentiginous melanocytic proliferations are identified, and in which the lesions do not precisely fit into the recognized histologic patterns that we recognize as malignant melanoma. I believe that as histopathologists and scientists, it is our responsibility to attempt to further classify these lesions and to determine their biological behavior. I believe that Doctors Davis and Zembowicz have defined a subset of such lesions, which if left untreated will persist and progress as melanomas. These lesions most probably represent a variant of lentigo maligna. Dr Milette is incorrect in his contention that these lesions were mistakenly diagnosed as junctional nevi when in fact they were always melanomas in situs , and therefore readily recognized from the outset. These lesions in fact do not conform to any of the criteria for the well-known histologic subtypes of melanoma, and only with careful follow-up, monitoring of the progression of these lesions, and generation of histologic criteria, can we proceed to label these lesions as melanoma, as outlined by Doctors Davis and Zembowicz. To simply say that all lentiginous melanocytic lesions are mela- nomas is tantamount saying that all sebaceous lesions should be called sebaceous carcinomas. Roy King, MD Knoxville Dermatopathology Laboratory and Departments of Pathology, University of Tennessee, Graduate School of Medicine, Knoxville, and Vanderbilt University, Nashville, TN, USA email: [email protected] 89

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J Cutan Pathol 2008: 35: 89Blackwell Munksgaard. Printed in Singapore

Copyright # Blackwell Munksgaard 2007

Journal of

Cutaneous Pathology

Letter to the Editor

ReplyTo the Editor,I believe that Dr Francois Milette has completely

missed the purpose of the paper by Doctors Davis andZembowicz (1). Themain gist ofDrMilette’s argument,as summarized in his concluding remarks, is that theauthors misdiagnosed melanoma in situ as a junctionalnevus and that the authors have concocted newdiagnostic terminology to hide their diagnoses or coverthem up. This reductionist position is simplistic at bestand anti-progressive at worst. Dr. Milette’s view that allthese cases outlined in the paper are diagnosticallystraightforward and easily diagnosed as melanoma insitu, completely nullifies the reality of the field ofmelanocytic lesions in which atypical lentiginousmelanocytic proliferations are difficult to classify. If onewere to simply classify all these lesions as melanoma, Ibelieve that we truly would have an epidemiologicalexplosion of case reports of melanomas. Doctors Davisand Zembowicz have attempted to generate criteria fora subset of atypical lentiginous melanocytic prolifer-ations which if left alone, will continue to persist andprogress, thus behaving in a malignant fashion. DrMilette disagrees with the criteria proposed in table 2 asnegative and irrelevant. The criteria generated in thetable reflect an attempt to reproduce reliable criteria fordiagnosing these problematic lesions. I do agree withDrMilette’s query of the use of the term �floating’ abovethebasal layerof the epidermis.However, the remainderof the criteria does provide a framework around whichto analyze similar lesions.DrMilette’s contention that the images in fig. 1 are

all diagnostic of melanoma in situ is puzzling. Firstly,fig. 1 is divided into three time periods over which theproliferation appears to increase in cellularity, how-ever, the overall picture is that of an atypicallentiginous junctional proliferation. There is no solarelastosis or effacement of the retiform epidermis,changes seen in lentigo maligna, or the typicalshotgun appearance of malignant melanoma of thesuperficial spreading type. I therefore, think that theseare not diagnostically straightforward or typical ofmelanoma in situ as previously classified. Dr Milette’spoint that only high magnifications are shown is welltaken and the authors perhapswould have been betterserved to submit more low-power fields. In fig. 2, thecaption does state that it is a Level 2melanoma, whichis in agreement with what DrMilette has ascertained.

With regards to the biological behavior, it isprecisely this fact that has led the authors to maintainthat these lesions do indeed behave in a malignantfashion. The time course of 12 years for their index todevelop into invasive melanoma, is precisely whatlead the authors to conclude that these were indeeda melanoma, and most probably a variant of a lentigomaligna. Our experience was indeed similar withthree of our index cases being initially diagnosed asatypical lentiginous nevi and the lesions persisting andprogressing over long periods of time (2).

In summary, the well-recognized patterns of cutane-ousmelanoma, namely, lentigomaligna type, superficialspreading type and acral lentiginous type, are well-defined in the literature, and for themost part are readilyrecognized as malignant melanoma. However, thereexist a substantial number of cases in which atypicallentiginous melanocytic proliferations are identified,and in which the lesions do not precisely fit into therecognized histologic patterns that we recognize asmalignant melanoma. I believe that as histopathologistsand scientists, it is our responsibility to attempt to furtherclassify these lesions and to determine their biologicalbehavior. I believe that Doctors Davis and Zembowiczhave defined a subset of such lesions, which if leftuntreatedwill persist and progress asmelanomas.Theselesions most probably represent a variant of lentigomaligna. Dr Milette is incorrect in his contention thatthese lesions were mistakenly diagnosed as junctionalnevi when in fact they were always melanomas in situs,and therefore readily recognized from the outset. Theselesions in fact donot conformtoanyof the criteria for thewell-known histologic subtypes of melanoma, and onlywith careful follow-up, monitoring of the progression ofthese lesions, and generation of histologic criteria, canwe proceed to label these lesions as melanoma, asoutlined by Doctors Davis and Zembowicz. To simplysay that all lentiginous melanocytic lesions are mela-nomas is tantamount saying that all sebaceous lesionsshould be called sebaceous carcinomas.

Roy King, MDKnoxville Dermatopathology Laboratory and

Departments of Pathology, University of Tennessee,Graduate School of Medicine, Knoxville, and

Vanderbilt University, Nashville, TN, USAemail: [email protected]

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