DOCSLIB.ORG

Spitz Nevus and Its Variants Gerardo Ferrara, Elvira Moscarella, Caterina M

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Spitz Nevus and Its Variants Gerardo Ferrara, Elvira Moscarella, Caterina M Chapter III.16 Spitz Nevus and Its Variants Gerardo Ferrara, Elvira Moscarella, Caterina M. Giorgio, III.16 Giuseppe Argenziano Contents autonomy of Reed nevus from Spitz nevus has been questioned since 1978, when Paniago- III.16.1 Definition . .151 Pereira et al. [8] underlined the occurrence of III.16.2 Clinical Features . .152 cases of spindle and/or epithelioid cell nevi with III.16.3 Dermoscopic Criteria. 153 heavy pigmentation, thereby ascribing Reed ne- vus to the morphological spectrum of Spitz ne- III.16.4 Relevant Clinical Differential vus. At present, some authors still maintain that Diagnosis. 158 Reed nevus is an entity that can be clearly dif- III.16.5 Histopathology. .159 ferentiated from pigmented spindle cell Spitz nevus [9–15]; however, a clinicopathological III.16.6 Management. .160 evaluation of a large case series has recently References. 161 shown that the histopathological distinction be- tween these two diagnostic categories is often matter of great debate and has no clinical and dermoscopic relevance [16]. We can therefore refer to Spitz nevus by classifying it into two III.16.1 Definition clinical variants, namely, the classical and the pigmented types (the latter also comprising Reed The eponymic designation “Spitz nevus” refers nevus). to a benign melanocytic proliferation, which Indisputably, some melanomas histopatho- was first described in 1948 by Sophie Spitz as logically resemble Spitz nevi to various extent “melanoma of the childhood” [1]. Along with [4]. When such similarities are striking from this original description, we presently consider both an architectural and a cytological point of as “classical” Spitz nevus a rapidly growing, view the term “spitzoid melanoma” is justified pink or flesh-colored papule or nodule of the [17]. A morphological spectrum of melanomas lower extremities or the face in childhood or with “spitzoid” features probably exists, in early adulthood [2–6]. Its histopathological which one end shows lesions with overtly atypi- hallmark is the presence of large spindle and/or cal histopathological features, i.e., lesions which epithelioid cells, usually in the paucity or ab- are readily identified as malignant on histo- sence of melanin. pathological examination At the opposite edge “Reed nevus” is another eponymic designa- of this spectrum, one can conceivably find (rare) tion for a benign melanocytic lesion described cases which can be diagnosed as malignant only by Reed et al. in 1975 as “pigmented spindle cell retrospectively, i.e., after the development of nevus” [7]. It is mostly found in young adults on metastases [17–19]. These lesions have been first the lower extremities as a rapidly growing referred to as “spindle cell and epithelioid cell brownish-black macule or papule [7]. Histo- nevi with atypia and metastasis” or “malignant pathologically, it is described as made up by in- (metastasizing) Spitz nevi” [19], and subse- terconnecting junctional fascicles of heavily quently as “atypical Spitz nevi/tumors” [18]. pigmented spindle cells [4, 7]. The nosological They could be considered as neoplasms with 152 G. Ferrara, E. Moscarella, C.M. Giorgio et al. “bland” histopathological features and meta- III.16.2 Clinical Features static potential limited to the regional lymph nodes [18–20]. The common (although not in- Spitz nevus is a solitary, round to oval, dome- III.16 variable) absence of further dissemination be- shaped papule, measuring up to 1 cm in diame- yond the regional lymph nodes has even raised ter. Its surface is smooth or keratotic/verrucous, the question about the true malignant nature of and occasionally even papillomatous. Although the lymph node “implants” from spitzoid neo- initially described as a non-pigmented lesion plasms [21]. At present, however, we have no [1], recent data underline that Spitz nevi are convincing scientific data which can allow to brown to black in 71.3–92.7% [16, 29] of histo- really challenge the dogma of the metastasis as logically examined cases. Such a high frequency an unequivocal sign of malignancy [22, 23]. of pigmented variants in surgical series could be The concept of an “intermediate” category of the result of a better clinical recognition due to spitzoid lesions placed in between benignity and dermoscopy (see below) coupled with a low ex- malignancy does not fit with the traditional di- cision rate of classical “pink” Spitz nevi in chil- chotomic (“benign vs malignant”) diagnostic dren. approach to histopathology. According to this As a rule, a rapidly growing, pink or reddish view, cases of “metastasizing nevi” are simply lesion of the head/neck or (lower) limbs is the diagnostic errors, because the distinction be- clinical presentation of classical Spitz nevus in tween Spitz nevi and melanoma, although children. A brown/black papule of the trunk or sometimes difficult, can – and therefore lower extremities is the common clinical picture must – be made [22, 24]. It is obvious, however, of pigmented Spitz nevus in young adults [5, 30, that such a “dual” diagnostic approach leads to 31]; transitional clinical features are also possi- lowering the diagnostic threshold for melano- ble. Large (>1 cm) nodular and/or ulcerated le- ma – and therefore to overdiagnosing melano- sions must be always regarded as worrisome ma – in order not to miss the histopathological even in childhood [32, 23]. recognition of metastasizing lesions with subtle Rare congenital cases have been reported [33, histopathological clues to malignancy. 34]. A halo phenomenon has also been described Ongoing molecular genetic studies on spit- [35]. Multiple, and sometimes eruptive [36], zoid neoplasms seem to be a promising diagnos- Spitz nevi can present in a clustered (agminated) tic tool. HRAS mutations/amplifications have [37] or a disseminated pattern [38]. Agminated been detected in 11.8% of Spitz nevi [25]. B-RAF Spitz nevi can also occur within a background and N-RAS mutations, which are frequently (diffuse) hyperpigmentation [39] or within a found in melanoma on skin without chronic speckled lentiginous nevus [40]. sun damage [26], are consistently absent in Spitz Spitz nevi have a low recurrence rate, even nevi [27, 28] and probably expressed in a minor- after incomplete excision [41]; however, some ity of spitzoid melanomas [28]. These data sug- cases of satellitosis [42] and giant nodule forma- gest that spitzoid neoplasms probably have a tion [43] have been reported following surgical different pathway to tumorigenesis than con- procedures. In our opinion, such unusual oc- ventional types of nevi and melanomas. currences could be even in keeping with a low (or very low) malignant potential of some of these lesions. Spitz Nevus and Its Variants Chapter III.16 153 Fig. III.16.1. a A pink lesion located on the thigh of a c A striking epidermal hyperplasia with junctional mela- 27-year-old woman. Dermoscopically there is a negative nocytic nests demarcated by half-moon peripheral clefts pigment network (reticular depigmentation) with dot- (“capping”). d At a higher magnification large Kamino ted vessels especially visible at the periphery. b A large, bodies are seen within the epidermis sharply circumscribed, plaque-like melanocytic lesion. III.16.3 Dermoscopic Criteria widely and regularly spaced gray-brown, small- to medium-sized globules. Six main dermoscopic patterns can be ascribed In frankly pigmented lesions, globules are to Spitz nevus, namely, vascular, globular, star- brown to black, large and regularly distributed burst, reticular, atypical, and homogeneous at the periphery (Fig. III.16.2). In most cases of [44]. pigmented Spitz nevi, peripheral globules are Classical Spitz nevus (Fig. III.16.1) is an fused with the central body of the lesion; these amelanotic or hypopigmented lesion with a vas- regular, “on focus” radial projections (so-called cular pattern composed of dotted vessels [45], streaks) are responsible for a “starburst” appear- which are responsible for its “definitional” pink ance (Fig. III.16.3). In a minority of cases, a color. Dotted vessels are monomorphic, regu- heavy pigmentation also gives rise to a regular larly distributed throughout the lesion, often black network, which rests above the lesion and grouped and surrounded by regularly intersect- can be removed by tape stripping (“superficial ing white lines, the so-called reticular depig- black network”; Fig. III.16.4) [46]. Several of mentation (Fig. III.16.1). A slight pigmentation these features can be simultaneously present can be present as a diffuse brownish hue with and/or irregularly distributed within a given le- 154 G. Ferrara, E. Moscarella, C.M. Giorgio et al. III.16 Fig. III.16.2. a A small pigmented plaque located on the arm of a 23-year-old man. Dermoscopically this is a symmetric lesion with striking brown to black globules especially visible at the periphery and grayish pigmenta- tion in the center. b A medium-sized, well-demarcated, plaque-like melanocytic lesion. c An epidermal hyper- plasia with “capping” of junctional nests. d Same features at the opposite side of the lesion. e Periadnexal extension of the melanocytic nests, a microscopic feature which Spitz nevus shares with congenital nevus as well as with melanoma Spitz Nevus and Its Variants Chapter III.16 155 Fig. III.16.3. a A small hyperpigmented plaque located nin pigment. c A slight epidermal hyperplasia with junc- on the thigh of a 43-year-old man. A starburst pattern tional nests of melanocytes shows no sharp separation is clearly visible by dermoscopy. b A small-
Load more

Recommended publications
  • Critical Evaluation of the So-Called “Junction Nevus”
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector CRITICAL EVALUATION OF THE SO-CALLED "JUNCTION NEVUS* S. WILLIAM BECKER, MS., M.D. The serious study of pigmented nevi was undertaken by many workers in the closing years of the 19th Century. All recognized that the microscopic picture of nevi differed from anything seen in other organs. The presence of nevus cells in both the epidermis and dermis led to concepts of origin at one or the other site, or at both sites. Dermal Origin: Demieville (1) believed that the nevus cells arose from adven- titial and endothelial cells of blood vessels. Bauer (2) and vonRecklinghausen (3) thought that the origin was from endothelium of lymph vessels rather than of blood vessels. Epidermal Origin: According to Abesser (4), Duranti, in 1871, was the first to suggest an epidermal origin of nevus cells. Kromayer (5) stated that the endo- thelium-like cells originate in the basal portion of the epidermis as "Bläschen- zellen", migrate to the dermis and develop connective tissue and elastic fibers, a change which he called "desmoplasia". Abesser (4) agreed that the cells origi- ated in the epithelium and lost their intercellular bridges, but migrated into the dermis as epithelium-like cells, and remained such. Unna (6) advanced the concept that the epithelial cells changed by losing their intercellular bridges and multiplied in groups, a process which he called "Ab- sonderung", then migrated as groups to the dermis, which he called "Abtrop- fung", thus forming pigmented nevi.
    [Show full text]
  • Atypical Mole Syndrome and Dysplastic Nevi: Identification of Populations at Risk for Developing Melanoma - Review Article
    CLINICS 2011;66(3):493-499 DOI:10.1590/S1807-59322011000300023 REVIEW Atypical mole syndrome and dysplastic nevi: identification of populations at risk for developing melanoma - review article Juliana Hypo´ lito Silva,I Bianca Costa Soares de Sa´,II Alexandre Leon Ribeiro de A´ vila,II Gilles Landman,III Joa˜ o Pedreira Duprat NetoII I Oncology School Celestino Bourroul - Hospital AC Camargo, Sa˜ o Paulo, SP, Brazil. II Skin Oncology Department - Hospital AC Camargo - Sa˜ o Paulo, SP, Brazil. III Pathology Department - Hospital AC Camargo - Sa˜ o Paulo, SP, Brazil. Atypical Mole Syndrome is the most important phenotypic risk factor for developing cutaneous melanoma, a malignancy that accounts for about 80% of deaths from skin cancer. Because the diagnosis of melanoma at an early stage is of great prognostic relevance, the identification of Atypical Mole Syndrome carriers is essential, as well as the creation of recommended preventative measures that must be taken by these patients. KEYWORDS: Dysplastic Nevus Syndrome; dysplastic nevi; melanoma; early diagnosis; Risk Factors. Silva JH, de Sa´ BC, Avila ALR, Landman G, Duprat Neto JP. Atypical mole syndrome and dysplastic nevi: identification of populations at risk for developing melanoma - review article. Clinics. 2011;66(3):493-499. Received for publication on November 23, 2010; First review completed on November 24, 2010; Accepted for publication on November 24, 2010 E-mail: [email protected] Tel.: 55 11 2189-5135 INTRODUCTION Several studies have shown that the presence of dysplas- tic nevi considerably increases the risk of developing The incidence of cutaneous melanoma has increased melanoma, which demonstrates that these lesions, aside rapidly worldwide.1-5 Although it corresponds to only 4% of 4 from being precursors to disease are also important risk all skin cancers, it accounts for 80% of skin cancer deaths.
    [Show full text]
  • Short Course 11 Pigmented Lesions of the Skin
    Rev Esp Patol 1999; Vol. 32, N~ 3: 447-453 © Prous Science, SA. © Sociedad Espafiola de Anatomfa Patol6gica Short Course 11 © Sociedad Espafiola de Citologia Pigmented lesions of the skin Chairperson F Contreras Spain Ca-chairpersons S McNutt USA and P McKee, USA. Problematic melanocytic nevi melanin pigment is often evident. Frequently, however, the lesion is solely intradermal when it may be confused with a fibrohistiocytic RH. McKee and F.R.C. Path tumor, particularly epithelloid cell fibrous histiocytoma (4). It is typi- cally composed of epitheliold nevus cells with abundant eosinophilic Brigham and Women’s Hospital, Harvard Medical School, Boston, cytoplasm and large, round, to oval vesicular nuclei containing pro- USA. minent eosinophilic nucleoli. Intranuclear cytoplasmic pseudoinclu- sions are common and mitotic figures are occasionally present. The nevus cells which are embedded in a dense, sclerotic connective tis- Whether the diagnosis of any particular nevus is problematic or not sue stroma, usually show maturation with depth. Less frequently the nevus is composed solely of spindle cells which may result in confu- depends upon a variety of factors, including the experience and enthusiasm of the pathologist, the nature of the specimen (shave vs. sion with atrophic fibrous histiocytoma. Desmoplastic nevus can be distinguished from epithelloid fibrous histiocytoma by its paucicellu- punch vs. excisional), the quality of the sections (and their staining), larity, absence of even a focal storiform growth pattern and SiQO pro- the hour of the day or day of the week in addition to the problems relating to the ever-increasing range of histological variants that we tein/HMB 45 expression.
    [Show full text]
  • Digital Epiluminescence Microscopy Monitoring of High-Risk Patients
    STUDY Digital Epiluminescence Microscopy Monitoring of High-Risk Patients June K. Robinson, MD; Brian J. Nickoloff, MD, PhD Objective: To examine the outcome of digital epilumi- dence in and comfort with dermatologic surveillance and nescence microscopic (DELM) surveillance of atypical skin self-examination performance were assessed. nevi in a high-risk population for 4 years. Results: During annual surveillance with DELM, 5.5% of Design: Atypical, flat melanocytic lesions in 100 pa- the lesions changed. Among the 193 excisional biopsy speci- tients at high risk of developing melanoma were fol- mens there were 4 melanomas in situ, 169 dysplastic nevi, lowed annually with DELM. Pigmentary changes or an and 20 common nevi. Confidence in and comfort with sur- increase in DELM diameter of 1 mm or greater was an veillance and skin self-examination improved after DELM. indication to perform an excisional biopsy. Conclusions: The criteria applied to detect substantial Setting: Cardinal Bernardin Cancer Center Melanoma DELM changes were an increase in DELM diameter of 1 Program, Loyola University Health System, Maywood. mm or greater and pigmentary changes, including ra- dial streaming, focal enlargement, peripheral black dots, Patients: A consecutive sample of 3482 lesions from 100 and “clumping” within the irregular pigment network. patients (aged 18-65 years) with at least 2 images of the Use of DELM enhanced confidence in and comfort with same lesion. care, which extended to performing more extensive skin self-examination. Main Outcome Measures:
    [Show full text]
  • Identification of HRAS Mutations and Absence of GNAQ Or GNA11
    Modern Pathology (2013) 26, 1320–1328 1320 & 2013 USCAP, Inc All rights reserved 0893-3952/13 $32.00 Identification of HRAS mutations and absence of GNAQ or GNA11 mutations in deep penetrating nevi Ryan P Bender1, Matthew J McGinniss2, Paula Esmay1, Elsa F Velazquez3,4 and Julie DR Reimann3,4 1Caris Life Sciences, Phoenix, AZ, USA; 2Genoptix Medical Laboratory, Carlsbad, CA, USA; 3Dermatopathology Division, Miraca Life Sciences Research Institute, Newton, MA, USA and 4Department of Dermatology, Tufts Medical Center, Boston, MA, USA HRAS is mutated in B15% of Spitz nevi, and GNAQ or GNA11 is mutated in blue nevi (46–83% and B7% respectively). Epithelioid blue nevi and deep penetrating nevi show features of both blue nevi (intradermal location, pigmentation) and Spitz nevi (epithelioid morphology). Epithelioid blue nevi and deep penetrating nevi can also show overlapping features with melanoma, posing a diagnostic challenge. Although epithelioid blue nevi are considered blue nevic variants, no GNAQ or GNA11 mutations have been reported. Classification of deep penetrating nevi as blue nevic variants has also been proposed, however, no GNAQ or GNA11 mutations have been reported and none have been tested for HRAS mutations. To better characterize these tumors, we performed mutational analysis for GNAQ, GNA11, and HRAS, with blue nevi and Spitz nevi as controls. Within deep penetrating nevi, none demonstrated GNAQ or GNA11 mutations (0/38). However, 6% revealed HRAS mutation (2/32). Twenty percent of epithelioid blue nevi contained a GNAQ mutation (2/10), while none displayed GNA11 or HRAS mutation. Eighty-seven percent of blue nevi contained a GNAQ mutation (26/30), 4% a GNA11 mutation (1/28), and none an HRAS mutation.
    [Show full text]
  • Melanomas Are Comprised of Multiple Biologically Distinct Categories
    Melanomas are comprised of multiple biologically distinct categories, which differ in cell of origin, age of onset, clinical and histologic presentation, pattern of metastasis, ethnic distribution, causative role of UV radiation, predisposing germ line alterations, mutational processes, and patterns of somatic mutations. Neoplasms are initiated by gain of function mutations in one of several primary oncogenes, typically leading to benign melanocytic nevi with characteristic histologic features. The progression of nevi is restrained by multiple tumor suppressive mechanisms. Secondary genetic alterations override these barriers and promote intermediate or overtly malignant tumors along distinct progression trajectories. The current knowledge about pathogenesis, clinical, histological and genetic features of primary melanocytic neoplasms is reviewed and integrated into a taxonomic framework. THE MOLECULAR PATHOLOGY OF MELANOMA: AN INTEGRATED TAXONOMY OF MELANOCYTIC NEOPLASIA Boris C. Bastian Corresponding Author: Boris C. Bastian, M.D. Ph.D. Gerson & Barbara Bass Bakar Distinguished Professor of Cancer Biology Departments of Dermatology and Pathology University of California, San Francisco UCSF Cardiovascular Research Institute 555 Mission Bay Blvd South Box 3118, Room 252K San Francisco, CA 94158-9001 [email protected] Key words: Genetics Pathogenesis Classification Mutation Nevi Table of Contents Molecular pathogenesis of melanocytic neoplasia .................................................... 1 Classification of melanocytic neoplasms
    [Show full text]
  • A Search for CDKN2A/P16ink4a Mutations in Melanocytic Nevi from Patients with Melanoma and Spouse Controls by Use of Laser-Captured Microdissection
    STUDY A Search for CDKN2A/p16INK4a Mutations in Melanocytic Nevi From Patients With Melanoma and Spouse Controls by Use of Laser-Captured Microdissection Hao Wang, MD, PhD; Richard B. Presland, PhD; Michael Piepkorn, MD, PhD Objective: To determine the frequency at which the CDKN2A were observed in any of the melanocytic CDKN2A coding region is mutated in the atypical nevi nevi. of persons with sporadic melanoma. Conclusions: Point mutations in CDKN2A are an un- Design: DNA samples, isolated by laser-captured mi- common event in the atypical nevi of persons with mela- crodissection of atypical nevi from 10 patients with newly noma. As such, the data may support a hypothesis of incident cases of sporadic melanoma and their spouses melanocytic nevus histogenesis, in which the melano- as matched controls, were used as templates for nested cytic nevus and malignant melanoma represent sepa- polymerase chain reaction amplification of CDKN2A rate, pleiotropic pathways resulting from common stimuli, exons 1 and 2. such as genomic damage from UV radiation. Results: No point mutations in the coding region of Arch Dermatol. 2005;141:177-180 ONCEPTUAL MODELS OF messenger RNA are expressed at seem- melanoma development ingly normal levels in atypical as well as ba- and progression incorpo- nal nevi, but at significantly reduced lev- rate common and atypi- els in many melanomas, including the cal (dysplastic) nevi as po- earliest recognizable stage, melanoma in Ctential stages in the evolution of the situ.3-5 Moreover, the phenotype of mul- malignant phenotype in melanocytic sys- tiple and/or enlarged nevi does not geneti- tems.1 Support for this hypothesis can be cally segregate with, nor readily link by found, among other lines of evidence, in the polymorphic markers to, the CDKN2A lo- 6,7 spatial coexistence of melanoma and nevi cus.
    [Show full text]
  • Genomic Copy Number Analysis of a Spectrum of Blue Nevi Identifies
    Modern Pathology (2016) 29, 227–239 © 2016 USCAP, Inc All rights reserved 0893-3952/16 $32.00 227 Genomic copy number analysis of a spectrum of blue nevi identifies recurrent aberrations of entire chromosomal arms in melanoma ex blue nevus May P Chan1,2, Aleodor A Andea1,2, Paul W Harms1,2, Alison B Durham2, Rajiv M Patel1,2, Min Wang1, Patrick Robichaud2, Gary J Fisher2, Timothy M Johnson2 and Douglas R Fullen1,2 1Department of Pathology, University of Michigan, Ann Arbor, MI, USA and 2Department of Dermatology, University of Michigan, Ann Arbor, MI, USA Blue nevi may display significant atypia or undergo malignant transformation. Morphologic diagnosis of this spectrum of lesions is notoriously difficult, and molecular tools are increasingly used to improve diagnostic accuracy. We studied copy number aberrations in a cohort of cellular blue nevi, atypical cellular blue nevi, and melanomas ex blue nevi using Affymetrix’s OncoScan platform. Cases with sufficient DNA were analyzed for GNAQ, GNA11, and HRAS mutations. Copy number aberrations were detected in 0 of 5 (0%) cellular blue nevi, 3 of 12 (25%) atypical cellular blue nevi, and 6 of 9 (67%) melanomas ex blue nevi. None of the atypical cellular blue nevi displayed more than one aberration, whereas complex aberrations involving four or more regions were seen exclusively in melanomas ex blue nevi. Gains and losses of entire chromosomal arms were identified in four of five melanomas ex blue nevi with copy number aberrations. In particular, gains of 1q, 4p, 6p, and 8q, and losses of 1p and 4q were each found in at least two melanomas.
    [Show full text]
  • Dysplastic Nevus Panel Discussion
    Dysplastic Nevus Panel Discussion Maxwell Fung, MD, Moderator Director, UC Davis Dermatopathology Service Kerri Rieger, MD PhD Stanford Dermatopathology Service Joshua Schulman, MD Director of Dermatopathology, Sacramento Veterans Affairs Medical Center Definitions, Diagnostic criteria Dysplastic nevus • Major criteria (required) • basilar proliferation of atypical melanocytes extending 3 rete ridges beyond a dermal component (if present) i.e. “shoulder” • intraepidermal melanocytic proliferation (lentiginous or epithelioid) • Minor criteria (≥ 2) • fusion of rete ridges • concentric/lamellar eosinophilic fibrosis • inflammatory host response • neovascularization Clemente C, et al. Histopathologic diagnosis of dysplastic nevi: concordance among pathologists convened by the WHO Melanoma Programme. Hum Pathol 1991;22:313-19. Naeyaert JM, Brochez L. Dysplastic nevi. N Eng J Med 2003;23:349:2233-2240 Atypical nevus/mole Fig 1. Duffy K, Grossman D. • Usually 4-12 mm The dysplastic nevus. J Am Acad Dermatol 2012;67:19:31-12. • Asymmetry • Irregular pigmentation • Irregular border pigmented • Ill-defined border seborrheic keratosis • Macular component, usually peripheral Dysplastic nevus syndrome atypical mole syndrome, B-K mole syndrome, familial melanoma syndrome, familial atypical multiple mole-melanoma (FAMMM) • OMIM #155600 NIH Consensus criteria Occurrence of melanoma in ≥1 first- or second-degree relatives Large number of nevi (often >50), some of which are clinically atypical (and) Nevi with certain distinct histologic features Dutch
    [Show full text]
  • Blue Nevi and Melanomas Natural Blue BLUE NEVUS Blue Nevus (BN)
    KJ Busam, M.D. Paris, 2017 Blue Nevi and Melanomas Natural Blue BLUE NEVUS Blue Nevus (BN) • Spectrum of blue nevi – Common, Sclerosing, Epithelioid, Cellular, Plaque type blue nevi • Differential diagnosis – Melanoma ex BN or simulating BN – BN vs other tumors – Biphenotypic/collision lesions Common Blue Nevus Clinical: - Circumscribed small bluish macule/papule - Preferred sites: Scalp, wrist, foot Pathology: - Predominantly reticular dermal lesion - Pigmented fusiform and dendritic cells - Admixed melanophages - Bland cytology Common Blue Nevus Blue Nevus Sclerosing Blue Nevus Pigm BN Cellular Blue Nevus - 49 yo woman - Buttock nodule CBN Cellular Blue Nevus Thrombi and stromal edema Multinucleated giant melanocytes Cellular Blue Nevus Hemorrhagic cystic (“aneurysmal”) change Amelanotic Cellular Blue Nevus 19 yo man with buttock lesion Atypical CBN Plaque-Type Blue Nevus Plaque-type Blue Nevus Plaque Type Blue Nevus Mucosal Blue Nevus Conjunctival Blue Nevus Nodal Blue Nevus Combined epithelioid BN Blue Nevus • M Tieche 1906; Virchow Arch Pathol Anat “Blaue Naevus” • B Upshaw 1947; Surgery “Extensive Blue Nevus” (plaque-type BN) • A Allen 1949; Cancer “ Cellular Blue Nevus” Blue Nevus – Mutation Analysis Type of Lesion GNAQ GNA11 Number Common BN 6.7% 65% 60 Cellular BN 8.3% 72.2% 36 Amelanotic BN 0% 70% 10 Nevus of Ota 5% 10% 20 Nevus of Ito 16.7% 0% 7 TOTAL 6.5% 55% 139 Van Raamsdonk et al NEJM 2010; 2191-9 Blue Nevus – Mutation Analysis Type of Blue Nevus GNAQ Number Common Blue Nevus 40% 4/10 Cellular Blue Nevus 44% 4/9 Hypomelanotic
    [Show full text]
  • Incidence of New and Changed Nevi and Melanomas Detected Using Baseline Images and Dermoscopy in Patients at High Risk for Melanoma
    STUDY Incidence of New and Changed Nevi and Melanomas Detected Using Baseline Images and Dermoscopy in Patients at High Risk for Melanoma Jeremy P. Banky, MBBS; John W. Kelly, MDBS; Dallas R. English, PhD; Josephine M. Yeatman, MBBS, FACD; John P. Dowling, MBBS, FRCPA Objective: To determine the incidence of new, changed, Results: The incidence of new, changed, and regressed and regressed nevi and melanomas in a cohort of pa- nevi decreased with increasing age (PϽ.001), whereas tients at high risk for melanoma using baseline total body the incidence of melanomas increased (P=.05). The num- photography and dermatoscopy. ber of dysplastic nevi at baseline was positively associ- ated with the incidence of changed nevi (PϽ.001) and Design: Cohort study of patients at high risk for mela- melanomas (P=.03). The use of baseline photography and noma who underwent baseline cutaneous photography dermatoscopy was associated with low biopsy rates and between January 1, 1992, and December 31, 1997, and early detection of melanomas. The development of mela- had at least 1 follow-up visit by December 31, 1998. noma in association with a preexisting nevus was not di- rectly correlated with a change in a preexisting lesion Setting: Private practice rooms of 1 dermatologist in con- monitored by baseline photography. junction with a public hospital-based, multidisciplinary melanoma clinic in Victoria, Australia. Conclusions: Nevi are dynamic, and only a small per- centage of all new and changed melanocytic lesions are Patients: A total of 309 patients who had at least 1 of the following risk factors for melanoma: personal his- melanomas.
    [Show full text]
  • S100A6 Protein Expression Is Different in Spitz Nevi and Melanomas Adriana Ribé, M.D., Ph.D., N
    S100A6 Protein Expression is Different in Spitz Nevi and Melanomas Adriana Ribé, M.D., Ph.D., N. Scott McNutt, M.D. Dermatopathology Division, Department of Pathology, New York Presbyterian Hospital—Cornell University Weill Medical College, New York, New York and melanomas, without differences. In summary, The Spitz nevus is a benign melanocytic lesion that a simple immunohistochemical test for S100A6 pro- can be identified reliably in many cases by conven- tein differentiated between Spitz nevi, melanomas, tional histopathological criteria. However, there are and melanocytic nevi. This marker could be used subsets of Spitz nevi and of malignant melanoma when the distinction is very difficult or controver- that closely resemble each other and represent di- sial in routine studies, especially when there is a agnostic challenges. S100 proteins are of interest junctional component. Further molecular analyses because of their involvement in neoplastic pro- of the S100A6 protein and gene should be per- cesses and their genes are clustered in chromosome formed to study the underlying genetic bases for 1q21. Chromosome 1 contains mutations in several such differences. types of tumors, including melanomas. The expres- sion of different S100 proteins (A2, A6 and A8/A9 or KEY WORDS: Melanocyte, Melanoma, S100, A12) was examined in 42 Spitz nevi, 105 melano- S100A6, Spindle and epithelioid cell nevus, Spitz mas, and 73 melanocytic nevi to test the hypothesis nevus. that their expression differs among these entities Mod Pathol 2003;16(5):505–511 and may contribute to the distinction between these entities. The results showed an up-regulation of The epithelioid and spindle cell nevus was first S100A6 protein in Spitz nevi, melanomas, and mela- described in 1948 by Spitz and named juvenile mel- nocytic nevi but with a different percentage of pos- anoma (1).
    [Show full text]