Immunohistochemical Studies of Atypical Conjunctival Melanocytic Nevi
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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. -
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. -
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: -
Optimal Management of Common Acquired Melanocytic Nevi (Moles): Current Perspectives
Clinical, Cosmetic and Investigational Dermatology Dovepress open access to scientific and medical research Open Access Full Text Article REVIEW Optimal management of common acquired melanocytic nevi (moles): current perspectives Kabir Sardana Abstract: Although common acquired melanocytic nevi are largely benign, they are probably Payal Chakravarty one of the most common indications for cosmetic surgery encountered by dermatologists. With Khushbu Goel recent advances, noninvasive tools can largely determine the potential for malignancy, although they cannot supplant histology. Although surgical shave excision with its myriad modifications Department of Dermatology and STD, Maulana Azad Medical College and has been in vogue for decades, the lack of an adequate histological sample, the largely blind Lok Nayak Hospital, New Delhi, Delhi, nature of the procedure, and the possibility of recurrence are persisting issues. Pigment-specific India lasers were initially used in the Q-switched mode, which was based on the thermal relaxation time of the melanocyte (size 7 µm; 1 µsec), which is not the primary target in melanocytic nevus. The cluster of nevus cells (100 µm) probably lends itself to treatment with a millisecond laser rather than a nanosecond laser. Thus, normal mode pigment-specific lasers and pulsed ablative lasers (CO2/erbium [Er]:yttrium aluminum garnet [YAG]) are more suited to treat acquired melanocytic nevi. The complexities of treating this disorder can be overcome by following a structured approach by using lasers that achieve the appropriate depth to treat the three subtypes of nevi: junctional, compound, and dermal. Thus, junctional nevi respond to Q-switched/normal mode pigment lasers, where for the compound and dermal nevi, pulsed ablative laser (CO2/ Er:YAG) may be needed. -
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 -
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. -
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. -
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 -
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. -
Inflammatory Juvenile Compound Conjunctival Nevi. a Clinicopathological Study and Literature Review
Rom J Morphol Embryol 2017, 58(3):in press R J M E EVIEW AND ASE ERIES Romanian Journal of R C S Morphology & Embryology http://www.rjme.ro/ Inflammatory juvenile compound conjunctival nevi. A clinicopathological study and literature review CLAUDIA FLORIDA COSTEA1,2), MIHAELA DANA TURLIUC3,4), GABRIELA DIMITRIU2), CAMELIA MARGARETA BOGDĂNICI1), ANCA MOŢOC2), MĂDĂLINA ADRIANA CHIHAIA2), CRISTINA DANCĂ2), ANDREI CUCU4), ALEXANDRU CĂRĂULEANU5), NICOLETA DUMITRESCU6), LUCIA INDREI7), ŞERBAN TURLIUC8) 1)Department of Ophthalmology, “Grigore T. Popa” University of Medicine and Pharmacy, Iaşi, Romania 2)2nd Ophthalmology Clinic, “Prof. Dr. Nicolae Oblu” Emergency Clinical Hospital, Iaşi, Romania 3)Department of Neurosurgery, “Grigore T. Popa” University of Medicine and Pharmacy, Iaşi, Romania 4)2nd Neurosurgery Clinic, “Prof. Dr. Nicolae Oblu” Emergency Clinical Hospital, Iaşi, Romania 5)Department of Obstetrics and Gynecology, “Grigore T. Popa” University of Medicine and Pharmacy, Iaşi, Romania 6)4th Year Student, Faculty of Medicine, “Grigore T. Popa” University of Medicine and Pharmacy, Iaşi, Romania 7)3rd Year Student, Faculty of Medicine, “Carol Davila” University of Medicine and Pharmacy, Bucharest, Romania 8)Department of Psychiatry, “Grigore T. Popa” University of Medicine and Pharmacy, Iaşi, Romania Abstract Aim: The conjunctival nevus affecting children and adolescents is a rare condition and the literature showed only few reports on this issue. The aim of this article is to determine the histopathological features for the correct diagnosis of an inflammatory juvenile compound nevus of the conjunctiva (IJCNC) in order to make the difference between this tumor and other lesions, like conjunctival melanoma or lymphoma, very similar from a gross point of view. -
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). -
Toma, 539 Acinic Cell Carcinoma Mucinous Adenocarcinoma Vs., 334
Cambridge University Press 978-0-521-87999-6 - Head and Neck Margaret Brandwein-Gensler Index More information INDEX acanthomatous/desmoplastic ameloblas- ameloblastomas benign neoplasia toma, 539 desmoplastic ameloblastoma, 539 juvenile nasopharyngeal angiofibroma, acinic cell carcinoma metastasizing ameloblastoma, 537 99–104 mucinous adenocarcinoma vs., 334–335 mural ameloblastoma, 533 salivary gland anlage tumor, 104–106 oncocytoma vs., 295–299 odonto-ameloblastoma, 551–553 benign peripheral nerve sheath tumors papillary cystic variant, vs. cystade- peripheral ameloblastoma, 534 (BPNST), 40–44 noma, 316–317 unicystic ameloblastoma, 532–533 benign sinonasal tract neoplasia, 28–48 salivary glands, 353–359 aneurysmal bone cyst (ABC), 584 benign peripheral nerve sheath tumor, adenocarcinoma not otherwise specified central GCRG vs., 590–591 40–44 (ANOS), 389–390 angiocentric T-cell lymphoma, 81 meningioma, 37–40 adenoid cystic carcinoma (ACC) angiomatoid/angioectatic polyps vs. JNAF, nasal glial heterotopia (NGH), 44–48 adenomatoid odontogenic tumor vs., 100–104 oncocytic Schneiderian papilloma 545 angiosarcoma vs. Kaposi’s sarcoma, 206 (OSP), 5, 33–36 basal cell adenocarcinoma vs., 372 antrochoanal polyp, 5–8 Schneiderian inverted papilloma, 28–32 basal cell adenoma vs., 293 apical periodontal cyst, 510–512 bisphosphonate osteonecrosis (BPP), canalicular adenoma vs., 294 arytenoid chondrosarcomas, 241 565–566 neuroendocrine carcinoma vs., 240–241 atrophic oral lichen planus, 126 blastomas of salivary glands, 319–325 atypical adenoma vs. parathyroid