Intradermal nevus with psammoma body formation.
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BACKGROUND: Apoptosis is important for maintenance of tissue homeostasis and often dysregulated in cutaneous neoplasms. The apoptosis inhibitor survivin is expressed in melanoma and non-melanoma skin cancers and benign keratinocytic lesions. Its expression has not been studied in melanocytic nevi. OBJECTIVE: We determined the expression pattern of survivin in benign melanocytic nevi in comparison to markers of proliferation and apoptosis. METHODS: Six cases of each of the following melanocytic nevi were retrieved from a dermatopathology archive: compound dysplastic nevus, intradermal nevus, compound nevus, neurotized intradermal nevus, and Spitz nevus. Survivin expression was evaluated by in situ hybridization. Apoptotic and proliferation indices were calculated by counting immunoreactive cells in terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling and proliferating cell nuclear antigen immunostained sections, respectively. RESULTS: All nevi, regardless of histologic type, expressed survivin. Compound melanocytic lesions expressed survivin in both epidermal and dermal compartments. The apoptotic rate was low for dysplastic, compound, and Spitz nevi, and apoptotic cells were not identified in any neurotized nevus. The proliferative index was highest for Spitz nevi, while all other nevi demonstrated rare positive cells. CONCLUSIONS: Survivin is consistently expressed in benign melanocytic lesions, while apoptotic cells are rarely identified, suggesting the dysregulation of apoptotic pathways with the accumulation of cells in these neoplasms.
Intradermal nevi are common benign pigmented skin tumors. Their occurrence within the external auditory canal is uncommon. The clinical and pathologic features of an intradermal nevus arising within the external auditory canal are presented, and the literature reviewed.
PURPOSE: To assess the relative frequency and clinicopathologic characteristics of benign conjunctival tumors. METHODS: A retrospective study of 80 consecutive patients admitted to our hospital with benign eyelid and conjunctival tumor between April 2000 and November 2002 was undertaken, and clinical records including age, sex and involved site of tumors and pathology slides of the patients were reviewed retrospectively. RESULTS: Twenty-three males and 33 females presented with benign eyelid tumors and 12 males and 12 females with conjunctival tumors. Mean age was 42.3 and 29.7 years, respectively. The lower eyelid was involved in 27 (48.2%) of eyelid tumors and the medial conjunctiva in 14 (58.3%) of conjunctival tumors. The most frequent tumor was intradermal nevus (44.6%), seborrheic keratosis (16.1%) and compound nevus (10.7%) in eyelid tumors, and compound nevus (29.2%) and intradermal nevus (25.0%) in conjunctival tumors. CONCLUSION: This report will provides a basic analysis of benign eyelid and conjunctival tumors.
A thirty-six-year-old man presented with a melanocytic nevus on his left shoulder. The lesion was excised and histopathologic examination showed an intradermal nevus with several infundibular cysts among the nevus cells. These cysts showed a cyst wall with epidermoid keratinization and a lumen filled by many cross-sectioned hair shafts. These findings were consistent with a diagnosis of trichostasis spinulosa within an intradermal melanocytic nevus. We note the relationship between these two disorders in the same lesion.
BACKGROUND: The role of benign melanocytic lesions as precursors and not only as risk markers for the development of cutaneous melanoma is controversial. OBJECTIVE: The purpose of the study was to assess the frequency of the histologic association of benign melanocytic lesions with cutaneous melanoma of a maximum thickness of 1.00 mm. The possibility that the spatial association of benign lesions with melanoma may be coincidental was also investigated. METHODS: The study subjects representing 289 cases of cutaneous melanoma of maximum thickness 1.00 mm (or less) were examined histologically for the presence of an associated benign melanocytic lesion(s), including lentiginous melanocytic proliferation; junctional, compound, or intradermal nevus; dysplastic nevus; and congenital nevus contiguous with or adjacent to the melanoma. The effects of age, tumor thickness, level of invasion, histologic type, and anatomic site on the association of benign melanocytic lesions with melanoma were assessed. In the control subjects 40 basal cell carcinomas and 38 compound nevi (not dysplastic) randomly chosen and matched for age (+/- 1 year) and site (head/neck, trunk, upper and lower limbs) with a melanoma case were examined to assess the proportion of these cases associated with benign lesions compared with the matched melanoma cases. RESULTS: A nevus was associated with melanoma in 51% of cases (n = 147). Of these, 82 (56%) were dysplastic nevi, 61 (41%) were common acquired nevi, and 4 (3%) were congenital nevi. Lentiginous melanocytic proliferation was present in the epidermis adjacent to 219 melanomas (75%) and in 44% of these cases (n = 97) a coexisting nevus was also present. CONCLUSION: The results of this study lend further support to the concept of common acquired nevi and dysplastic nevi as precursors of cutaneous melanoma. In addition, lesions diagnosed clinically as simple lentigo and solar lentigo may be important as potential precursors of melanoma, particularly in the elderly.
The present ultrastructural evaluation of 12 acquired intradermal melanocytic nevi revealed that in contrast to the nested epithelioid melanocytic nevus cells of the upper dermis, the spindle nevus cells of the deep dermis showed perineurial differentiation, exhibiting a spindly configuration characterized by a melanosome-free cytoplasm that showed extremely slender bipolar contour and contained abundant intermediate filaments, a decreased number of cytoplasmic organelles, and, significantly, a fair number of plasmalemmal pinocytotic vesicles. The nevic corpuscles were found to consist of laminated slender cytoplasm showing subcellular conformation similar to that of the spindle nevus cells. By immunohistochemistry, many spindle nevus cells and nevic corpuscles were immunoreactive for nerve growth factor receptor. All the nevus cells were immunoreactive for vimentin and S-100 protein, and negative for protein gene product 9.5, epithelial membrane antigen, Leu-7, and myelin basic protein. Characteristically, protein gene product 9.5 immunohistochemistry revealed numerous immunoreactive axons intermingled with the spindle nevus cells in the deep portion. All the PGP9.5-immunoreactive axons were observed by immunoelectron microscope to be unmyelinated and always ensheathed by a thin cytoplasmic process of Schwann cells but not nevus cells. These findings indicate that differentiation plasticity exists in the various nevus cells, with the epithelioid nevus cells and the spindle nevus cells displaying more ultrastructural and immunophenotypical characteristics of melanocyte and perineurial cells, respectively, suggesting that a pluripotential cell of neural crest origin accounts for the histogenesis of this lesion.
Features of peripheral nerve sheath differentiation such as neuroid cords, nerve corpuscles, fascicle-like structures, and, exceptionally, palisading have been reported in melanocytic nevi. We report an intradermal melanocytic nevus with prominent Verocay-like bodies. The upper portion of the neoplasm was composed of typical round intradermal nevus cells, many of which were pigmented. Within the deeper portion, there was a nonpigmented spindle cell proliferation with prominent Verocay bodies, simulating a neurilemmoma. Typical nevus nests merged with neurilemmoma-like areas. The entire lesion stained positively for S-100 and Mart-1 proteins and negatively for HMB-45 stain. Diffuse Mart-1 positivity excluded a collision of a melanocytic lesion with a neurilemmoma. The histopathologic features of this nevus further support a close relation between nevus cells and Schwann cells.
Several skin diseases and tumors were immunohistochemically studied with the use of monoclonal antibodies against myelin proteins and neurofilament proteins. In prurigo nodularis, many nerve fibers were found embedded in dense inflammatory cell infiltration. Abnormal innervation was observed in piloleiomyoma. The axons were demonstrated within the cytoplasm of granular cells of granular cell schwannoma. In neurofibroma, tumor cells had myelin proteins in their cytoplasms. Many cells and fibers that contained myelin proteins were demonstrated in nevus cell nevus, especially in compound nevus and intradermal nevus, and it was suggested that schwannian cells may be the origin of some nevus cells.
A mouse monoclonal antibody, FKH1, was produced to detect cytoplasmic melanoma-associated antigen. FKH1 was raised using cultured human melanoma cell line KHm-6 as immunogen. Reactivity of this antibody was assessed by immunohistochemical techniques. Positive reactions were seen against 5 human melanoma cell lines and cultured human epidermal melanocyte. It stained cytoplasm of melanoma cells in a diffuse and granular pattern with indirect immunofluorescence. Immunoelectron microscopy showed diffuse distribution of immuno-reactant in the cytoplasm of KHm-1 cells excluding melanosomes and other subcellular organelles. In immunoblotting, FKH1 bound with proteins having molecular weight of 71 kd and 55 kd extracted from KHm-6 cells. Reactivity against frozen and alcohol-fixed paraffin-embedded melanocytic tumors was also tested with indirect immunofluorescence or ABC (avidin biotin peroxidase complex) techniques. All cases of frozen sections from benign and malignant melanocytic tumors including 2 cases of amelanotic melanoma showed positive staining with FKH1. In fixed tissues, reactivity was 16/19 (84.2%) in malignant melanoma and 30/44 (68.2%) in other melanocytic tumors. FKH1 did not react against normal melanocytes, C-type nevus cell, intradermal nevus pigmentosus with neuroid structure and neurofibroma. It was demonstrated that FKH1 recognized proliferative melanocytes originated from melanoblast or melanoblastic nevoblast. FKH1 failed to stain normal human peripheral nerves and nonmelanocytic tumors except APUDoma and malignant Merkel cell tumor. In halo nevus, nevus cells were clearly distinguished from intermingling inflammatory cell infiltrate. It was suggested that FKH1 is a useful monoclonal antibody in diagnosing human malignant melanoma, particularly in evaluating tumor thickness of Breslow more precisely.
A case is reported of complex hamartoma with the aspect of a giant pigmented nevus, localized in one of the lower extremities. Histological examination revealed the involvement of different embryonal layers in order to give rise to dissimilar types of nevi: flat pigmented nevus, intradermal cellular nevus, epidermal verrucous nevus, Jadassohn's sebaceous nevus; Hoffman-Zurhelle's superficial lipomatous nevus, and fibrous hamartoma of the manifested at infancy. This malformation and more specifically the nevus cells constitute the subsequent transformation into an infiltrating malignant blastoma (malignant melanoma).
BACKGROUND AND OBJECTIVE: Few reports about melanocytic lesions treatment by means of noncoherent-intense-pulsed light (NCIPL) have been published. Here we evaluate the clinical results of a relapsing hairy intradermal melanocytic nevus treated with a noncoherent-intense-pulsed light source. STUDY DESIGN/MATERIALS AND METHODS: A facial repigmented hairy intradermal melanocytic nevus that relapsed after shave excision, received four treatment sessions of a noncoherent-intense-pulsed light source (EpiLight, ESC Medical Systems Ltd, Israel) with the following parameters: 755 nm, a fluence energy of 40-42.5 J/cm(2), triple mode, a pulse width of 3.8 ms, and a delay of 20 ms, at 4-week intervals. RESULTS: Complete pigment clearance and hair removal was obtained. We have neither observed repigmentation nor hair regrowth after a 6 month-follow-up. No side effects were documented. CONCLUSIONS: Noncoherent-intense-pulse light is an effective treatment for hairy-pigmented melanocytic nevus.
Sixteen cases of blue nevi were investigated using the anti-melanoma specific antibody HMB-45. This antibody has been found to react with junctional but not with intradermal nevus cells, and with fetal and neonatal, but not with adult, melanocytes. Our study shows that HMB-45 also reacts with cells of the blue nevus, a unique type of intradermal nevus. The origin of blue nevus cells is controversial, and the results of this study support the hypothesis that blue nevus cells are not of purely melanocytic or Schwannian origin, but are derived from a precursor cell that has some common features of both melanocyte and Schwann cell.
Dyskeratosis follicularis like changes are reported on a pigmented intradermal naevus (follicular infundibulum) from the nose of a 23 years old woman with no other stigmata of Darier's disease. These findings are discussed at the light of Ackerman's concept of focal acantholytic dyskeratosis and the relevant literature is reviewed.
40 cases each of malignant melanoma. Spitz's nevus and benign intradermal nevus were examined using an interactive image analysis system. 60 consecutive nuclei were evaluated in the upper and lower portion of the melanocytic lesions. Besides basic karyometric data, a 'maturation parameter' (MP) expressing the previously described 'maturation to the depth' was assessed in each individual case, by calculating the ratio of the nuclear area in the deep portion and in the superficial portion. When the three parameters (superficial nuclear area, deep nuclear area and maturation parameter) were evaluated separately (k-nearest neighbour method), the efficiency of the superficial nuclear area was only 19%, compared with 72% for the deep nuclear area and 94% for the maturation parameter. Combination of the maturation parameter and the deep nuclear area provided an efficiency of 98% with a sensitivity of 98% and a specificity of 97%. The results indicate that the maturation parameter is superior to conventional karyometric data in the differentiation between benign and malignant melanocytic lesions.