Immunohistochemical expression of cyclooxygenage-2 in melanocytic skin lesions

Background Several reports have shown expression of cyclooxygenase‐2 (COX‐2) in malignant skin tumors. COX‐2 has also recently been reported as a marker of malignant melanoma (MM). Objective Our aim was to investigate whether there is a difference in the immunohistochemical expression of COX‐2 between malignant and benign melanocytic lesions of the skin. Methods We selected 40 archival cases of MM including 10 cases of superficial spreading melanoma, 10 of lentigo maligna melanoma, 10 of nodular melanoma, and 10 of acral lentiginous melanoma. For comparison, we also selected 35 benign melanocytic lesions, which included 15 nonatypical nevi and 10 atypical nevi. The remaining 10 cases were Spitz nevi. COX‐2 immunohistochemical staining was performed, and intensities were assessed quantitatively. Results The MM group and the benign melanocytic nevi group showed a highly statistically significant difference in the intensity of COX‐2 expression (P < 0.0001). Staining intensity in the dermal component of MM cases also showed a tendency to increase with increasing tumor depth. By contrast, the intensity of the dermal component in the melanocytic nevi group decreased with increasing depth as the nevus cells matured from type A to type C cells. No statistical difference was noted between the MM and Spitz nevi cases (P = 0.20). Conclusions Malignant melanoma shows stronger immunohistochemical expression of COX‐2 than benign melanocytic nevi. Although COX‐2 cannot be used alone to differentiate MM from melanocytic nevi, it may serve as an aid in the differential diagnosis of melanocytic skin lesions.     

Immunoperoxidase technique modified by counterstain with azure B as a diagnostic aid in evaluating heavily pigmented melanocytic neoplasms

Heavily-pigmented melanocytic neoplasms are difficult to evaluate on routine hematoxylin and eosin stained slides because pigmented melanocytes are difficult to distinguish from the numerous melanophages that are usually seen in the background of these lesions. Immunoperoxidase staining for S100 protein or HMB-45 antibody using diaminobenzidine (DAB) as chromogen, which forms a brown product, does not adequately distinguish melanocytes from melanophages. We modified this technique by replacing hematoxylin as the counterstain with azure B, which stains melanin green-blue. Thus, positive melanocytes appear brown while melanin granules in their cytoplasm are green-blue. However, negative melanophages only stain green-blue. This technique is useful in evaluating heavily pigmented melanocytic lesions such as malignant melanomas, melanosis of regressing malignant melanoma, residual malignant melanoma in areas of granulation tissue with melanophages, blue nevi, pigmented spindle cell variant of Spitz's nevi and combined nevi.     

Agminated Spitz Nevi: Case Report and Review of the Literature

Spitz nevi are benign melanocytic lesions with many histologic similarities to malignant melanoma. A case of agminated Spitz nevi on a 2‐year‐old boy's left cheek is reported and 41 other cases of agminated Spitz nevi are reviewed. In this case, two biopsies were performed on two different‐appearing lesions and the results of both biopsies showed Spitz nevi.     

Epidermal consumption in benign and malignant melanocytic neoplasms

Consumption of the epidermis associated with effacement of the rete ridge pattern has been cited as a useful criterion in the diagnosis of melanoma, but the significance of consumption in the absence of rete ridge effacement is unknown. We evaluated 701 melanocytic neoplasms for presence and ‘grade’ of consumption by melanocytic nests relative to diagnosis, body location, gender and age. We defined 1+ consumption as collections of melanocytes occupying greater than two thirds of the viable epidermis, with or without loss of the rete ridge pattern. Nests extending to the bottom of, within, and through the granular layer were graded 2+, 3+ and 4+, respectively. Consumption was more frequent and higher grades were found in melanomas followed by Spitz nevi compared with conventional melanocytic nevi (p < 0.001). Melanomas with higher Breslow thickness showed higher grades (p < 0.05). In conventional nevi, consumption occurred most frequently in back (13.7%), acral (11.9%) and scalp (9.8%) locations. Consumption without the requirement for rete ridge effacement occurs more frequently and at higher grades in melanoma. Higher grades correlate with higher Breslow thickness. Consumption is also common in Spitz nevi and occurs at lower grades in conventional (non‐Spitz) nevi, especially on the back, the scalp and at acral sites.     

Distinctive eosinophilic cytoplasmic inclusion bodies in melanocytic nevi: an immunohistochemical and ultrastructural study

Background: We sought to further determine the histochemical, immunohistochemical and ultrastructural properties of eosinophilic cytoplasmic inclusion bodies in melanocytic nevi. Methods: Skin specimens from four patients with a known diagnosis of conventional melanocytic nevus (3) or Spitz nevus (1) and containing intracytoplasmic eosinophilic inclusion bodies were selected. In addition, melanomas (25), Spitz nevi (10) and blue nevi (4) were examined to determine the frequency of the inclusions. Results: Inclusions tended to be located in multinucleated melanocytes with abundant vacuolated cytoplasm. In conventional (hematoxylin and eosin‐stained) sections, the degree of density and eosinophilia of intracytoplasmic inclusions varied with size. Periodic acid‐Schiff, Fontana and Congo red stains showed no reactivity. All bodies were immunoreactive for ubiquitin but negative for tyrosinase, keratin and vimentin. Ultrastructurally, inclusion bodies were non‐membrane bound, ranged from 4 to 7 µm, and were comprised of radiating filamentous structures with or without an electron‐dense core. Electron probe x‐ray microanalysis revealed no significant peaks. None of additional melanomas, Spitz nevi and blue nevi that were evaluated showed similar inclusions. Conclusions: The inclusion bodies described herein bear no resemblance to other cytoplasmic inclusion bodies previously described in melanocytic lesions. There is no discernible relationship to melanosomes by ultrastructural analysis. We postulate a relationship with dysfunction of ubiquitin‐mediated protein degradation occurring in melanocytes. Shon W, Wada DA, Gibson LE, Flotte TJ, Scheithauer BW. Distinctive eosinophilic cytoplasmic inclusion bodies in melanocytic nevi: an immunohistochemical and ultrastructural study.     

Proliferative activity in melanocytic nevi from patients grouped by age with clinical follow‐up

Any mitotic activity in a melanocytic nevus is a source of concern about the biologic potential of that lesion, especially in an adult. Previously diagnosed benign melanocytic nevi in individuals from six different age groups were re‐examined; mitotic figures were counted in routine hematoxylin and eosin‐stained sections; Ki‐67 nuclear positivity was assessed by immunohistochemistry. Mitoses were seen in 0–14.3% of nevi in all groups of patients >1 year of age; 55.6% (5/9 cases) of nevi in patients <1‐year old had mitoses identified histologically. Ki‐67‐positive melanocytes were seen in all cases of those lesions in infants (less than 1‐year old) and only in a minority of lesions from the other age groups. The maximum and mean numbers of Ki‐67‐positive melanocytes per square millimeter were highest in patients <1‐year old (16.7 and 5.6, respectively), and decreased in all other groups. Follow‐up data were available in the majority of the patients. There were no examples of malignant melanoma in the various age groups. We conclude that proliferative activity in benign melanocytic nevi decreases with age, however, proliferative activity can be seen at any age and its significance must be judged in the context of other histopathologic features.     

The morphologic spectrum of germline‐mutated BAP1‐inactivated melanocytic tumors includes lesions with conventional nevic melanocytes: A case report and review of literature

Germline mutations in BRCA1‐associated protein 1 (BAP1) are associated with several neoplasms, including BAP1‐inactivated melanocytic tumors (BIMTs). BIMTs are classically described as biphenotypic melanocytic proliferations with BAP1‐deficient large epithelioid and rhabdoid melanocytes showing various degrees of cytologic atypia. This morphology has been traditionally classified as “spitzoid” despite the various differences between these lesions and the more classic Spitz nevi. Herein, we report a case of an otherwise healthy 11‐year‐old female patient with a family history of several malignancies who presented with multiple pink to brown papules. Histologic and immunohistochemical evaluation identified three lesions with loss of nuclear BAP1 staining. The histologic spectrum of these lesions included junctional spitzoid cells within a triphenotypic proliferation and a separate lesion composed entirely of dermal small to medium‐sized epithelioid melanocytes with maturation. BAP1 gene sequencing revealed a germline frameshift pathogenic BAP1 mutation, denoted c.1717delC. This case provides further evidence that not all BIMTs conform to classic morphological criteria and that the morphologic spectrum includes lesions resembling conventional nevi. As BIMTs can serve as an early marker of the BAP1 hereditary tumor predisposition syndrome, we believe a need exists for a more comprehensive combined clinical and pathological approach for BIMT identification.     

Spitz Nevi and Other Spitzoid Neoplasms in Children: Overview of Incidence Data and Diagnostic Criteria

Spitz nevi are benign melanocytic neoplasms characterized by epithelioid or spindle melanocytes or both. In some rare cases their presentation overlaps with the clinical and histopathologic features of malignant melanoma, so a differential diagnosis can be difficult to make. Intermediate forms between Spitz nevi and malignant melanoma, with unpredictable behavior, have been called atypical Spitz tumors. A literature search was performed to review the clinical, dermoscopic, genetic, and histopathologic aspects of spitzoid tumors. Spitz nevi mainly occur in children, with no predilection for sex, and in young women. Common sites are the head and lower arms, where Spitz nevi present as pink nodules or hyperpigmented plaques. Spitzoid lesions may have diverse dermoscopic patterns: vascular, starburst, globular, atypical, reticular, negative homogeneous, or targetoid. The management of spitzoid lesions can be invasive or conservative; surgical excision is usually reserved for those with doubtful features, whereas clinical and dermoscopic follow‐up is preferred for typical pediatric Spitz nevi. The role of sentinel lymph node biopsy in atypical Spitz tumors is debated. Immunohistochemistry and new molecular techniques such as comparative genomic hybridization, polymerase chain reaction, and fluorescence in situ hybridization offer new diagnostic perspectives, investigating genetic alterations that are specific for malignant melanoma or for Spitz nevi.     

IMP‐3 expression in melanocytic lesions

Background: Insulin‐like growth factor‐II mRNA‐binding protein 3 (IMP‐3 ), a member of the insulin‐like growth factor mRNA‐binding protein family, is expressed in several human malignancies, including melanomas. However, the expression of IMP‐3 has not been explored in melanoma in situ, various histologic subtypes of invasive melanomas and atypical Spitz tumors. Methods: IMP‐3 immunostain was performed in 157 melanocytic lesions. Results: Nearly all benign (8/8), dysplastic (8/8) and Spitz nevi (8/9) were negative for IMP‐3. Focal IMP‐3 positivity was observed in 5/12 melanoma in situ and 4/15 superficial melanomas (Breslow depth ≤1 mm). Half (10/20) of deep melanomas (Breslow depth >1 mm) and 25/52 metastatic melanomas demonstrated strong IMP‐3 staining. IMP‐3 expression differs significantly between non‐desmoplastic melanomas (superficial and deep) and benign or dysplastic or Spitz nevi (p = 0.0427, respectively). Four of 23 desmoplastic melanomas expressed IMP‐3 , which was significantly different from deep melanomas (p = 0.0109). IMP‐3 stained 7 of 10 atypical Spitz tumors. The difference between atypical Spitz tumors and Spitz nevi was statistically significant (p = 0.0256). Conclusion: A malignant circumstance, such as non‐desmoplastic melanoma or atypical Spitz tumor, can be inferred when IMP‐3 is expressed, suggesting potential diagnostic value of IMP‐3 in melanocytic lesions. Yu L, Xu H, Wasco MJ, Bourne PA, Ma L. IMP‐3 expression in melanocytic lesions.     

Genital lentigines and melanocytic nevi with superimposed lichen sclerosus: a diagnostic challenge

BACKGROUND: Benign pigmented lesions of the genitalia, such as genital lentigines and melanocytic nevi, often show clinical and histopathologic features highly suggestive of malignant melanoma (MM). Superimposed changes of lichen sclerosus (LS) may cause real concern and lead to an erroneous diagnosis of MM. OBJECTIVE: This study was performed to assess clinicopathologic characteristics of genital lentigines and melanocytic nevi with associated LS. METHODS: We performed a retrospective review of 5 cases. RESULTS: Histopathologic sections of the 2 cases of genital lentigines with concurrent changes of LS showed a lichenoid lymphocytic infiltrate and pigment incontinence with melanophages in a fibrosed papillary dermis, features reminiscent of completely regressed MM. The 3 cases of genital melanocytic nevi and superimposed LS were sharply circumscribed, relatively symmetric, but revealed confluent nests varying in size and shape and pagetoid upward spread of melanocytic nests and single melanocytes. Changes of LS extended beyond the melanocytic proliferation. CONCLUSION: Genital lentigines and melanocytic nevi with associated LS may show features that mimic MM.     

Diagnostic significance of the blue hue in dermoscopy of melanocytic lesions: a dermoscopic-pathologic study.

In epiluminescence microscopy, the perception of a blue hue is generally considered a clue to malignancy, especially in clinically equivocal melanocytic skin lesions. However, melanocytic nevi can seldom show a blue hue under dermoscopy. The aim of the current study was to evaluate the histopathologic correlates of the blue hue seen in dermoscopy, to clarify its significance and diagnostic value. From a series of 224 consecutive pigmented skin lesions submitted to surgical excision, we selected all the melanocytic skin lesions (n. 36), blue nevi excluded, characterized by the presence of a blue hue dermoscopically. In agreement with recent refinement of dermoscopic semeiology, all cases were further classified in cases showing blue areas and cases showing blue-whitish veil by experts observers blinded to the final diagnosis. Histopathologically, the series included 23 (63.9%) melanocytic nevi and 13 (36.1%) melanomas. For each lesion, several histopathologic parameters related to both epidermal and dermal alterations were assessed. Blue areas were found in 21 melanocytic nevi and 7 melanomas, whereas blue-whitish veil was found in 6 melanomas and 2 nevi. Careful dermoscopic-histopathologic correlation demonstrated that blue areas are related to the presence of large amounts of melanin pigment, either within melanophages (in the context of areas of regression) or within pigmented melanocytes in the superficial dermis. Conversely, the histopathologic correlate of the blue-whitish veil resulted in the presence of an acanthotic epidermis with compact orthokeratosis overlying large amounts of melanin in the dermis. Such melanin was found not only within melanocytes but also in large clusters of melanophages within areas of regression in the dermis. In conclusion, the majority of melanocytic lesions characterized by the presence of blue areas were histopathologically diagnosed as melanocytic nevi whereas the presence of blue-whitish veil was highly indicative of malignant melanoma diagnosis (specificity 91% vs. 9% of blue areas; sensitivity 75% vs. 25% of blue areas). Thus, these two features of blue hue under dermoscopy cannot be longer considered as synonymous in dermoscopy setting, being associated with different histopathologic alterations and different diagnostic information.     

Large Congenital Melanotic Nevi in an Extremity with Neurocutaneous Melanocytosis

Abstract:   A 14-day-old boy presented with a large congenital melanocytic nevus over his left thigh with approximately 17 satellite nevi distributed over the rest of his skin surface. Six weeks later, he developed generalized tonic–clonic seizures and additional satellite nevi became apparent ( n  > 20). A subsequent brain magnetic resonance imaging demonstrated right temporal T1 hyperintense signal abnormality. At 4 months of age the patient underwent a lumbar puncture that was normal without evidence of melanocytes or tumor. Nevertheless, a few days later he underwent resection of his right medial temporal lesion which demonstrated melanocytosis in the temporal lobe as well as melanocytosis in subependymal areas in other parts of the brain and ventricles, confirming the suspected diagnosis of neurocutaneous melanocytosis. Our case supports previous studies that conclude that the number of satellite nevi is a greater predictor of neurocutaneous melanocytosis than is the location of large congenital melanocytic nevus. In our case, cerebrospinal fluid studies were not reliable even in the face of florid neurocutaneous melanocytosis involving the leptomeninges and ventricles.     

Sclerosing nevus with pseudomelanomatous features

Background: Among the pigmented lesions with a central area of scar, we found a group of cases histologically characterized by striking architectural alteration of the melanocytic component, but with no cytological atypia and mitotically quiescent. The aim of the current study was to assess the biological nature of such lesions. Methods: We selected 19 of these melanocytic neoplasms that had the following characteristics: (a) a clinically evident whitish central area suggestive of regression (with no history of a previous surgical procedure or trauma), (b) histological features of fibrous scar‐like tissue at the center of the lesion, (c) the presence of large, confluent and unusually shaped melanocytic nests at the dermoepidermal junction and in the dermis, (d) a pagetoid spread of melanocytes above the epidermal basal layer and (e) remnants of nevus tissue at the border of the scar. The lesions showed no evidence of cytological atypia, expansive nodules of melanocytes, significant numbers of mitoses or cellular necrosis. Results: All the cases have been followed up and none have recurred or metastasized. Histologically, these neoplasms have important similarities with the so‐called recurrent nevus, nevi on lichen sclerosus and nevi developed during or following cutaneous inflammatory and sclerosing processes. The origin of the scar in each case was obscure but was probably related to minor unnoticed trauma or to chronic friction on a nevus. In few cases, the fibrosis was probably the result of partial regression of the nevus or a sequel to folliculitis. The pseudomelanomatous features appear to be related to the presence of the scar, as already reported for nevi that are involved in fibrotic or scarring processes. In our study, the nevi involved in the fibrotic process were congenital nevi and common or dysplastic nevi. One case was a Spitz nevus. Conclusions: From our data we concluded that, despite their worrisome clinical and histological aspect, the lesions described in this case series were most probably benign melanocytic nevi, involved by a fibrotic process combined with pseudomelanomatous proliferation. The lack of cytological atypia, mitoses and expansive nodules allowed us to differentiate these lesions from regressing melanomas.     

Desmoplastic melanocytic nevi with lymphocytic aggregates

Desmoplastic melanocytic nevi can be difficult to distinguish from desmoplastic melanoma. The presence of lymphocytic aggregates in association with a sclerosing melanocytic proliferation is commonly regarded as a feature in support of a diagnosis of desmoplastic melanoma. However, the finding is not specific for melanoma. Herein we report six cases of sclerosing melanocytic nevi with associated lymphocytic aggregates. They occurred in five women and one man, ranging in age from 11 to 61 years. Three lesions were sclerosing Spitz nevi; one was an amelanotic sclerosing blue nevus, one an acquired intradermal sclerosing nevus, and one was a congenital compound melanocytic nevus with sclerosis of its dermal component. The lesions were interpreted as benign, i.e. melanocytic nevi, because of their histopathologic attributes (symmetric silhouette, benign cytologic features) and results from immunohistochemical studies (all lesions strongly expressed Melan-A and p16) and fluorescence in situ hybridization (FISH). Three lesions tested by FISH lacked copy number changes of 11p, 6q or 6p. None of the lesions recurred. The cases highlight that contextual information is essential for the diagnosis of desmoplastic melanoma and sclerosing nevus. The presence of lymphocytic aggregates per se does not prove that a sclerosing melanocytic proliferation is malignant.     

Expression of p-27 (kip1) in nevi and melanomas

Histopathologic criteria are usually sufficient for the accurate distinction of benign from malignant melanocytic lesions of the skin. A minority of cases, however, particularly Spitz nevi, continue to pose a vexing diagnostic challenge. Recent research, however, suggests that p27 (kip1), a cell cycle inhibitory protein, may prove helpful in predicting the biologic behavior of a diverse array of human neoplasms. We analyzed 63 melanocytic lesions of the skin (21 Spitz compound nevi, 21 compound nevi, 21 melanomas, and a variety of other benign and malignant cutaneous neoplasms as a control group) for expression of p27 (kip1). The distribution of immunoreactivity was analyzed by quantifying nuclear staining in each case without knowledge of the diagnosis or outcome. Clinical history and follow-up information were obtained by chart review. There was no difference in the expression of p27 between Spitz nevi (labeling index=38.4+/-4.0), compound nevi (labeling index=40.1+/-4.8), and melanoma (labeling index=42.3+/-5.1). Logistic regression failed to show any difference in p27 labeling index between the nevi and melanoma (p=0.736). These results indicate that antibodies to p27 are not useful in distinguishing between these melanocytic lesions.     

Genome profiling of melanocytic tumors using multiplex ligation-dependent probe amplification (MLPA): Its usefulness as an adjunctive diagnostic tool for melanocytic tumors

BACKGROUND: The histopathology of melanocytic tumors sometimes presents diagnostic problems. Applicable parameters other than routine pathology are needed. OBJECTIVE: We assessed the feasibility of multiplex ligation-dependent probe amplification (MLPA), a novel PCR-based genome profiling method, in the classification of melanocytic tumors. METHOD: We extracted DNA from paraffin-embedded tissue sections of 24 primary melanomas, 14 Spitz nevi and 17 common melanocytic nevi. We analyzed the copy number gains or losses of a total of 76 genes spanning almost all chromosome arms using commercially available MLPA kits. RESULTS: Although four melanocytic nevi and three Spitz nevi did not yield sufficient DNA for reliable analysis due to small tumor size, the MLPA analysis was feasible and applicable to the remaining 88% of samples. We found multiple genetic aberrations in primary melanomas. The total number of aberrations in each tumor ranged from 1 to 32 (average, 12.04). All but two melanomas showed aberrations at more than three genetic loci. Seventeen (70.8%) of the 24 melanomas showed a copy number loss of either the CDKN2A or CDKN2B gene on chromosome 9p21. All the Spitz nevi and 7 (50%) of 14 common melanocytic nevi had copy number changes at one or two gene loci (average, 1.04). The receiver operator characteristic curve analysis showed that the threshold value of copy number aberrations corresponding to 98% specificity for melanoma was 2.42 and the sensitivity using this threshold value was 92.5%. CONCLUSIONS: MLPA could be used as an adjunctive diagnostic tool for melanocytic tumors.     

Expression of activated Akt in benign nevi, Spitz nevi and melanomas

BACKGROUND: Activated Akt expression (p-Akt) is reportedly increased in many melanomas as compared with benign nevi. The purpose of this study was to evaluate and compare p-Akt immunohistological staining in benign nevi, Spitz nevi and primary melanomas. METHODS: Immunostaining for phosphorylated Akt was performed in 41 melanocytic lesions previously classified as benign intradermal nevus (14 lesions), Spitz nevus (9 lesions) or melanoma (18 lesions). Lesions were graded for intensity of p-Akt staining by two independent observers (0, no staining; 1, slightly positive; 2, moderately positive; 3, highly positive). Scores were averaged, and statistical analyses were performed. RESULTS: Benign nevi showed less staining (mean score 1.18) compared with Spitz nevi (mean score 2.11) and melanomas (mean score 2.19). This difference was statistically significant between benign nevi and melanomas (p = 0.0047) and benign nevi and Spitz nevi (p = 0.0271). No statistical difference was detected in staining between Spitz nevi and melanomas (p = 0.8309). CONCLUSIONS: Activated Akt expression is increased in Spitz nevi and melanomas as compared with benign intradermal nevi, but is unlikely to prove useful in differentiating between the former.     

The relationship between melanocytes and peripheral nerve sheath cells (Part I): melanocytic nevus (excluding so-called "blue nevus") with peripheral nerve sheath differentiation

Among thousands of specimens of melanocytic nevi, not including giant congenital melanocytic nevus or blue nevus, 42 melanocytic nevi that showed peripheral nerve sheath differentiation were collected. The patterns of melanocytic nevi with peripheral nerve sheath differentiation may be classified into three groups: 1) "neurotized and neural nevi" with nests of "neuroid cords" and "nevic corpuscles" (the most common pattern); 2) nerve fascicle-like structures with no relation to neurotized and neural nevi; and 3) palisading melanocytes of a nevus in nests of conventional melanocytic nevi (a rare pattern). Each pattern may represent a different expression of nerve sheath differentiation in melanocytic nevi. Some melanocytic nevi with nerve fascicle-like structures show discrete structures closely resembling authentic nerve fascicles, confirming a close relationship between melanocytes and peripheral nerve sheath cells (Schwann cells and probably perineurial cells in part) and suggesting derivation of the two types of cells from common precursor cells of the neural crest and their de novo development in the dermis rather than by Abtropfung of melanocytes from the epidermis. In addition, the high prevalence of Unna, Miescher, and superficial congenital nevi in melanocytic nevi with peripheral nerve sheath differentiation suggests a different character or process for these congenital melanocytic nevi than for Clark and Spitz nevi (junctional and compound types).     

Melan‐A positive dermal cells in malignant melanoma in situ

The presence of Melan‐A positive dermal cells in excisions for melanoma in situ represents a frequent conundrum for pathologists. These cells may represent superficially invasive melanoma, benign, incidental, dermal nevi or non‐specific staining of dermal melanophages. Occasionally, rare, Melan‐A positive dermal cells are present which do not clearly correspond to the above three categories. Our objective was to further characterize these Melan‐A positive dermal cells. To do this, immunoperoxidase staining for Melan‐A and SOX‐10 was performed on 188‐cutaneous excisions, including examples of melanoma in situ, atypical junctional melanocytic hyperplasia and non‐melanocytic tumors. These were evaluated for the presence of Melan‐A and SOX‐10 positive dermal cells. Dermal cells, positive for both markers, were identified in 17% of the excisions. The cells were present in 10% of cases from the melanocytic group and 31% of the cases from the non‐melanocytic group. These cells did not exhibit cytologic atypia and resembled neither the co‐existing neoplasm nor melanophages. We conclude that positivity of these rare Melan‐A positive cells for SOX‐10 argues that they represent true melanocytes and not non‐specific staining. The absence of cytologic atypia in these cells and their presence in excisions of non‐melanocytic neoplasms argues that they are benign, reactive, dermal melanocytes.     

Immunohistochemical expression of p16 in desmoplastic melanoma

Desmoplastic melanoma can be difficult to distinguish from desmoplastic melanocytic nevi both clinically and histopathologically. Several attempts have been made to explore the use of ancillary studies to facilitate this distinction. Prior work has suggested that immunohistochemical expression of p16 could help distinguish sclerosing Spitz nevi from desmoplastic melanomas. We re‐evaluated the expression of p16 in 22 desmoplastic melanomas (13 mixed and 9 pure desmoplastic tumors) and five desmoplastic melanocytic nevi (three desmoplastic Spitz nevi and two congenital melanocytic nevi with prominent dermal sclerosis). All desmoplastic melanocytic nevi were strongly immunoreactive for p16. Of the 22 desmoplastic melanomas, 6 tumors failed to label for p16, 10 were focally positive, but 6 tumors were diffusely immunoreactive. The latter finding is relevant, as it points to limitations in the diagnostic value of immunohistochemical staining for p16 for the diagnosis of desmoplastic melanocytic proliferations. Diffuse staining for p16 is not restricted to desmoplastic Spitz nevi but can also occur in a subset of desmoplastic melanomas, and this warrants caution in the use of this marker for diagnostic purposes.