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Dermal melanocytosis includes various congenital and acquired pigmentary disorders characterized by dermal dendritic melanocytes. Blue nevi typically present as papulonodular lesions, whereas other dermal melanocytoses manifest as patches. This report describes a case of a blue nevus associated with acquired dermal melanocytosis on the back of a 46-year-old Japanese woman. The patient presented with a black nodule on a blue-greyish hyperpigmented area on the upper back. Histopathological analysis of the nodule confirmed a common blue nevus, whereas the adjacent hyperpigmented area showed features consistent with acquired dermal melanocytosis. Blue nevi and acquired dermal melanocytoses share a common pathophysiology involving ectopic melanocyte accumulation during embryogenesis. The coexistence of blue nevus and acquired dermal melanocytosis on the back is rare, highlighting the broad spectrum of dermal melanocytosis and the variability of its clinical manifestations. Recognition of such unusual presentations is critical for appropriate diagnosis and management.

NRAS Q61 mutations are driver genetic alterations associated with common melanocytic nevi. Herein, we describe a case of NRAS-mutant melanocytic tumor with a blue nevus-like morphology. A 71-year-old Japanese man presented with a 4.6-mm nodule on his back. Histopathological examination revealed a dense distribution of spindle-shaped melanocytes in the upper dermis and a sparse distribution of dendritic melanocytes in the mid-dermis. The vertical periadnexal extension reached the deep dermis at the center of the tumor. A small junctional component, hyperpigmentation, sclerotic stroma, mild nuclear atypia, and a few mitotic figures were observed. Immunohistochemical examination revealed no PRAME expression and preserved p16 expression. Diffuse RASQ61R immunoreactivity was observed in these tumor cells. Nuclear β-catenin expression was not observed. Targeted RNA sequencing revealed two mutations, NRAS c.182A>G (Q61R) and FGFR2 c.-157A>G, but no other pathogenic alterations such as BRAF, GNAQ, GNA11, CTNNB1, PRKAR1A, or IDH1 mutations or kinase gene fusions. The histopathology fits that of compound-type blue nevus, which is called \"Kamino nevus\"; however, this tumor was genetically considered to be on the spectrum of conventional acquired melanocytic nevi but not on that of blue nevi. Morphologically, NRAS-driven melanocytic nevi resemble blue nevi without IDH1R132C coexistence.

Background: Agmination and/or satellitosis in pigmented blue lesions is a phenomenon rarely mentioned in the literature and not well known. This phenomenon can be expressed by several benign and malignant pigmented blue lesions, such as blue nevi, Spitz nevi, melanocytoma and melanoma. On this spectrum, dermoscopy, reflectance confocal microscopy (RCM) and dynamic Optical coherence tomography (D-OCT) represent non-invasive imaging technologies, which may help clinicians in the diagnosis of melanoma and non-melanoma skin cancers in daily clinical practice. Methods: Currently, in the literature there is a lack of new data about agminated blue lesions and blues lesions with satellitosis, as well as the lack of a recent and updated review of the literature about this topic. Therefore, considering that clinicians must be confident with the diagnosis of these rare skin lesions, we decided to carry out this work. Results: In this paper, four new cases of agminated pigmented cutaneous lesions were described. Moreover, a review of the current literature on this topic was performed. Conclusions: A clinical-pathological correlation is often needed to reach a correct diagnosis; currently, dermoscopy and non-invasive diagnostic techniques, such as reflectance confocal microscopy and optical coherence tomography, due to the depth of these skin lesions in the dermis, can only make a partial and limited contribution.

Fusion genes involving homologs of protein kinase C (PKC) have been identified in a variety of tumors. We report the clinical and histologic presentation of 51 cutaneous melanocytic neoplasms with a PKC fusion gene (involving PRKCA in 35 cases, PRKCB in 15 cases, and PRKCG in a single case). Most tumors were in young adults (median age, 29.5 years; range, 1-73 years) but some presented in newborns. Histologically, 42 tumors were classified as benign, presenting predominantly as biphasic dermal proliferation (88%) with nests of small melanocytes surrounded by fibrosis with haphazardly arranged spindled and dendritic melanocytes, resembling those reported as \"combined blue nevi.\" Most tumors (60%) were heavily pigmented and in 15%, hyperpigmented epithelioid melanocytes were present at the dermoepidermal junction. Two lesions were paucicellular and showed marked sclerosis. Three tumors, including 2 proliferating nodules, were considered intermediate grade. Six tumors had sheets of atypical melanocytes infiltrating the dermis and were classified as melanomas. Two of the melanomas displayed loss of BAP1 nuclear expression. The median follow-up time was 12 months, with 1 patient alive with metastatic disease and 1 dying of their melanoma. These results suggest that melanocytic tumors with PKC fusion genes have characteristic histopathologic features, which are more similar to blue nevi than to pigmented epithelioid melanocytomas. As is the case with GNA-mutated blue nevi, they can progress to melanomas via BAP1 inactivation and metastasize.

Activating mutations in GNAQ, GNA11, CYSLTR2, and PLCB4 genes are regarded as the main oncogenic drivers of blue nevi (BN) and blue malignant melanocytic tumors. Here we report 4 cases of blue melanocytic neoplasms devoid of these mutations but harboring GRM1 gene fusions. In this short series, there was no gender predominance (sex ratio, 1). The mean age at diagnosis was 40 years (range, 12-72). Tumors were located on the face (n = 2), forearm (n = 1), and dorsum of the foot (n = 1). Clinically, a plaque-like pre-existing BN was found in 2 cases, including a deep location; another case presented as an Ota nevus. Two cases were diagnosed as melanoma ex-BN, one as an atypical BN, and one as a plaque-like BN. Microscopic examination revealed a dermal proliferation of dendritic melanocytes in a sclerotic stroma. A dermal cellular nodule with atypia and mitotic activity was observed in 3 cases. Genetic investigation by whole exome RNA sequencing revealed MYO10::GRM1 (n = 2) and ZEB2::GRM1 (n = 1) fusions. A GRM1 rearrangement was identified by fluorescence in situ hybridization in the remaining case. SF3B1 comutations were present in the 2 melanomas, and both had a MYO10::GRM1 fusion. Array comparative genomic hybridization was feasible for 3 cases and displayed multiple copy number alterations in the 2 melanomas and limited copy number alterations in the atypical BN, all genomic profiles compatible with those of classical blue lesions. GRM1 was overexpressed in all cases compared with a control group of blue lesions with other typical mutations. Both melanomas rapidly developed visceral metastases following diagnosis, with a fatal outcome in one case and tumor progression under palliative care in the other. These data suggest that GRM1 gene fusions could represent an additional rare oncogenic driver in the setting of BN, mutually exclusive of classical canonical mutations, especially in plaque-type or Ota subtypes.

Blue nevi, which are characterized by collections of pigment-producing melanocytes in the dermis, have a variety of clinicopathological characteristics. Plaque-type blue nevus (PTBN) is a variant of blue nevi. PTBN presents at birth or arises in early childhood, and it shows a combination of the features found in common blue nevus and cellular blue nevus. It is typically found on the dorsal surface of the hands and feet or on the head and neck, and it is usually benign and stable over time. However, reports have occasionally described malignant melanomas developing in or associated with a PTBN. Malignant blue nevi are most commonly found on the scalp. We report the case of an 88-year-old woman with a malignant melanoma associated with a PTBN of the cheek.

A 3-year-old boy presented with bluish patch and scattered blue spots on the left side of his face. After several sessions of laser treatment, the azury patch in the periorbital area became even darker. Histopathology showed many bipolar, pigment-laden dendritic cells scattered in the papillary and upper reticular dermis. Immunohistochemically, these cells were positive for S100, SOX-10, melan-A, P16, and HMB-45. The positive rate of Ki-67 was less than 5%. Finally, the lesion was diagnosed with nevus of Ota concurrent with common blue nevus. Therefore, for cases of the nevus of Ota with poor response to laser treatment, the possible coexisting diseases should be suspected.

UNASSIGNED: Acquired melanocytic nevi are common eyelid lesions; however, their clinical presentation is not well documented.
UNASSIGNED: In this retrospective study, clinical records were reviewed in patients evaluated between 2005 and 2022.
UNASSIGNED: Eyelid margin nevi (n = 150) were more commonly excised in female (78%) and Caucasian (86%) patients. Change in appearance/size were frequent presenting complaints, and 17% experienced ocular symptoms. Referring diagnosis included other benign lesions (11.3%), and concern for malignancy (16.7%). Many individuals (38.7%) noted their lesion for ≤5 years. Nevi were distributed across the 4 margins (9% peripunctal), and 88% had a regular base. Visible pigmentation was more common in non-Caucasians (95.2%) than Caucasians (41.1%). Lashes grew through 60.7% of nevi and were often misdirected.Nevi were treated with superficial excision and cauterization. Histologic subtypes included: dermal (86.6%), compound (9.4%), blue (2.7%), junctional (0.7%), lentiginous dysplastic (0.7%). An irregular base (p=0.042) and pigmentation (p=0.056) were more common in compound than dermal nevi. Lash line quality and appearance were improved in the majority of patients returning for follow-up, although postoperative trichiasis, marginal erythema, and residual pigmentation were observed.
UNASSIGNED: Melanocytic nevi commonly involve the eyelid margins and have a variety of presentations and appearances. Existing nevi can change, and new lesions appear throughout adulthood. Stable, benign appearing nevi can be observed. Shave excision provides a diagnosis and improved appearance for symptomatic or suspicious lesions, with few serious complications. Malignant transformation is rare, although evidence for recurrence warrants further evaluation.

UNASSIGNED: Blue nevi are a heterogeneous group of lesions that can display a variety of different clinicopathological characteristics. Although attempts are made to classify each lesion into defined subtypes, there can be overlap between the subtypes. The clinical , dermoscopic and histolopathologic features of a case of proliferative nodule arising within blue nevus is discussed. Running title: Blue nevi are an heterogeneous group of melanocytic lesions blue tinctorial properties. Proliferative nodules are rare benign lesions often present at birth as a component of a large congenital melanocytic nevi, congenital or acquired nevi. We first report a case of proliferative nodule arising within blue nevus.