Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Melan-A (MART1) gene encodes an antigen recognized by cytotoxic T cells. Although its expression in metastatic melanoma has been documented in the literature by several investigators, little is known about its distribution in primary melanomas and benign melanocytic nevi. In this study, we evaluated Melan-A expression immunohistochemically on sections from paraffin-embedded material of 50 benign nevi and 40 primary cutaneous melanomas using the monoclonal antibody A103. To evaluate a potential role of A103 in the differential diagnosis of melanocytic from nonmelanocytic tumors, we also analyzed a number of benign and malignant peripheral nerve sheath tumors, fibrohistiocytic tumors, and leiomyosarcomas. Immunoreactivity with A103 was present in all "nonneurotized" nevi and in all nondesmoplastic primary melanomas, both in the intraepidermal and the dermal component. Only two nevi that underwent prominent neurotization showed no staining with A103. Although all melanomas with epithelioid cells tended to be strongly positive with A103, only 4 of 13 spindle cell and desmoplastic melanomas (all positive with anti-S-100 and negative with HMB-45) were immunoreactive with A103 (two focally, two diffusely). None of the nonmelanocytic lesions expressed Melan-A. Our results confirm that Melan-A protein is broadly expressed in the majority of benign and malignant melanocytic lesions and suggest that A103 can be helpful diagnostically, not only for metastatic tumors, but also for primary skin lesions. Its use in distinguishing between melanocytic and peripheral nerve sheath tumors, however, is limited because of the low or absent expression of Melan-A in nevi that underwent neurotization and spindle cell and desmoplastic melanomas.
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PMID:Expression of melan-A (MART1) in benign melanocytic nevi and primary cutaneous malignant melanoma. 970 77

Overexposure to short- and long-wave ultraviolet radiations (UVB, UVA) may contribute to melanoma development through combined genotoxic and mitogenic effects in melanocytes. This study compares the impact of UVA-1 versus UVB, and single versus fractionated exposures on melanocyte proliferation in hairless SKH-2 mice. A single erythemal dose was compared with an equal dose fractionated over 8 d, and dose-dependency was studied. Proliferation (Ki-67 positive-sign) in melanocytes (melanoma antigen recognized by T-cells-1 positive or micropthalmia transcription factor positive) was ascertained in double-labeled skin sections. Single erythemal UVB exposures caused a delayed, dose-dependent increase of melanocyte proliferation. The highest, 17-fold, increase (from 0.05% to 0.8% of melanocytes) occurred 4 d after UVB exposure, without any detectable effect on overall melanocyte numbers. Correspondingly, DNA repair-deficient xeroderma pigmentosum A (Xpa) mice proved exquisitely sensitive to melanocyte proliferation induction by UVB exposure. No discernable effects were measured from fractionated suberythemal UVB exposures, or from any UVA-1 exposure regimen. Hence, melanocyte proliferation appears to be most efficiently induced by a single UVB overexposure. Moreover, the ineffectiveness of UVA-1 radiation and the enhanced sensitivity of Xpa mice point at pyrimidine dimers as causative DNA lesions. Consequently, murine nevi and melanoma are expected to be most effectively induced by intermittent UVB overexposures.
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PMID:Single UVB overexposure stimulates melanocyte proliferation in murine skin, in contrast to fractionated or UVA-1 exposure. 1565 80

Smooth muscle hamartoma (SMH) is a rare benign congenital or acquired lesion sometimes associated with Becker's nevus (Becker's melanosis). We report an unusual lesion with combined features of SMH and melanocytic nevus. The patient is a 49-year-old male with a history of a changing 'mole' on the left upper back. Clinical examination showed a solitary 1.2-cm nodule with central gray pigmentation. Histological examination showed a relatively well-circumscribed intradermal lesion. The superficial portion of the lesion consisted of melanocytes with nevoid morphology. The melanocytes had congenital pattern of distribution. Lesional melanocytes acquired a spindled morphology in the deeper dermis. The base of the lesion consisted of intersecting smooth muscle fascicles focally admixed with spindled melanocytes. The melanocytic component strongly expressed melanoma antigen recognized by T-cells-1 (MART-1) and HMB-45. The smooth muscle component was strongly positive for smooth muscle actin and h-caldesmon. Neither components showed significant cytological atypia or mitotic activity. Unlike a recently reported case of SMH combined with a melanocytic nevus and basal cell carcinoma, the current lesion did not occur in association with a Becker's nevus.
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PMID:Smooth muscle hamartoma associated with a congenital pattern melanocytic nevus, a case report and review of the literature. 1854 54

We report 2 cases of benign intradermal melanocytic nevi with discrete glandular elements and mucin deposition engendering a diagnostic dilemma. The preliminary differential included entrapment of adnexal structures, collision with an adnexal neoplasm such as adenoid cystic carcinoma or metastatic adenocarcinoma. A colloidal iron special stain confirmed the deposition of mucin; however, a pankeratin AE1/AE3 immunohistochemical cocktail was surprisingly negative. Closer cytological examination of the discrete "glands" combined with nearby pseudoangiomatous (almost kaposiform) change hinted at melanocytic origin, which was confirmed with a positive melanoma antigen recognized by T-cells 1 immunohistochemical stain. Histopathological variations in melanocytic morphology include balloon cell formation, pseudoangiomatous change, lipomatous change, nevus of Nanta (osteonevus) with osseous metaplasia, neurotization, cartilaginous nevus, calcification, increased elastic tissue, psamomma body formation, amyloid deposition, eczematous changes (Meyerson nevus), granular cell change and ancient change/atypia. Mucin deposition, tubule and pseudoacini formation, and now discrete adenoid cystic-like "glands" may also be seen, all of which are important to recognize to avoid misdiagnosis.
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PMID:Two cases of discrete adenoid pseudogland formation within benign intradermal melanocytic nevi. 2962 14