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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experienced ophthalmologists who appropriately employ ancillary diagnostic testing, including fluorescein angiography, ocular ultrasonography, MRI, and fine needle aspiration biopsy, are remarkably accurate in the diagnosis of intraocular neoplasms. Recognizing the classic clinical features of the more commonly encountered lesions, such as choroidal melanoma, choroidal nevus, metastatic carcinoma to choroid, lymphoid tumors, and circumscribed choroidal hemangioma, and understanding the applicability and limitations of the various diagnostic tests are the keys to accurate detection.
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PMID:Differential diagnosis of choroidal neoplasms. 182 11

The dysplastic nevus in nonfamilial melanoma is a clinicopathologic entity consistently demonstrating an eightfold or greater association with malignant melanoma. The present report quantifies the relationship between nuclear atypia and 16 architectural and cytoplasmic features in 153 pigmented nevi removed from a similar number of patients with newly diagnosed nonfamilial melanoma. All lesions were evaluated by one dermatopathologist, and most lesions were reviewed by a second dermatopathologist. Nuclear atypia of nevomelanocytes was defined as at least three of the following: nuclear enlargement, pleomorphism, hyperchromatism, and prominent nucleoli easily observed throughout each lesion. Seventeen percent of the total nevi had such atypia. On univariate analysis, 11 parameters (lentiginous hyperplasia of the epidermis, basal melanocytic hyperplasia, junctional nest disarray, fusion [bridging] of theques, suprabasal melanocytes, lymphoid response, prominent vascularity, fibroplasia, abundant cytoplasm, "dusty" cytoplasm, and large melanin granules) showed an association with nuclear atypia (P less than .05). However, on multivariate analysis only five parameters continued to be important: basal melanocytic hyperplasia, junctional nest disarray, melanophages (inverse correlation), prominent vascularity, and large melanin granules. These data support the idea that multiple histopathologic characteristics, correlating objectively with nuclear atypia, are important for the diagnosis of dysplastic nevi. In our view, the minimal essential histologic criteria for dysplastic nevi based on these findings include nuclear atypia and abnormal patterns of intraepidermal nevomelanocytic proliferation (ie, basal melanocytic hyperplasia and/or junctional nest disarray).
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PMID:Correlation of histologic architectural and cytoplasmic features with nuclear atypia in atypical (dysplastic) nevomelanocytic nevi. 203 99

The author has performed study on the histogenesis of the nevus cells in the nevocellular nevi. In the study, specimens of the intradermal nevi in 124 cases were evaluated histologically and immunohistochemically and the following results were obtained: 1) Findings of hematoxylin eosin staining It was observed that three types of cells, including type A cells (epidermoid type cells), type B cells (lymphoid type cells), type C cells (neuroid type cells) were found to run through an intermediate stage from the upper part to the lower part of the nevocellular structure, although they disclosed different histological structures. In 39 (31.5%) of the 124 cases, Meissner's corpuscle-like cells were confirmed. 2) Findings of immunohistochemical staining i. Of the type A, type B and type C cells, the S-100 alpha protein stain was essentially negative. Meissner's corpuscle-like cells were selectively positive by this stain. ii. Although no particular difference was noted in the staining of S-100 protein between the type A and type B cells, a somewhat greater proportion of positive cells was noted in type C cells. In the Meissner's corpuscle-like cells, a notably higher positive conversion of cells was observed as compared to those of the three other types of cells. iii. Type A, type B and type C cells compared more or less similarly for the positive ratio of neuron-specific enolase but the ratio was unusually high in the Meissner's corpuscle-like cells. 3) Findings from routine electron microscopic staining i. Similar to the light microscopic findings, the nevus cells were found to change in shape uninterruptedly from the upper layer to the lower layer of the dermis. Unusually marked changes were noted both in the number and shape of the melanosome and premelanosome in the cytoplasm. ii. In the Meissner's corpuscle-like cells both melanosomes and premelanosomes were missing but a finding suggestive of a neuroid structure was affirmed. As noted above, the results of the histological, immunohistological and electron microscopic studies were in support of the general findings suggestive of a gradual shift of the nevus cells from the upper layer to the lower layer in the dermis, which prompted the author to support the so-called "neural crest origin hypothesis".
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PMID:[Histological and immunohistochemical studies on nevocellular nevi in the dermis. With special reference to the histogenesis of nevus cells]. 232 79

The current study was undertaken to characterize the expression of trophoblast-lymphocyte cross-reactive antigens on normal, molar, and malignant trophoblast. A panel of monoclonal antibodies directed against lymphoid cell markers were tested in immunofluorescence assay on cryostat sections of placenta and mole and on monolayers of choriocarcinoma cells. NKH-1, a monoclonal antibody to natural killer cells, reacted with both molar and placental villous trophoblast and with two choriocarcinoma cell lines. NKH-2, a monoclonal antibody reactive with a subset of natural killer cells, did not react with placental villous trophoblast but reacted with molar villous trophoblast in three of five moles tested and with both choriocarcinoma cell lines. B5, a monoclonal antibody which reacts with activated B cells, reacted with both choriocarcinoma cell lines but did not react with normal placental or molar trophoblast. MY7, a monoclonal antibody to myeloid colony-forming cells, reacted with only one of the choriocarcinoma cell lines. Trophoblast-lymphocyte cross-reactive antigens may be important in the immunobiology of gestational trophoblastic disease by modulating interactions between the trophoblast and the maternal immune system.
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PMID:Cross-reactivity of monoclonal antibodies directed against lymphocyte markers with trophoblast cells of normal placenta, hydatidiform mole, and gestational choriocarcinoma. 282 98

The majority of melanocytic tumours are easily diagnosed but they become a problem when they are amelanotic and the tumour cells resemble those of other tumours. This applies particularly to secondary melanoma. Detection of S100 protein is a useful identifying marker. S100 protein, so named for its solubility in saturated ammonium sulphate, is derived from brain tissue. It is a dimer and belongs to a calcium binding group of proteins. The protein was first thought to be in neural or neural crest derived tissues but has been found in chondrocytes, adipocytes, myoepithelial cells, dendritic cells of lymphoid tissue, Langerhans cells and T lymphocytes. The protein is present in a high proportion of malignant melanomas and nevocytic nevi of skin, but is less positive in eye melanomas. It is present in gliomas, Schwannomas and neurofibromas but not in neurone derived tumours such as neuroblastomas. Chondromas, chondrosarcomas, liposarcomas, some osteogenic sarcomas and some histiocytic tumours are positive. The tumours that do not contain S100 protein are listed. Pending development of melanoma-directed monoclonal antibodies, the use of anti-serum to S100 protein plus anti-keratin and anti-leukocyte reagents is useful in the identification of tumours of doubtful histogenesis.
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PMID:S-100 protein as a marker for melanocytic and other tumours. 299 6

MacG1 is a mouse monoclonal antibody (mAb) directed against a ganglioside, which is differentially expressed by macrophages infiltrating malignant melanomas and benign melanocytic lesions. mAb MacG1 was obtained by immunization with liposomes containing a mixture of gangliosides extracted from malignant melanoma. The antibody was selected for binding to melanoma gangliosides and for reactivity with frozen tissue sections of malignant melanoma. mAb MacG1 showed reactivity in 25 of 46 melanomas examined but in only 1 of 51 nevi tested. The mAb did not react with melanoma cells but did with cytoplasmic granules and deposits associated with large dispersed cells, which were also found in some nonmelanomatous tumors and in some lymphoid tissues. Using mAbs directed against differentiation antigens these cells were identified as macrophages. In nearly all reactive tissues MacG1-positive macrophages accounted for a minority of the total macrophages. The difference in reactivity between malignant melanomas and nevi could not be explained by the variable numbers of total macrophages in these lesions. It is suggested that mAb MacG1 may define a functionally distinct subpopulation of tumor-infiltrating macrophages. Staining of cells other than macrophages was observed in some normal and malignant neural tissues. MacG1 bound to a monosialoganglioside extracted from melanoma and reacted only with NeuAc alpha 2-3Gal beta 1-4Glc-Cer when tested with a panel of ganglioside standards.
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PMID:MACG1, a mouse monoclonal antibody detecting a monosialoganglioside expressed in tumor-infiltrating macrophages. 335 14

The hereditary dysplastic nevus syndrome (DNS) is a well-characterized disorder in which affected individuals have increased numbers of premalignant (dysplastic) nevi and a markedly increased risk of developing cutaneous melanoma. Seeking evidence of a systemic disorder in DNS, we examined the effect of ultraviolet radiation on cultured lymphoid cells. Epstein-Barr virus-transformed lymphoblastoid cell lines from patients with hereditary DNS had similar survival values following treatment with 2.3 to 9.0 J of 254-nm ultraviolet radiation per m2 as did lines from control individuals. Mutagenesis at the hypoxanthineguanine phosphoribosyltransferase locus was assessed by measuring the induction of resistance to thioguanine using a microtiter well assay. Three lymphoblastoid cell lines from patients with hereditary DNS and melanoma had a 2- to 3-fold greater frequency of induced mutants per clonable cell than three normal lines following exposure to 4.5 to 9.0 J of ultraviolet radiation per m2. Expanded clones of mutated DNS lymphoblastoid cell lines had less than 6% of normal hypoxanthine-guanine phosphoribosyltransferase activity. Inhibition and recovery of DNA synthesis following ultraviolet exposure were similar in 2 DNS and 2 normal lines. Repair by DNS lines of ultraviolet-induced DNA damage was in the normal range as measured by alkaline elution. Thus, hereditary DNS exhibits in vitro hypermutability which may reflect increased susceptibility to ultraviolet-induced somatic mutations in vivo. This abnormality may be related to the increased melanoma susceptibility of patients with hereditary DNS.
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PMID:Hereditary dysplastic nevus syndrome: lymphoid cell ultraviolet hypermutability in association with increased melanoma susceptibility. 394 Jun 25

A 54-year-old white man had a slowly growing painless epibulbar mass that clinically mimicked a lymphangioma. Morphologically, the paucicellular tumor contained stellate and spindly cells, mast cells, and dilated lymphatic channels embedded in a loose collagenous matrix. The clinical differential diagnosis included lymphangioma, amelanotic nevus, lymphoma, reactive lymphoid hyperplasia, dermoid, lipoma, and botryoid rhabdomyosarcoma. Pathologically, lymphangioma, myxoid neurofibroma, and spindle cell lipoma were all considered. The authors discuss the clinical and histopathologic features of the various tumors, and confirmation of the diagnosis of conjunctival myxoma by differential alcian blue staining properties dependent on critical electrolyte concentration.
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PMID:Conjunctival myxoma. A clinicopathologic study. 667 44

The records of 200 consecutive patients referred to the Ocular Oncology Service of Wills Eye Hospital because of an iris lesion suspected of being an iris melanoma were reviewed. On clinical evaluation, 24% of the lesions met the criteria for the diagnosis of iris melanoma and 76% were diagnosed as simulating lesions (pseudomelanomas). The most common pseudomelanomas included primary iris cyst (38%), iris nevus (31%), essential iris atrophy (5.7%), iris foreign body (4.5%), peripheral anterior synechia (2.5%), and iris metastasis (2.5%). Less frequently encountered pseudomelanomas included aphakic iris cysts, leiomyoma, melanocytoma, reactive lymphoid hyperplasia, adenoma of iris pigment epithelium, iridoschisis, and other miscellaneous entities. The clinical features that are helpful in differentiating the more common iris pseudomelanomas from true melanomas are discussed. Correct clinical identification of these simulating lesions may prevent unnecessary surgery or other treatment.
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PMID:The differential diagnosis of malignant melanoma of the iris. A clinical study of 200 patients. 688 62

140.240, an IgG2a mouse monoclonal antibody raised against a cultured human melanoma cell line, was highly specific for melanoma cells as determined by direct and absorption analyses in a mixed hemadsorption assay. Supernatants of doubly cloned hybridomas producing antibody 140.240 reacted with all cultured and fresh melanomas tested but failed to react with a variety of carcinomas, sarcomas, lymphomas, leukemias and other tumors of neuroectodermal origin. This antibody did not react with B-lymphoid cell lines, ruling out HLA-DR specificity. Non-reactivity of antibody 140.240 with peripheral blood lymphocytes obtained from the donor of the immunizing melanoma line excluded the possibility of detecting histocompatibility antigens. Nevus cells were also non-reactive. However, antibody 140.240 did identify an antigenic determinant on tissue homogenates prepared from fetuses of 10-14 weeks' gestation. The antigen involved was shed by cultured melanoma lines and, by immunoprecipitation analysis of radiolabelled lysates, had a molecular weight of approximately 87kdal. Thus, the structure identified by monoclonal antibody 140.240 is a melanoma-specific oncofetal antigen.
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PMID:Human melanoma-specific oncofetal antigen defined by a mouse monoclonal antibody. 715 20


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