Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ganglioside GD3 was distributed widely on melanocytes, naevi, and practically all melanomas. Not all the cells in melanoma appeared to express GD3, so that treatment with MAbs to GD3 could be expected to leave foci of tumor cells resistant to the effects of the MAbs. GM3 had a similar distribution of GD3 on melanoma, but was expressed on a lower percentage of cells in individual tumors. Expression of GM3 appeared to be suppressed on melanoma and naevus cells in the epidermis. Addition of MAbs to GM3 to those against GD3 in the treatment of melanoma may increase the lytic effect against cells coexpressing both gangliosides, but as GM3 did not appear to be expressed on GM3 -ve cells, the percentage of resistant cells may not be decreased. GD2 was expressed on only approximately 25% of primaries and less than 50% of metastases. In individual tumors there was some evidence of reciprocal expression of GD3 and GD2, so the combination of MAbs to GD3 and GD2 may decrease the percentage of melanoma cells that are resistant to either MAb alone. Both GD3 and GD2, but not GM3, was expressed on lymphocytes around melanoma metastases in LNs and around melanomas in skin. GD2 was detected on a large percentage of lymphocytes around metastases in lymph nodes, but not in the skin, suggesting that the gangliosides GD2 and GD3 may be expressed on different subsets of T-lymphocytes. These findings, together with previous studies showing that the MAbs can enhance lymphocyte responses to a variety of stimuli, provide support for the hypothesis that the clinical effects of the MAbs may reflect activation of host responses against the tumor. Further analysis of the role of gangliosides in lymphocyte function is needed.
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PMID:Ganglioside antigens in tissue sections of skin, naevi, and melanoma--implications for treatment of melanoma. 167 56

Neurofibromas, schwannomas, and neurotized melanocytic nevi may closely resemble one another at the light microscopic level. We studied 10 neurofibromas, 10 schwannomas, and 10 partially neurotized melanocytic nevi immunohistochemically using an antibody directed against factor XIIIa to determine if this antibody might provide a useful method of differentiating these lesions. The cases were also stained with S100 protein. All of the neurofibromas stained intensely for factor XIIIa. The proportion of cells staining within the tumors varied from 30% to 70%. In contrast, none of the schwannomas and neurotized nevi studied demonstrated staining of tumor cells with this antibody. S100 protein was expressed by 100% of neurofibromas, schwannomas, and melanocytic nevi. Our findings suggest that factor XIIIa may provide a reliable and practical means of differentiating cutaneous neurofibromas from neurotized nevi and cutaneous schwannomas. Distinguishing between these different tumor types may be important in some clinical situations, particularly with respect to rendering a diagnosis of von Recklinghausen's neurofibromatosis. The differences in the immunohistochemical profiles of neurofibromas and neurotized nevi support the concept that these tumors are histogenetically distinct, despite their similar histologic appearances.
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PMID:Immunohistochemical demonstration of factor XIIIa expression in neurofibromas. A practical means of differentiating these tumors from neurotized melanocytic nevi and schwannomas. 197 68

A case of Spitz's nevus with eosinophilic globules was examined using antibodies for several components of the basement membrane. Aggregated tumor cells revealed the same characteristics as normal nevocytic nevi, that is, they were surrounded by laminin and type-IV collagen, whereas type-VII collagen was absent. All of these components of basement membranes, including type-VII collagen, were also found in eosinophilic globules, which were densely stained by these antibodies. It is assumed that these eosinophilic globules are essentially composed of basement membrane components, which are probably synthesized by epidermal and possibly also by melanocytic tumor cells.
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PMID:Identification of basement membrane components in eosinophilic globules in a case of Spitz's nevus. 169 20

Silver staining of nucleolar organizer regions is an objective method for evaluating the malignancy of a variety of tumors. We studied 126 ciliochoroidal melanomas, three coincidental nevi that occurred in eyes with melanomas, and one magnocellular nevus collected from the Collaborative Ocular Melanoma Study to determine the effectiveness of the silver-stained nucleolar organizer region technique in assessing the malignant potential of these tumors. Malignant lesions demonstrated higher mean silver-stained nucleolar organizer region counts (4.347) than benign nevi (1.855) (P less than or equal to .0001). Among malignant melanomas, mixed-cell melanomas had slightly higher counts than spindle-cell melanomas (P less than or equal to .0001), but this difference was not important clinically. Results were also compared to other histopathologic variables, which disclosed correlation of silver-stained nucleolar organizer regions with mitoses and tumor size. Comparison with computerized cytomorphometric analyses of prognosis also disclosed significant correlation. This technique may prove to be a useful adjunct in the assessment of malignancy and treatment response of uveal melanomas.
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PMID:The value of nucleolar organizer regions in uveal melanoma. The Collaborative Ocular Melanoma Study Group. 170 Jun 11

The authors describe a case of choroid plexus hemangioma in a 49-year-old male. Computed tomographic scan showed an isodense mass at the trigone of the right lateral ventricle with homogeneous enhancement. He also displayed a port-wine nevus on the ipsilateral side of the face. At operation, the tumor was found not to adhere to the lateral ventricular wall but to be connected to the choroid plexus, and was colored similarly to the facial nevus. Histological examination showed a capillary hemangioma with many crowded capillaries. This case was not included in the category of Sturge-Weber syndrome but is thought to be closely related, considering the syndrome from the viewpoint of generalized neurocutaneous hemangiomatosis.
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PMID:Choroid plexus hemangioma with port-wine nevus of the face: relationship to Sturge-Weber syndrome--case report. 170 63

100%, 75%, 50%, 25% and 12.5% oxidized dextran T10 (Dex T10) were used as intermediate carriers for conjugating drug daunorubicin (DNR) and antibody anti-human thymocytic globulin (AHTG), to form different immunoconjugates, AHTG:Dex:DNR. It was demonstrated that the conjugate with 25% oxidized Dex T10 as intermediate carrier linked more DNR molecules than the others. The degree of its substitution was 10-11 moles of DNR per mole of AHTG. Moreover, because the amount to reducing agent sodium borohydride (NaBH4), required for the reduction reaction, was relatively small, its damaging effect on AHTG and DNR was lessened accordingly. The antitumor effect of AHTG:Dex:DNR in vitro was tested by using 24-h cytotoxicity assay, with CEM as target cell. Cytotoxic effect of the conjugate was proven and the LD50 was 10.68 micrograms/ml. However, it showed only slight cytotoxic effect on non-target cell K562. When 10 min cytotoxicity assay was performed to show the specific tumor-killing effect of the conjugate, it revealed an obvious cytotoxic activity toward CEM, with the LD50 being 14.79 micrograms/ml, but hardly toward K562. These results suggest that AHTG:Dex:DNR possesses specific cytotoxic effect.
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PMID:Preparation of AHTG-DNR conjugates and their antitumor effect in vitro. 171 85

A total of 145 melanocytic tumors (nevus, 38; primary malignant melanoma, 72; metastatic malignant melanoma, 35) were stained with Ki 67 monoclonal antibody using a three-step immunoperoxidase technique. For each case, mean numerical density and maximum numerical density of Ki 67 positive nuclei (number per mm3) were quantitatively evaluated using interactive image analysis. Maximum numerical densities revealed highly significant differences. Within the group of primary malignant melanomas, there was a significant correlation between proliferative activity and maximum tumor thickness. Further, a 'Ki 67-prognostic index' was assessed in each case of primary malignant melanoma, calculating the product of the Breslow index and maximum numerical density/1000 (103 +/- 12; range 1-694). In a prospective, short-term evaluation of primary malignant melanomas, there was a significant difference concerning 'Ki 67-prognostic index' between disease-free survival and occurrence of metastases. After a follow-up time of 24 months, only 63% of the patients with a 'Ki 67-prognostic index' greater than 25 were disease-free, whereas no patient with a 'Ki 67-prognostic index' less than 25 was found to have metastases. We conclude: assessment of the maximum numerical density of Ki 67 reflects the degree of malignancy in melanocytic skin tumors; within primary malignant melanomas, maximum numerical density of Ki 67 positive cells correlates with well-established prognostic parameters (tumor thickness, level of invasion, mitotic rate); assessment of the 'Ki 67-prognostic index' may be of additional prognostic value for patients with primary malignant melanoma.
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PMID:Ki 67 immunostaining in melanocytic skin tumors. Correlation with histologic parameters. 171 49

gamma-Immune protein-10 (gamma-IP10) is a cytokine whose expression has been shown to be induced by interferon-gamma. It is a member of a group of closely related cytokines (e.g., interleukin 8 and platelet factor 4) with chemotactic properties. gamma-IP10 has been detected in keratinocytes, lymphocytes, monocytes, and endothelial cells in immunologically mediated processes, such as positive tuberculin skin tests, and in growth-activated keratinocytes, such as in psoriasis. Keratinocytes in normal epidermis do not produce gamma-IP10. We tested the hypothesis that keratinocytes adjacent to dysplastic nevi and melanomas would produce gamma-IP10, perhaps as part of an immune response to a tumor, and that this response would not be seen in ordinary melanocytic nevi. We used an affinity-purified, polyclonal rabbit anti-gamma-IP10 antibody to examine 10 nevi with moderate to severe histologic dysplasia, one superficial spreading melanoma, and 10 compound melanocytic nevi with no features of dysplasia. As predicted, keratinocytes surrounding all of the cytologically atypical melanocytic lesions displayed strong staining with gamma-IP10. There was no staining of keratinocytes adjacent to ordinary melanocytic nevi. The observed keratinocyte staining with gamma-IP10 may be related to a host immune response to antigenically abnormal cells.
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PMID:Detection of cytokine-induced protein gamma-immune protein-10 (gamma-IP10) in atypical melanocytic proliferations. 172 47

Antigen expression was studied by immunohistochemistry in 133 human melanocytic skin lesions to gain insight into the initial steps of tumor development, i.e. in particular the change from melanocytes to benign nevi. We refer to the proposed progression model of Clark and co-workers. The following types of antigens were investigated: (i) intermediate filament antigens (vimentin), (ii) melanoma-associated antigens (HMB-45, NKI/C3, MA-930, LS59), (iii) proliferation-associated antigens (S-100, Ki67, Ro/SSA, calmodulin), (iv) progression-associated antigens (HLA-DR, ICAM-1), and (v) basal membrane antigens (bullous pemphigoid antigen, laminin, fibronectin, collagen type IV). The intensity of expression and the topography of immunoreactive pigment cells were compared with the stage of tumor progression. Special attention was paid to the early steps of this process, i.e. the disturbance of the epidermal melanin unit and the development of melanocytic ("nevocellular")nevi. A dramatic shift of antigen expression (antigen types [i] to [v]) was noted in benign nevi compared with melanocytes. Nevi with cellular atypia disclosed a tendency towards an increased percentage of tumor cells reactive for melanoma- and progression-related antigens (types [ii] and [iv]). However, there was no clear cut level of distinction of antigen expression (types [i] to [v]) between benign and primary malignant melanocytic tumors. So-called dysplastic nevi resembled benign tumors or melanocytes rather than malignant melanoma. Metastatic melanoma of skin showed a relatively high number of Ki67-positive, cycling melanoma cells. The results have a bearing on the concepts of melanocytic nevus ontogenesis and "maturation". It appears that melanocytes lose maturity on their way down to the dermis in contrast to traditional concepts (Abtropfung); this might be of importance for our understanding of melanoma development in association with melanocytic nevi. Our findings are discussed with regard to Clark's model of tumor progression.
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PMID:The initial steps of tumor progression in melanocytic lineage: a histochemical approach. 174 97

In a retrospective study, cutaneous melanocytic tumors from 18 horses, less than 2 years old, were examined histopathologically and clinical follow-up requested. Melanocytomas (benign melanomas) occurred in a variety of breeds and in horses of varied coat color. The age of the horses at the time of biopsy ranged from 3 weeks old to 2 years old. Four melanocytomas were congenital, 11 melanocytomas were acquired by 1 year of age, and three were acquired prior to 2 years of age. Of the 18 horses, five were male, and 13 were female. All tumors were solitary and located on the legs or trunk; none were in the perineal region. Ulceration of the overlying epidermis was common. Tumors were generally localized and were not encapsulated. The tumors had a variety of cell patterns ranging from sheets, to streams, or nests of melanocytes. Cellular morphologic findings also ranged from epithelioid, to a mixture of epithelioid and spindle cells or to a spindle pattern. The nuclei were large and euchromatic, especially in the epithelioid cells. Several tumors had moderate cellular pleomorphism and binucleate cells. Mitotic activity was generally low (less than 1/high-powered field), but was readily detected (1-2/high-powered field) in bleached sections of four cases. Melanin pigmentation varied from mild to heavy. Melanophages were admixed with the tumor cells or in the adjacent tissue. Follow-up information was obtained on 15/18 horses and revealed that 14/15 horses were free of recurrence following excision. One neoplasm, that was poorly demarcated and had a spindle cell pattern, was not completely resected and continued to grow. These melanocytic tumors in young horses are distinct from melanomas in aged horses in their location, epithelial involvement, and age of horses affected. The majority of these tumors appear to be benign and share features of melanocytic nevi of human beings.
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PMID:Congenital and acquired melanocytomas (benign melanomas) in eighteen young horses. 175 Jan 61


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