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)

We review two patients with unusual pilosebaceous and spindle cell neoplasms. Both lesions were on the nose and were clinically similar to angiofibroma. Immunoperoxidase (S-100 protein, vimentin, immunostain for actin) and special stains (Masson's trichrome, periodic acid-Schiff, and Bielschowsky silver stain) were used to evaluate the lesions. The histologic differential diagnosis included neural nevi, trichogenic myxoma, trichodiscoma, benign neural and vascular tumors, and dermal scar formation. Our patients, we believe, had single asymptomatic smooth, skin-colored papules; this condition was recently termed "neurofollicular hamartoma."
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PMID:Neurofollicular hamartoma. A clinicopathological study. 165 45

In an immunocytochemical investigation of the expression of glial fibrillary acidic protein (GFAP) in non-nervous system tissues ten anti-GFAP antibodies were used on a range of normal adult organs from different species. All four polyclonal and six monoclonal antibodies revealed the expression of GFAP in cells of the zona fasciculata and reticularis of the adrenal cortex and Leydig cells of the Syrian hamster. The Chinese hamster, mole, rat, mouse, guinea pig, rabbit, pig, duck and man were negative. Co-expression of immunoreactivity for GFAP and vimentin was observed in adrenocortical and Leydig cells of the Syrian hamster but there were differences in the staining patterns of these intermediate filament proteins. Expression of GFAP in adrenal cortex of Syrian hamster is confirmed by immunoblot and limited proteolysis analysis which reveal a light form which is immunochemically indistinguishable from its counterpart in the central nervous system. The results presented here suggest a new model for the study of the possible role of GFAP expression in cells known to be sites of steroid synthesis.
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PMID:Glial fibrillary acidic protein immunoreactivity in adrenocortical and Leydig cells of the Syrian golden hamster (Mesocricetus auratus). 172 Jan 32

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

The cytoskeleton is considered to be important for maintaining cell shape and facilitating cell movement. In the present study, the expression of cytoskeletal components is examined in benign and malignant melanocytic skin tumors. Paraffin sections of 75 cases (25 each of nevocellular nevus, primary malignant melanoma, and cutaneous metastases of malignant melanoma) were stained with antibodies to tubulin, myosin, actin, and vimentin using a three-step immunoperoxidase method. The staining results were assessed independently for tumor cells and stroma cells in comparison to inbuilt reference structures. Vimentin is found in all melanocytic lesions in the tumor as well as in the stroma cells. In malignant lesions, the tumor cell staining intensity varies between neighboring regions; particularly in malignant melanoma the staining is pronounced in the tumor periphery (chi 2 test: p less than 0.05). Actin is only weakly positive in nevus cells and primary melanoma tumor cells, but strongly expressed in metastatic tumor cells (p less than 0.001). Nevus fibroblasts are only weakly positive, whereas the stroma fibroblasts in the malignant lesions are strongly positive (p less than 0.001). The same is true for myosin and tubulin expression in dermal fibroblasts (p less than 0.001), whereas the tumor cells are equally (weakly) positive in all melanocytic lesions. Our study shows that there are significant differences in the immunohistochemical expression of cytoskeletal components in various melanocytic tumors. There is an elevated expression of vimentin and actin in the tumor cells, particularly of metastatic lesions. However, the most pronounced differences are found in the dermal fibroblasts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Expression of cytoskeletal components in melanocytic skin lesions. An immunohistochemical study. 202 88

Fourteen cases of naevocytic naevi with anastomising lacunae suggestive of vascular spaces are reported. The cells lining these lacunae were consistent with naevus cells, being positive for vimentin and S100 protein and negative for factor VIII-related antigen and Ulex europaeus I. The cells were not surrounded by laminin or type IV collagen. We suggest the formation of these vascular-like spaces may be due to defective production or increased degradation of components of the basement membrane with a consequent lack of cohesion.
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PMID:Naevocytic naevi with vascular-like spaces. 206 45

A review was conducted of 335 malignant melanomas to identify variant morphologic patterns that might be confused with other tumors. In all, 27 predominantly amelanotic neoplasms with unusual histologic features were selected for additional study. These included nine with an adenoid or pseudopapillary pattern, seven small cell neoplasms, five with prominent myxoid stroma, four with a hemangiopericytoma-like appearance, and two composed of neoplastic cells with a signet-ring configuration. A diagnosis of melanoma was confirmed in all cases by Fontana-Masson strains for melanin pigment, electron microscopic examination, or the results of immunohistochemical analyses for cytokeratin, vimentin, S-100 protein, and the HMB-45 antigen. One tumor was associated with a congenital hairy melanocytic nevus, five were vulvovaginal lesions, four arose in the sinonasal tract, and one occurred in the rectum. Four of the specified microscopic patterns were observed in both primary and secondary neoplasms; the two signet-ring cell melanomas were recurrent lesions. The authors conclude that malignant melanomas may assume the histologic guise of adenocarcinomas, small cell carcinomas, and sarcomas, in a variety of tissue sites. Special studies designed to detect melanocytic differentiation are therefore appropriate in diverse differential diagnostic settings.
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PMID:Morphologic diversity in malignant melanomas. 224 3

One hundred cutaneous tumors were investigated immunohistopathologically for the expression of intermediate filament (IF) proteins. Epithelial tumors, such as basocellular and squamous cell carcinomas, cutaneous adnexal tumors, and metastatic carcinomas showed keratin positivity in a varying number of tumor cells with two keratin antibodies with different specificities. Neoplastic cells of fibrohistiocytic tumors, pigmented nevi, melanomas, hemangiomas, glomus tumors, and lymphomas were positive for vimentin, but not for keratin or desmin. Cutaneous leiomyomas and leiomyosarcomas, on the other hand, were positive for desmin. The results show that the typing of IFs enables the differential diagnosis between carcinomas and sarcomas or melanomas, epidermal appendage tumors, and mesenchymal tumors, and between fibrohistiocytic and leiomyocytic tumors, and therefore are of diagnostic value in histopathologic problems of the skin.
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PMID:Antibodies to intermediate filament proteins. The differential diagnosis of cutaneous tumors. 240 82

Immunohistochemical analyses were performed on 64 nevocellular nevi (12 compound nevi and 52 intradermal nevi). S-100 protein and its alpha- and beta-subunits were almost always demonstrated in type A, B and C cells, and the staining intensity tended to increase in the type C cells. Neuron-specific enolase was detected in each type of cell; however, the population of positive cells was smaller among type C cells. Beta 2-microglobulin was occasionally demonstrated, but only in type A cells. Vimentin was frequently revealed in every type of cell. Neither myelin basic protein nor glial fibrillary acidic protein was observed in any type of cell. In contrast, normal epidermal melanocytes were positive for vimentin, but negative for S-100 protein and its subunits and neuron-specific enolase. Schwann cells were positive for S-100 protein and its beta-subunit, but negative for the alpha-subunit. Thus, the nevus cells shared a common nature with epidermal melanocytes and Schwann cells which originate from the neural crest; however, the former cells were somewhat different from the latter two kinds and from benign and malignant tumors derived from these cells in the expression of these antigenic substances. Such differences in the expression of antigenic substances may be due to dysontogenic manifestations in nevus cells.
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PMID:[Immunohistochemical study of nevocellular nevi]. 268 14

Solitary mastocytoma (mast cell naevus) of the skin represents a relatively rare dermal tumour. Its occurrence on the lower eyelid is exceptional. We report the case of a 4 month old male infant who exhibited a firm, yellowish nodule (1 cm in maximum diameter) on the lower lid of the right eye from birth. Histologically, the tumour consisted of strongly metachromatic tissue mast cells (TMC) infiltrating the whole dermis, the adjacent subcutaneous tissue and the lid muscle. Since comparable skin lesions in other sites were not observed, a diagnosis of solitary mastocytoma was made. Immunocytological investigations revealed strong reactivity of the TMC to antisera against vimentin, common leucocyte antigen (CLA), alpha 1-antitrypsin (alpha 1-AT) and alpha 1-antichymotrypsin (alpha 1-ACT). A minor proportion of the TMC reacted to antisera against lysozyme and KiB3. Surprisingly, the TMC also reacted to antisera against certain regulatory peptides (RP), namely adrenocorticotropic hormone (ACTH), peptide histidine isoleucine (PHI), leu-enkephalin and met-enkephalin. However, absorption controls revealed that the immunostaining for ACTH and the two enkephalins was non-specific. The immunocytological phenotype of TMC suggests a close relationship to the myeloid-monocytic lineage, but a possible relationship between TMC and the diffuse neuroendocrine system needs further investigation.
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PMID:Solitary mastocytoma of the eyelid. A case report with special reference to the immunocytology of human tissue mast cells, and a review of the literature. 312 Apr 1

The ability of the intermediate filament subunit protein vimentin to bind synthetic oligonucleotide telomere models containing repeat sequences from Oxytricha (T4G4), Saccharomyces (TGTGTG3), or Tetrahymena (T2G4) was investigated in vitro with a filter binding assay and a gel overlay assay. At low ionic strength, vimentin bound these oligonucleotides with high affinity. At higher ionic strength, the vimentin-oligonucleotide complex was less stable, such that approximately 30% of the initial binding remained at 150 mM KCl. One mole of vimentin tetramer bound approximately 1 mol of telomere oligonucleotide. Vimentin bound well oligonucleotides containing either a random duplex or random 3'-overhang, but showed a reduced affinity for a blunt-ended oligonucleotide. A control random sequence oligonucleotide was not bound by vimentin. The oligonucleotide-binding site of vimentin was shown to be localized in the non-alpha-helical N-terminal domain by assays employing purified proteolytic fragments of vimentin. Preliminary results in the gel overlay assay show that other members of the intermediate filament family, nuclear lamins A-C, all bind the synthetic oligonucleotide containing the telomere repeat sequence of Oxytricha.
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PMID:The binding in vitro of the intermediate filament protein vimentin to synthetic oligonucleotides containing telomere sequences. 326 81


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