Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0278883 (metastatic melanoma)
 6,224 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

22 undifferentiated tumours of the Salivary Gland Register (University of Hamburg) were studied by conventional light microscopical and immunocytochemical methods to elucidate the heterogeneity of this tumour group. The following observations were made in this collective: 18 tumours displayed one or more markers for the epithelial character and were classified as carcinomas. 10 carcinomas were considered as primary ones and 8 were considered as secondary ones (metastatic or invasive "per continuitatem"). Primary carcinomas were subclassified as poorly differentiated variants of a distinctive type of salivary gland tumours, as follows: 6 cases of carcinoma in pleomorphic adenoma, and one case each of mucoepidermoid tumour, adenocarcinoma, salivary duct carcinoma and epidermoid carcinoma. Secondary carcinomas were subclassified as follows: 3 epidermoid carcinomas, 3 nasopharyngeal carcinomas and 2 bronchial carcinomas. One tumour positive for S-100 protein and NSE (Neuron-specific enolase) was classified as a metastatic melanoma. Another tumour positive for vimentin and actin was classified as a rhabdomyosarcoma of the periglandular tissue. Two tumours lacked any markers studied here and were regarded as a malignant paraganglioma and an undifferentiated lymphoma, respectively. The differential diagnosis of the undifferentiated tumours of salivary glands and the special problems of this tumour group are discussed.
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PMID:Undifferentiated tumours of salivary glands. Immunocytochemical investigations and differential diagnosis of 22 cases. 303 6

Three different human tumor lines in culture, a rhabdomyosarcoma, a bronchogenic carcinoma and a metastatic melanoma, release proteins (transforming growth factors, TGFs) into the medium that confer the transformed phenotype on untransformed fibroblasts. These proteins are acid and heat-stable; produce profound morphologic changes in rat and human fibroblasts; and enable normal anchorage-dependent cells to grow in agar. Removal of the transforming protein results in a reversion of cell phenotype. The major activity interacts with epidermal growth factor (EGF) cell membrane receptors. The peptides from these tumor cells are similar in their action to the sarcoma growth factor (SGF) released by murine sarcoma virus-transformed rodent cells. The most anchorage-independent tumor cells released the most TGFs. EGF-related TGFs were not detectable in fluids from cultures of cells with high numbers of free EGF membrane receptors (normal human fibroblasts and human carcinomas).
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PMID:Transforming growth factors produced by certain human tumor cells: polypeptides that interact with epidermal growth factor receptors. 625 71

Transforming growth factors (TGFs) stimulate cells to divide in monolayer cultures and to form colonies that grow progressively in soft agar. TGFs are a family of polypeptide hormones that, in vitro, confer on fibroblasts and epithelial cells properties associated with the transformed phenotype. They have been isolated from the supernatant fluids of several human and animal carcinoma and sarcoma cells. TGFs interact with epidermal growth factor (EGF) membrane receptors. They are not detectable in culture fluids from cells that contain high numbers of free EGF cell membrane receptors. One TGF is sarcoma growth factor (SGF), which is released by murine sarcoma virus-transformed cells. Studies have shown EGF and SGF to be two distinct growth factors despite the fact that SGF exerts its effects by specifically interacting with EGF receptors. Addition of SGF to normal indicator cells results in expression of the transformed phenotype. The effects of SGF are reversible; the cells resume their normal growth pattern when the growth factor is removed. Three different human tumor cell lines in culture, a rhabdomyosarcoma, a bronchogenic carcinoma, and a metastatic melanoma, release TGFs that also confer the transformed phenotype on normal fibroblasts. One would expect that, as research into this area continues, new TGFs and their interaction with different specific cell membrane receptors will be described.
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PMID:Sarcoma growth factor and other transforming peptides produced by human cells: interactions with membrane receptors. 629 3

We performed immunohistochemical analysis for KIT in 365 soft tissue sarcomas. Most tumors evaluated were completely negative for KIT, including all cases of leiomyosarcoma, rhabdomyosarcoma, myxofibrosarcoma, liposarcoma, solitary fibrous tumor, synovial sarcoma, dermatofibrosarcoma protuberans, schwannoma, malignant peripheral nerve sheath tumor, clear cell sarcoma, low-grade endometrial stromal sarcoma, and follicular dendritic cell sarcoma. Tumors showing occasional immunoreactivity for KIT included extraskeletal myxoid chondrosarcoma (2/20), Ewing sarcoma/malignant primitive peripheral neuroectodermal tumor (4/20), melanotic schwannoma (3/5), metastatic melanoma (4/20), and angiosarcoma (5/20). In most cases, staining for KIT was focal. Rare tumor cells showing KIT positivity were identified in a small number of other tumors. This study demonstrates very limited expression of KIT in soft tissue tumors other than gastrointestinal stromal tumors and underscores the discriminatory value of KIT immunohistochemical analysis for differential diagnosis. As some of these findings differ markedly from previous reports, it is evident again that variations in immunohistochemical technique can lead to major discrepancies in positive staining. Since treatment eligibility for selective tyrosine kinase inhibitors such as STI571 hinges on positive immunostaining, standardization and reproducibility of meaningful results are critically important.
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PMID:Immunohistochemical staining for KIT (CD117) in soft tissue sarcomas is very limited in distribution. 1221 91

A 40-yr-old woman with an asymptomatic sinonasal rhabdomyosarcoma (RMS) initially presented with submental nodal metastasis. The fine-needle aspiration (FNA) and the subsequent biopsy of the nodal metastasis were misinterpreted as metastatic carcinoma because the primary tumor was occult, the tumor cells were exclusively round cells with a nested arrangement, and rhabdomyoblasts were absent. The correct diagnosis of metastatic RMS became apparent when the primary sinonasal tumor, detected in a CT, was biopsy proven to be an alveolar RMS. Retrospectively, there were helpful clues to the correct diagnosis in the nodal FNA and biopsy. When FNA cytology or biopsy histology of a lymph node suggests metastatic carcinoma but the tumor cells are nonimmunoreactive to carcinoma markers, the differential diagnosis should be expanded to include not only metastatic melanoma but also metastatic sarcoma and lymphoma. Cytologically, the presence of multinucleated giant tumor cells, including the rosette forms, in the FNA smears should alert the cytopathologist to the possibilities of sarcoma and anaplastic large cell lymphoma.
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PMID:Rhabdomyosarcoma in an adult presenting with nodal metastasis: a pitfall in fine-needle aspiration cytology of lymph nodes. 1583 Mar 59

Sox10 transcription factor is expressed in schwannian and melanocytic lineages and is important in their development and can be used as a marker for corresponding tumors. In addition, it has been reported in subsets of myoepithelial/basal cell epithelial neoplasms, but its expression remains incompletely characterized. In this study, we examined Sox10 expression in 5134 human neoplasms spanning a wide spectrum of neuroectodermal, mesenchymal, lymphoid, and epithelial tumors. A new rabbit monoclonal antibody (clone EP268) and Leica Bond Max automation were used on multitumor block libraries containing 30 to 70 cases per slide. Sox10 was consistently expressed in benign Schwann cell tumors of soft tissue and the gastrointestinal tract and in metastatic melanoma and was variably present in malignant peripheral nerve sheath tumors. In contrast, Sox10 was absent in many potential mimics of nerve sheath tumors such as cellular neurothekeoma, meningioma, gastrointestinal stromal tumors, perivascular epithelioid cell tumor and a variety of fibroblastic-myofibroblastic tumors. Sox10 was virtually absent in mesenchymal tumors but occasionally seen in alveolar rhabdomyosarcoma. In epithelial tumors of soft tissue, Sox10 was expressed only in myoepitheliomas, although often absent in malignant variants. Carcinomas, other than basal cell-type breast cancers, were only rarely positive but included 6% of squamous carcinomas of head and neck and 7% of pulmonary small cell carcinomas. Furthermore, Sox10 was often focally expressed in embryonal carcinoma reflecting a primitive Sox10-positive phenotype or neuroectodermal differentiation. Expression of Sox10 in entrapped non-neoplastic Schwann cells or melanocytes in various neoplasms has to be considered in diagnosing Sox10-positive tumors. The Sox10 antibody belongs in a modern immunohistochemical panel for the diagnosis of soft tissue and epithelial tumors.
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PMID:Sox10--a marker for not only schwannian and melanocytic neoplasms but also myoepithelial cell tumors of soft tissue: a systematic analysis of 5134 tumors. 2572

Metastatic malignant melanoma is notorious for its phenotypic diversity and loss of differentiation markers. We herein summarized our experience with 14 metastatic melanomas showing complete loss of immunohistochemical melanocytic markers (with or without heterologous differentiation). Patients included 11 men and 3 women aged 24 to 78 years (median, 67 y). Thirteen patients had histologically confirmed primary skin melanoma, and 1 had metastatic melanoma of unknown primary. Undifferentiated metastasis was diagnosed synchronous to primary tumor (n=1), following skin melanoma by 3 months to 9 years (n=11) and preceding it by 1 year (n=1). Sites of undifferentiated metastases were axillary (3), inguinal (1), or submandibular (1) lymph nodes, digestive tract (2), bone/soft tissue (2), lung/pleura (2), and disseminated (n=3). Histology of metastases mimicked undifferentiated pleomorphic or spindle cell sarcoma with variable myxoid and giant cell areas (n=10) and cytokeratin-positive undifferentiated small cell sarcoma (n=1). Three cases showed heterologous dedifferentiation: pleomorphic rhabdomyosarcoma (n=1), teratocarcinosarcoma-like with prominent rhabdomyoblasts (n=1), and adenocarcinoma-like with metaplastic bone (n=1). All cases were negative for S100, melanoma cocktail, HMB45, Melan A, and SOX10. Other markers showed following results: smooth muscle actin (1/14), p16 (1/14), TP53 (2/12), pancytokeratin (4/14), desmin (5/14), h-caldesmon (0/9), and MDM2/CDK4 (0/5). SMARCB1 was intact in 8/8 cases. Genotyping showed BRAF(V600E) mutation (5/14), NRAS mutation (5/14), and BRAF/NRAS wild-type (4/14). In conclusion, undifferentiated/dedifferentiated metastatic melanoma is likely underrecognized and frequently mistaken for undifferentiated sarcoma or other neoplasms. Diagnosis of undifferentiated sarcoma at sites where melanoma metastasis are frequent (eg, inguinal and axillary region) should be made with great caution and warrants exploration of the remote history. Genotyping is a helpful surrogate marker in classifying such difficult cases. In the light of available targeted therapies, recognition of undifferentiated/dedifferentiated metastatic melanoma is mandatory for appropriate treatment.
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PMID:Metastatic Malignant Melanoma With Complete Loss of Differentiation Markers (Undifferentiated/Dedifferentiated Melanoma): Analysis of 14 Patients Emphasizing Phenotypic Plasticity and the Value of Molecular Testing as Surrogate Diagnostic Marker. 2703 13