Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sentinel lymph node (SLN) biopsy has become an increasingly important procedure used in the primary staging of malignant melanoma. However, micrometastases in a lymph node can be easily missed on routine H&E-stained sections. Therefore, S-100 and HMB-45 IHC stains are standardly performed on grossly negative SLNs for detection of metastatic melanoma. Each of these IHC markers, however, is not ideal. The authors investigated whether the newer IHC marker Melan-A would improve the detection of metastatic melanoma in SLN biopsies. Forty lymph nodes previously diagnosed with metastatic melanoma were retrospectively evaluated for S-100, HMB-45, and Melan-A expression. In addition, 42 SLN biopsies for metastatic melanoma detection were prospectively collected and evaluated for S-100, HMB-45, and Melan-A expression. All lymph nodes with metastatic melanoma from the retrospective study demonstrated S-100 reactivity. Five of the lymph nodes with metastatic melanoma from the retrospective study failed to express either HMB-45 or Melan-A, all of which displayed a desmoplastic morphology. One of the metastases positive for S-100 and HMB-45 failed to show reactivity with Melan-A (3%). The prospective study found 10 lymph nodes from 42 cases to be positive for metastatic melanoma, which were positive for S-100 (100%). Nine of the involved lymph nodes were positive for HMB-45(90%), and nine were positive for Melan-A (90%). Melan-A, although very specific, cannot replace the use of S-100 and HMB-45 for the detection of metastatic melanoma in SLNs. It can, however, substitute for HMB-45 with equally good results.
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PMID:Can Melan-A replace S-100 and HMB-45 in the evaluation of sentinel lymph nodes from patients with malignant melanoma? 1693 24

Perivascular epithelioid cell tumor (PEComa) is rare entity and has been described only recently. By immunohistochemistry and genetics it belongs to the family of tumours which comprises angiomyolipoma, clear cell "sugar" tumor of lung, lymphangioleiomyomatosis and clear cell myomelanotic tumor of ligamentum falciforme/teres hepatis. We describe an unusual case of hepatic PEComa arising in a 55-year-old woman with previous history of glioblastoma. Histologically the tumor grew in expansive way, and was composed of clear and eosinophilic epithelioid cels, without vascular or lipomatous component characteristic of angiomyolipoma. There was mild nuclear pleomorphism, sporadic mitotic activity and haemorrhage without necrosis. On immunohistochemistry, the tumor was HMB-45+50, Melan-A and smooth muscle actin positive. Tyrosinase, S-100 protein, cytokeratin coctail, EMA, vimentin, muscle specific actin, CD10, TTF-1, hepatocyte, desmin and cyclin D1 were negative. Sporadic nuclear p53 positivity was seen. The main differential diagnosis of hepatic PEComa includes clear cell variant of liver cell adenoma and hepatocellular carcinoma, metastases of various clear cell carcinomas and metastasis of malignant melanoma. In respect of uncertain biologic potential of PEComa, long term follow up is indicated.
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PMID:[Perivascular epithelioid cell tumor (PEComa) of the liver: a case report and review of the literature]. 1737 Apr 72

HLA-A2-restricted cytolytic T cells specific for the immunodominant human tumor Ag Melan-A(MART-1) can kill most HLA-matched melanoma cells, through recognition of two naturally occurring antigenic variants, i.e., Melan-A nonamer AAGIGILTV and decamer EAAGIGILTV peptides. Several previous studies have suggested a high degree of TCR cross-reactivity to the two peptides. In this study, we describe for the first time that some T cell clones are exclusively nonamer specific, because they are not labeled by A2/decamer-tetramers and do not recognize the decamer when presented endogenously. Functional assays with peptides gave misleading results, possibly because decamers were cleaved by exopeptidases. Interestingly, nonapeptide-specific T cell clones were rarely Valpha2.1 positive (only 1 of 19 clones), in contrast to the known strong bias for Valpha2.1-positive TCRs found in decamer-specific clones (59 of 69 clones). Molecular modeling revealed that nonapeptide-specific TCRs formed unfavorable interactions with the decapeptide, whereas decapeptide-specific TCRs productively created a hydrogen bond between CDR1alpha and glutamic acid (E) of the decapeptide. Ex vivo analysis of T cells from melanoma metastases demonstrated that both nonamer and decamer-specific T cells were enriched to substantial frequencies in vivo, and representative clones showed efficient tumor cell recognition and killing. We conclude that the two peptides should be regarded as distinct epitopes when analyzing tumor immunity and developing immunotherapy against melanoma.
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PMID:A novel population of human melanoma-specific CD8 T cells recognizes Melan-AMART-1 immunodominant nonapeptide but not the corresponding decapeptide. 1802 9

Melanoma can show a broad spectrum of immunoreactivity and exhibit aberrant expression of antigens or changes in immunophenotype, particularly at metastatic sites. We studied 70 primary melanomas and their metastases with a broad panel of immunohistochemical markers using a tissue microarray technique to determine possible antigenic shift between the primary lesions and their metastases. Representative tissue cores were taken and processed from each case, and the tissue microarrays were stained by standard methods using antibodies to vimentin, bcl-2, CD117, carcinoembryonic antigen, epithelial membrane antigen, S-100 protein, HMB-45, cytokeratin AE1/AE3, Melan-A, TTF-1, CD99, and tyrosinase. Histologically, all the melanomas were of the classic epithelioid type. A slight increase in the expression of Melan-A was noted in metastatic lesions as opposed to the primary tumors (63% vs. 48.4%). Expression of other melanoma-associated markers, including S-100 protein and tyrosinase was only slightly decreased at metastatic sites as opposed to the primary tumor. Increased aberrant expression of epithelial-associated markers, including epithelial membrane antigen and cytokeratin AE1/AE3 was also noted in the metastases. bcl-2, CD117, and TTF-1 also showed a modest increase in antigenic expression at metastatic sites over the primary lesions. The results of this study demonstrated minimal antigenic shift between primary and metastatic melanoma for some of the more conventional melanocytic markers, it showed increased expression of aberrant markers and oncogene expression at metastatic sites.
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PMID:Expression of immunohistochemical markers in primary and metastatic malignant melanoma: a comparative study in 70 patients using a tissue microarray technique. 1809 85

Acral myxoinflammatory fibroblastic sarcoma (AMIFS) is a low-grade sarcoma that presents mostly in distal extremities of middle-aged patients. The clinicopathologic features, immunohistochemical profile and follow-up data of five cases (three men and two women; age 39-65 years) are presented. The tumors presented as a slow-growing, poorly circumscribed, subcutaneous masses in the hands (three), foot (one) and calf (one), with dermal involvement in two cases. They had myxoid and hyaline stroma with dense acute and chronic inflammation. Spindle cells, large bizarre ganglion-like cells and multivacuolated cells were seen. Variable reactivity in lesional cells were noted for vimentin, Alpha-1-antitrypsin (A1AT), factor XIIIa, CD68, CD95, CD117, Alpha-1-antichymotrypsin (A1ACT), CD34, AE1/3, S-100 protein, EBER, CD63 and CD15. MIB-1 showed 5-30% nuclear labeling. They were negative for cytokeratin AE1/3, smooth muscle actin, CD30, ALK-1, EMA, desmin, CMV, HMB-45 and Melan-A. Follow up ranged from 2 weeks to 95 months (mean 54). One patient was lost to follow up; three underwent excision and one patient had below the knee amputation. Two patients developed metastases (one died of disease), and two patients are alive without evidence of disease. AMIFS are rare tumors that may involve joints and tendons leading to clinical diagnosis of ganglion cyst or tenosynovitis.
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PMID:Acral myxoinflammatory fibroblastic sarcomas: are they all low-grade neoplasms? 1819 Apr 43

We report an autopsy case of malignant epithelioid angiomyolipoma in a 36-year-old male tuberous sclerosis patient. He had been diagnosed to have a bilateral renal tumor 20 years previously. The left kidney had been surgically resected at the age of 34, and the left renal tumor was pathologically diagnosed as classic angiomyolipoma and epithelioid angiomyolipoma. He suddenly died of cardiac arrest, and at autopsy the right kidney weighed 7120 g. The tumor presented with massive necrosis invading the inferior vena cava, but was not hemorrhagic. Microscopic examination revealed tumor cells varying in size with a predominantly solid proliferation pattern and marked atypical large cells with vesicular nuclei and abundant eosinophilic cytoplasm. Mitotic figures were often encountered, and atypical forms were also present. Metastatic lesions were identified in the right lung, liver, diaphragm, and mesentery. Immunohistochemical examination showed epithelioid angiomyolipoma cells that were focally reactive for HMB-45 and showed diffuse positive staining for Melan-A. No mutation was detected in the p53 gene by polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) analysis despite diffuse immunoreactivity for p53. This case was proven to be malignant because of the occurrence of distant metastases, and showed that p53 mutations are not always associated with malignant transformation in epithelioid angiomyolipoma.
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PMID:Malignant epithelioid angiomyolipoma of the kidney in a patient with tuberous sclerosis: an autopsy case report with p53 gene mutation analysis. 1854 41

Although neoplastic cells with a plasmacytoid appearance have been reported in a variety of tumors, to the best of our knowledge, a plasmacytoid squamous cell carcinoma (SCC) of the vulva or skin has heretofore not been described. We document the case of a 92-year-old female patient with a history of multiple excisions for vulvar verrucous and SCCs, who presented with a 3-cm, symptomatic, polypoid mass of the left upper vulva. Histologically, sheets of dyscohesive relatively monotonous plasmacytoid and spindle cells were found dispersed throughout the dermis. The neoplastic cells expressed cytokeratins AE3, 5/6, and 903, p63, and the plasma cell markers CD138 (syndecan-1) and VS38. The neoplastic cells did not label with S-100 protein, Melan-A, smooth muscle actin, desmin, Kappa and Lambda light chains, epithelial membrane antigen, MOC-31, uroplakin III, thrombomodulin, and E-cadherin. Based on the tumor location, morphology, and immunohistochemical results, the diagnosis of plasmacytoid SCC of the vulva was rendered. Six months after complete excision, she developed regional inguinal lymph node and pulmonary metastases and died. Like other plasmacytoid malignancies, vulvar plasmacytoid SCC is a rare and likely aggressive variant of SCC, which can pose significant diagnostic challenges. Squamous cell carcinoma should also be considered in the differential diagnosis of neoplasms with plasmacytoid cytology. To correctly classify plasmacytoid malignancies, a wide panel of immunohistochemical markers must be used.
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PMID:Plasmacytoid squamous cell carcinoma of the vulva. 1875 57

Epidermodysplasia verruciformis (EV) is a rare autosomal-recessive condition associated with a predisposition to infection with specific types of human papillomaviruses. A spectrum of wart-like lesions on the face, dorsa of the hands, and legs are characteristic clinical findings. Lesions usually develop in early childhood, persist, and may eventuate in cutaneous squamous cell carcinoma, usually in sun-exposed areas. These lesions are locally destructive and sometimes metastasize. We present a case of a 34-year-old African American woman with EV with a 9-month history of a right index finger ungual longitudinal pigmented band and nail splitting. Biopsy showed hyperkeratotic and parakeratotic subungual epithelium with verrucous hyperplasia. The superficial keratinocytes showed koilocytic changes. In addition, there was extensive, focally full-thickness keratinocyte dysmaturation with variable nuclear atypia and numerous mitotic figures, without apparent invasion. An associated melanocytic hyperplasia (confirmed by Melan-A stain), composed of large, pigment-laden dendritic melanocytes, was present without appreciable atypia or pagetoid spread. The findings are of a squamous cell carcinoma in situ arising in association with EV with incidental melanocytic hyperplasia. To the best of our knowledge, this is first report of a subungual presentation of this condition with associated melanonychia.
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PMID:Subungual Bowen disease in a patient with epidermodysplasia verruciformis presenting clinically as longitudinal melanonychia. 1903 34

A 59-year-old woman presented with a large mediastinal mass. At thoracotomy, the mass was found tightly adherent to the esophageal wall and right lower lobe of the lung. Histological examination showed a solid tumor composed of closely packed nests of cells with clear and eosinophilic cytoplasm, which were strongly and diffusely positive for S100 protein but negative for HMB45 and Melan-A. The diagnosis of clear cell sarcoma was supported by demonstrating the presence of an EWS gene rearrangement by fluorescence in situ hybridization. There was no evidence that this lesion represented metastatic disease. To the best of our knowledge, primary mediastinal clear cell sarcoma has not been previously reported in the literature. We present the case and discuss the differential diagnosis.
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PMID:Clear cell sarcoma of the mediastinum. 1943

The diagnosis of malignant melanoma can be challenging given the wide variation in morphologic features and immunohistochemical stains are often used to confirm the diagnosis. We report a case of melanoma with loss of staining for S100 protein, HMB-45, and Melan-A, with retained expression of tyrosinase. Regional lymph node metastases showed positive S100 protein staining. Although the loss of phenotypic markers including S100 protein has been reported in metastatic melanoma, loss of S100 in primary melanoma is rare. Discordant staining between primary and metastatic lesions further emphasizes the protean nature of melanoma.
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PMID:S100, HMB-45, and Melan-A negative primary melanoma. 1993 Sep 94


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