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)

Immunohistochemical techniques may aid in the diagnosis of poorly differentiated metastatic tumors. Anti-carcinoembryonic antigen (CEA) antibodies have been used in the identification of epithelial neoplasms. However, recent unpublished data report CEA reactivity in malignant melanoma and melanoma cell lines. We studied 28 cases of known metastatic malignant melanoma with an antibody panel for CEA (polyclonal and monoclonal), AE1:3, S-100, and HMB-45. Reactivity for CEA (polyclonal) was seen in 15 of 28 (53%) cases: nine exhibited strong diffuse positivity, five moderate focal positivity, and one globular cytoplasmic staining. Focal reactivity for cytokeratin (AE1:3) was seen in three of 28 cases. HMB-45 staining was present in 23 of 28 (82%, including strong positivity in the cytokeratin-reactive cases). Staining for S-100 protein was strong in all cases. No staining was seen for CEA (monoclonal). CEA immunoreactivity is seen in a significant number of metastatic malignant melanoma cases. This may be due to CEA expression by tumor cells, or crossreactivity of the polyclonal antibody with substances such as nonspecific crossreacting antigen (NCA) that share antigenic sites with CEA. These findings emphasize the need for care in interpreting immunohistochemical results. Immunohistochemical evaluation of CEA should not be made alone, but only as part of a diagnostic antibody panel.
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PMID:CEA immunoreactivity in metastatic malignant melanoma. 834 88

The ultrastructural and immunohistochemical findings are reported in two ovarian myxomas, one of which was also associated with a sclerosing stromal tumor of the same ovary. Both neoplasms showed a myxoid, moderately cellular proliferation of spindle and stellate cells interspersed with areas of fibrosis and hemorrhage as well as delicate vascular spaces. Ultrastructurally, stellate neoplastic cells with irregular nuclei and occasional nucleoli were embedded in a mucinous and loose collagen matrix. Their cytoplasm showed abundant intracytoplasmic thin filaments that rarely condensed into poorly formed dense bodies. These thin filaments correlated with immunoreactivity for muscle-specific actin and vimentin. The neoplastic cells showed no immunoreactivity with antibodies to desmin, S-100 protein, cytokeratin AE1:AE3, factor VIII-related protein, or placental alkaline phosphatase. These ultrastructural and immunohistochemical findings are consistent with myofibroblastic differentiation. These ancillary studies exclude important, clinically more aggressive differential considerations such as myxoid rhabdomyosarcoma, myxoid liposarcoma, myxoid neural tumors, mucinous adenocarcinoma showing pseudomyxomatous change, and myxoid-appearing endodermal sinus (yolk sac) tumor.
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PMID:Ovarian myxoma: ultrastructural and immunohistochemical findings. 150 39

Gliosarcomas are mixed tumors with malignant glial and mesenchymal elements. The number of GFAP-positive tumor cells decreases with the increase of sarcomatous components, until whole areas may be GFAP negative. These distinct differentiations may, however, lead to false interpretations in small tissue samples. In this connection, it is of interest that, according to other reports, glial tumors may be positive for different anti-keratin antibodies and this prompted us to undertake a systematic investigation of the immunoreactivity of gliosarcomas using a panel of well-characterized monoclonal antibodies against cytokeratins (KL1, AE 1/3, Lu-5, CK-19, CK MNF 116 and Ma-903). These cases were further studied with the anti-epithelial non-cytokeratin antibodies EMA, HEA 125, Ber-EP4, CEA as well as the melanoma-antibody HMB-45, Leu-M1, GFAP and vimentin. As screening study we examined 20 cerebral metastatic carcinomas, 21 malignant gliomas (including 6 gliosarcomas) and 3 metastatic melanomas with the monoclonal antibodies KL1 and HMB-45. All cerebral metastatic carcinomas and 4/6 gliosarcomas were positive for KL1, whereas all melanomas, 2 metastatic carcinomas and 3 gliosarcomas showed an immunostaining with HMB-45. All gliosarcomas were positive with at least one of the tested anti-cytokeratin antibodies. The gliosarcomas did not show an immunoreaction in any of the cases when CEA, HEA 125, Ber-EP4, EMA or Leu M1 were applied. In our opinion, the monoclonal antibodies HEA 125 and Ber-EP4 could obviously be helpful in differentiating gliosarcomas from metastatic carcinomas.
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PMID:Epithelial and melanoma antigens in gliosarcoma. An immunohistochemical study. 159 90

The clinicopathologic features of 44 serous borderline tumors (SBT) of the ovary were evaluated. Nineteen were Stages II and III, and 9 had invasive peritoneal implants. All 19 patients received chemotherapy and 4, who had invasive implants, died of disease after 3, 4.3, 8, and 9 years. The other 25 patients were free of tumor 1-14 years (mean, 5.3 years) after surgery. Coexpression of low molecular weight keratins (AE1, CAM 5.2) and vimentin was found in all tumors and their implants. No significant differences were found between SBT with different volume-corrected mitotic indices (M/Vi) with respect to gross features, presence or absence of implants, stage, and survival. Cytometric DNA analysis also was performed on the primary ovarian tumors and the implants. Twenty-one primary tumors had diploid or tetraploid histograms, and 23 had aneuploid histograms. DNA ploidy of the primary ovarian tumors did not correlate with gross features, the presence or absence of implants, M/Vi, stage, and survival. The data from this study confirm that most SBT are clinically benign, but SBT with invasive implants may behave aggressively. Expression of intermediate filaments, M/Vi, and DNA ploidy evaluation of the primary ovarian tumors seem to be of no value in predicting prognosis. However, four of seven patients with aneuploid DNA implants died of tumor.
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PMID:Serous borderline tumors of the ovary. A clinicopathologic, immunohistochemical, and quantitative study of 44 cases. 160 37

Poorly differentiated Sertoli-stromal cell tumors and carcinosarcomas of the ovary both show biphasic epithelial and stromal patterns and may both show heterologous stromal elements, presenting a difficult diagnosis. We studied the immunohistochemical profile of Sertoli cell differentiation in human testes and applied these findings to the ovarian tumors. Eleven Sertoli-stromal cell tumors, six carcinosarcomas of the ovary, and 11 testes (six fetal, one infant, and four adult) were studied using antibodies to cytokeratin AE1:AE3 (AE1:3), cytokeratin CAM 5.2 (CAM), epithelial membrane antigen (EMA), vimentin, desmin, muscle-specific actin (MSA), S-100 protein (S-100), CA 19-9, CA 125, carcinoembryonic antigen monoclonal (CEA-M), carcinoembryonic antigen polyclonal (CEA-P), and placental alkaline phosphatase (PLAP). In the fetal testes, immature gonadal stroma and sex cord areas stained with vimentin (six of six cases), AE1:3 (five of six cases), and CAM (six of six cases). Sertoli cells in immature gonadal stroma areas, sex cords, and seminiferous tubules of normal fetal, infant, or adult testes never showed immunoreactivity for EMA, S-100, CA 19-9, CA 125, CEA-M, CEA-P, or PLAP. All Sertoli-stromal cell tumors stained with AE1:3 and CAM in areas of Sertoli cell differentiation (11 of 11 cases) but did not stain with EMA, PLAP, CEA-P, CEA-M, CA 19-9, CA 125, or S-100 (none of 11 cases). Carcinosarcomas expressed AE1:3 and CAM in all epithelial areas (six of six cases) and most stromal areas (five of six cases). Carcinomatous areas of carcinosarcoma also showed immunoreactivity for EMA (six of six cases), CA 125 (two of six cases), PLAP (two of six cases), CEA-P (two of six cases), and CEA-M (one of six cases), while stromal areas of carcinosarcoma expressed EMA (four of six cases) and S-100 (four of six cases). Heterologous stromal elements were present in three of 11 Sertoli-stromal cell tumors (two showed skeletal muscle and one showed both skeletal muscle and cartilage differentiation) and in four of six carcinosarcomas (one skeletal muscle, one cartilage, and two cartilage and skeletal muscle). All skeletal muscle heterologous elements expressed desmin, vimentin, and MSA. The heterologous cartilage in carcinosarcoma stained with S-100 (three of three), while the one case of heterologous cartilage in Sertoli-stromal cell tumor did not. These results suggest that ovarian Sertoli-stromal cell tumor can be distinguished from carcinosarcoma by the absence of staining for EMA, PLAP, CEA, CA 125, or CA 19-9 in epithelial areas of Sertoli-stromal cell tumor.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Utility of immunohistochemistry in distinguishing ovarian sertoli-stromal cell tumors from carcinosarcomas. 161 79

Epidermotropic neuroendocrine carcinoma (NEC) is rare. Based on such a case in an 88-year-old woman with a facial NEC showing epidermotropism with a pagetoid growth pattern, we asked whether several similar tumors involving the epidermis could be easily differentiated by immunohistochemical methods. We constructed a panel of control cases (2 each) for NEC, clear cell Bowen's disease (CCBD), Paget's disease (PD), superficial basal cell carcinoma (SBCC), cutaneous T-cell lymphoma (CTTL), and superficial spreading malignant melanoma (SSMM) to compare with our patient. A panel of antibodies including epithelial membrane antigen (EMA), neuron specific enolase (NSE), AE1/3 cytokeratin (CK), carcinoembryonic antigen (CEA), leukocyte common antigen (LCA), S-100, and HMB-45 were applied. Cutaneous NEC controls and our patient's tumor were strongly positive for EMA and NSE and had paranuclear dot-like cytoplasmic positivity for CK. CCBD was moderate to strong for CK. PD was strong for CEA. SBCC was essentially negative for all. CTLL was strong for LCA. SSMM was strong for S-100 and HMB-45. Controls were either negative or weak for the antibodies not mentioned. We conclude that this antibody panel can reliably differentiate these epidermotropic or juxtaepidermal tumors in diagnostic dermatopathology and should be applied to lesions requiring separation beyond H & E capabilities, especially with superficial shave biopsies showing small cell "Pagetoid" growth patterns.
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PMID:Epidermotropic neuroendocrine carcinoma. Immunohistochemical differentiation from simulators, including malignant melanoma. 164 47

Merkel cell carcinoma is a primary cutaneous neuroendocrine carcinoma occurring commonly in the head and neck of middle-aged and elderly patients. While not very rare, this disease has never been reported in Taiwan. We report the clinical and pathologic features of three patients with Merkel cell carcinoma. The patients included one male (aged 56) and two females (aged 70, 80). The primary sites of the tumors were the hand in one patient and the head and neck in two. Two patients had regional lymph node metastasis. Case 1 had concurrent chronic arsenicalism with multiple Bowen's disease and squamous cell carcinoma of the skin. Histopathology revealed tumor cell infiltration throughout the dermis. In two cases, the tumor cells were small, round and non-cohesive, like lymphocytic infiltrates. In Case 3, however, they were large, oval and formed in nests. The tumor cells were keratin (AE1), neuron-specific enolase and chromogranin positive by immunohistochemical staining. Electronmicroscopy in Case 1 revealed a few cytoplasmic intermediate filaments and neurosecretory granules. Therapy consisted of radiation in 2 patients and surgery in 1; one died during radiotherapy, the other two survived and showed no signs of recurrence at 10 and 21 months.
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PMID:[Merkel cell carcinoma: report of three cases]. 168 94

Six cases of conjunctival spindle cell carcinoma, a rare variant of squamous cell carcinoma, were studied. The median age of the three men and three women was 63.5 years. The tumors appeared as a single nodule in some patients or diffusely involved the conjunctiva in others. Two of the four individuals with intraocular extension presented with phthisis bulbi. Polyclonal antikeratin antibody was helpful and gave the most consistent results when compared with monoclonal antikeratin antibodies, AE1/3 and PKK1. The electron microscopic study of four lesions also established the epithelial nature of the tumor cells. Intracytoplasmic tonofilaments and a few desmosomes were present. Histopathologically, this variant of squamous cell carcinoma is difficult to distinguish from other spindle cell tumors, and this study demonstrates the value of immunohistochemistry and electron microscopy in supporting the correct diagnosis.
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PMID:Spindle cell carcinoma of the conjunctiva. An immunohistochemical and ultrastructural study of six cases. 169 22

The authors studied by immunohistochemistry the intermediate filament (IF) protein profile of 66 frozen samples of breast tissue, including normal parenchyma, all variants of fibrocystic disease (FCD), fibroadenomas, cystosarcoma phylloides, and ductal and lobular carcinomas. Monoclonal antibodies (MAbs) to cytokeratins included MAb KA 1, which binds to polypeptide 5 in a complex with polypeptide 14 and recognizes preferentially myoepithelial cells; MAb KA4, which binds to polypeptides 14, 15, 16 and 19; individual MAbs to polypeptides 7, 13, and 16, 17, 18, and 19, and the MAb mixture AE1/AE3. The authors also applied three MAbs to vimentin (Vim), and three MAbs to glial filament protein (GFP). Selected samples were studied by double-label immunofluorescence microscopy and by staining sequential sections with some of the said MAbs, an MAb to alpha-smooth muscle actin, and well-characterized polyclonal antibodies for the possible coexpression of diverse types of cytoskeletal proteins. Gel electrophoresis and immunoblot analysis also were performed. All samples reacted for cytokeratins with MAbs AE1/AE3, although the reaction did not involve all cells. Monoclonal antibody KA4 stained preferentially the luminal-secretory cells in the normal breast and in FCD, whereas it stained the vast majority of cells in all carcinomas. Monoclonal antibody KA1 stained preferentially the basal-myoepithelial cells of the normal breast and FCD while staining tumor cell subpopulations in 4 of 31 carcinomas. Vimentin-positive cells were found in 8 of 12 normal breasts and in 12 of 20 FCD; in most cases, Vim-reactive cells appeared to be myoepithelial, but occasional luminal cells were also stained. Variable subpopulations of Vim-positive cells were noted in 9 of 20 ductal and in 1 of 7 lobular carcinomas. Glial filament protein-reactive cells were found in normal breast lobules and ducts and in 15 of 20 cases of FCD; with rare exceptions, GFP-reactivity was restricted to basally located, myoepithelial-appearing cells. Occasional GFP-reactive cells were found in 3 of 31 carcinomas. Evaluation of sequential sections and double-label immunofluorescence microscopy showed the coexpression of certain cytokeratins (possibly including polypeptides 14 and 17) with vimentin and alpha-smooth muscle actin together with GFP in some myoepithelial cells. The presence of GFP in myoepithelial cells was confirmed by gel electrophoresis and immunoblotting. Our results indicate that coexpression of cytokeratin with vimentin and/or GFP is comparatively frequent in normal basal-myoepithelial cells of the breast.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Coexpression patterns of vimentin and glial filament protein with cytokeratins in the normal, hyperplastic, and neoplastic breast. 170 Jun 18

A panel of seven monoclonal antibodies including anti-vimentin, anti-keratin markers AE1/AE3 and EAB902, human milk fat globule (HMFG-2), B72.3, anti-carcinoembryonic antigen (CEA), and anti-Leu-M1 were used for an immunoperoxidase staining assay to determine their value in the differentiation of pleural mesothelioma from lung adenocarcinoma. Anti-vimentin positively identified 86% of the mesotheliomas and none of the adenocarcinomas. AE1/AE3, EAB902, and B72.3 reacted with a high percentage of both mesothelioma and adenocarcinoma specimens. With HMFG-2, both membrane and cytoplasmic staining was observed in 92% of the adenocarcinomas and in 14% of the mesotheliomas, whereas 26% of the mesotheliomas only exhibited membrane staining. Eighty percent of the adenocarcinomas and 8% of the mesothelioma tissues stained with anti-Leu-M1. Anti-CEA did not react with any of the 50 mesotheliomas tested but did react with 95% of the lung adenocarcinomas tested. From this study, it was concluded that anti-CEA and anti-Leu-M1 were the most effective of the seven tumor markers evaluated; and that 100% of the pleural mesothelioma tissues could be correctly differentiated from lung adenocarcinomas using a panel consisting of anti-vimentin, HMFG-2, anti-CEA and anti-Leu-M1 monoclonal antibodies.
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PMID:Immunohistochemical evaluation of seven monoclonal antibodies for differentiation of pleural mesothelioma from lung adenocarcinoma. 170 54


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