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Query: UMLS:C0027651 (tumor)
 685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of localized fibrous tumor (LFT) (localized fibrous mesothelioma) of the liver in an 83-year-old woman is presented. The tumor was 15 x 9 x 8 cm and was confined to the left lateral segment of the liver. Occasional mitotic figures (MF) (2 to 3 per 50 high-power fields [HPF]) were present. Strong, diffuse vimentin positivity was demonstrated by immunohistochemistry. Immunoreactivity for cytokeratins (AE1-3), epithelial membrane antigen (EMA), desmin, and desmosomal proteins (desmoplakin I + II) was absent. Electron microscopic examination showed a mesenchymal appearance of the majority of neoplastic cells, with a few ultrastructural features suggestive of mesothelial differentiation. These findings supported a submesothelial origin of the tumor. After a partial hepatectomy with total gross and microscopic removal of the tumor, the patient was alive without recurrence at 2 years, 5 months later. A review of the English literature showed six additional cases that are probably similar. Currently, all tumors have been clinically benign, although follow-up information has been limited.
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PMID:Localized fibrous tumor (localized fibrous mesothelioma) of the liver. 247 68

We have undertaken an analysis of hemidesmosomes (HD) and their associated structures, intermediate filaments (IF) and anchoring fibrils (AF), in various types of basal cell carcinoma (BCC). Using a combination of electron microscopy and immunofluorescence microscopy we show that there is a correlation between the loss of HD and tumor type (i.e., in solid and infiltrative BCC hemidesmosomes are present, sometimes in reduced numbers), while there appears to be a lack of hemidesmosomes in cells of sclerosing specimens. Moreover, even though there is a loss of cytoplasmic constituents of the HD in sclerosing forms of BCC, this is not the case with regard to collagen VII, a component of AF, which are normally associated with the extracellular side of the HD. Collagen VII is localized to the basement membrane zone of tumor cells in the absence of the cytoplasmic constituents of HD. Furthermore, deposits of collagen VII occur in the connective tissue close to tumor cell populations in all but one of the BCC specimens we analyzed. In addition to modifications in HD and AF in BCC tissue, there are changes in the cytoskeletal elements of both tumor cells and the normal appearing epidermis that overlies tumor areas. In sclerosing BCC microfilaments are commonly observed along the basal portions of tumor cells where they abut the connective tissue. IF are often found interacting with these microfilaments. Indirect immunofluorescence analysis of tumor tissue using a monoclonal keratin antibody preparation, AE1, which in normal epidermis stains basal cells, reveals that AE1 antibodies only weakly stain tumor cells. Moreover, in the epidermis that overlies tumor cell regions AE1 antibodies stain suprabasal cells and not basal cells. This change in staining pattern generated by AE1 antibodies appears to depend upon the proximity of tumor cells. These results are discussed in relation to the organization of the HD and its associated AF and IF. The possibility that HD, IF, and AF antibody preparations may be of diagnostic use is raised.
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PMID:Hemidesmosomes, collagen VII, and intermediate filaments in basal cell carcinoma. 247 65

Ovarian endometrioid carcinomas resembling sex cord-stromal tumors (ECSCSs) may simulate Sertoli cell tumors, Sertoli-Leydig cell tumors (SLCTs), and adult granulosa cell tumors (AGCTs), both clinically and pathologically. Differing clinical features and histologic findings are almost always successful in distinguishing these tumor types, although in some cases the differential diagnosis is difficult. Immunohistochemical staining of 17 ECSCSs, 14 Sertoli cell tumors or SLCTs, and 15 AGCTs was performed with the use of antibodies against cytokeratins (AE1/AE3, 902, and CAM 5.2), epithelial tumor-associated antigens (EMA, OM-1, B72.3, and carcinoembryonic antigen B1.1), vimentin, S-100, neuron-specific enolase, and lysozyme to determine the immunohistochemical profile of each tumor type and to define further the nature of the sex cord-like components in ECSCSs. All 17 ECSCSs, none of the 15 AGCTs, and one of 14 Sertoli cell tumors or SLCTs stained with EMA. Staining for OM-1 was almost as helpful diagnostically, with positive results for 15 of 17 ECSCSs, 0/15 AGCTs, and 1/14 Sertoli cell or SLCTs. Antikeratins were immunoreactive with all the ECSCSs as well as some of the AGCTs and Sertoli cell tumors or SLCTs. The B72.3 and B1.1 were immunoreactive with some ECSCSs and Sertoli cell tumors, but were nonreactive with AGCTs. Neuron-specific enolase was demonstrated in 11 of 17 ECSCSs, two of 14 Sertoli cell tumors or SLCTs, and 0 of 15 AGCTs. Vimentin, S-100, and lysozyme were least helpful in the differential diagnosis. These studies suggest that an immunohistochemical approach may be useful in the differentiation of ECSCSs and sex cord-stromal tumors. Furthermore, it supports the conclusion that the sex cord-like cells in ECSCSs are not Sertoli or granulosa cells, but cells of surface epithelial type growing in architectural patterns similar to those of sex cord-stromal tumors.
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PMID:Ovarian endometrioid carcinomas resembling sex cord-stromal tumors. An immunohistochemical study. 247 93

We studied 23 cases of capillary hemangioblastoma (CHB) of the cerebellum with 17 immunohistochemical cell markers in an attempt to define the nature of the so-called "stromal" cells. These cases were compared to four cases of intracranial metastatic renal cell carcinoma (RCC), which may mimic CHB histologically. The 17 markers studied included vimentin (VIM), Factor VIII-related antigen (FVIIIR:Ag), blood group antigens A, B, and H, Ulex I lectin (Ulex), Alkaline Phosphatase (Alk P), neurofilament protein (NF), glial fibrillary acidic protein (GFAP), S-100 protein (S-100), nerve growth factor receptor (NGFR), muscle-specific actin (MSA), desmin (Des), monoclonal keratin (MKER, including Cam 5.2 and AE1/3), epithelial membrane antigen (EMA), and chromogranin (Chrom). No significant stromal cell staining was seen by markers for endothelial, epithelial, chromaffin, or smooth muscle origin. In some cases individual cells demonstrated positivity for GFAP (4/22) and S-100 protein (13/23); these cells were generally stellate and located near the periphery, and we conclude that these were the result of entrapment of surrounding cerebellum. No case demonstrated NF in stromal cells. However, nearly all cases of CHB showed stromal cell staining with VIM (19/22). In contrast, all of the cases of RCC showed significant staining for at least one marker of epithelial origin (3/4 for MKER and 4/4 for EMA). We conclude that the stromal cell of CHB is neither endothelial, neural, epithelial, pericytic, nor neuroendocrine in origin, and is instead of undifferentiated mesenchymal origin. The designation of this tumor as an "hemangioblastoma," although a misnomer, is firmly established in the literature and should probably be retained.
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PMID:A detailed immunohistochemical analysis of cerebellar hemangioblastoma: an undifferentiated mesenchymal tumor. 247 46

Acetone-fixed frozen sections of 15 malignant melanomas of the skin with metastases were studied immunohistochemically for the presence of different types of intermediate filament proteins, synaptophysin, muscle cell actins, and desmoplakins. One of the melanomas was a primary toe tumor, and the others mainly regional lymph node metastases. The original diagnosis of melanoma was reconfirmed in each case, and the melanoma diagnosis of the metastases was verified by S100 protein immunostaining in all cases and by a monoclonal antibody to melanoma cells (NK1C3) in 7 cases. All melanomas were prominently vimentin-positive. In 10 of 15 cases, immunoreactive keratin could be demonstrated with antibody CAM 5.2. The presence of keratins was confirmed in selected cases with three other monoclonal antibodies including AE1, PKK1, and a monoclonal antibody specific for keratin number 18. Desmoplakin, another marker of epithelial differentiation, was not found in melanoma cells. Two melanomas contained neurofilament-positive tumor cells, which were however negative for synaptophysin. Desmin, muscle actins, and glial fibrillary acidic protein were not found in the neoplastic cells. On the basis of the present results one could conclude that the protein composition of the cytoskeleton of melanomas is more complex than has been previously thought and most importantly that melanomas may contain keratins.
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PMID:Immunohistochemical spectrum of malignant melanoma. The common presence of keratins. 248 Nov 51

A monoclonal antikeratin antibody, EKH4, was produced from a hybridoma cell line which was established by fusing P3X63SAg8 mouse myeloma cells with spleen cells of mice immunized with human trichilemmoma cells. Immunoblot analysis showed that EKH4 antibody reacts predominantly with 50 kilodalton keratin polypeptide in normal epidermis. By indirect immunofluorescence and immunoperoxidase techniques, EKH4 antibody reacted with the lower 2-3 cell layers of the epidermis as well as most cells of pilosebaceous follicle of human and animal skin. Tumor cells of human basal cell epitheliomas and squamous cell carcinomas were also stained with this antibody. The staining was much more regular and intense compared with an available monoclonal antikeratin antibody, AE1. In the lesion of epidermal proliferative disorders, such as psoriasis and actinic keratosis, the entire epidermis instead of the lower layers was stained with EKH4 antibody. Normal skin overlying or adjacent to epithelial tumors also showed positive staining in the entire epidermis. By using indirect immunoperoxidase technique, EKH4 also stained alcohol-fixed, paraffin-embedded tissue sections.
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PMID:Monoclonal antikeratin antibody: production, characterization, and immunohistochemical application. 258 61

The clinical and pathologic findings of four cases of palpable sclerosing adenosis of the breast, called "adenosis tumor", are reported. Adenosis tumor is a rare lesion that clinically and sometimes histologically is misinterpreted as mammary carcinoma. In our study, adenosis tumor was detected in four women of 35-39 years (average 37 years). All cases were treated by local excision. None of the lesions had recurred at follow-up, 1-3 years later. Microscopically the most frequent growth pattern was classical sclerosing adenosis. Other findings were epitheliosis, collagenous spherulosis, microcysts, apocrine metaplasia and radial scars. Only in one case were detected foci of lobular carcinoma in situ. With immunoperoxidase staining, the proliferating cells stained positively for cytokeratin (AE1/AE3) and actin, revealing epithelial and myoepithelial differentiation. Coexpression of actin, S-100 protein and GFAP was detected in numerous stromal myofibroblast-like cells. In sclerosing adenosis and in radial scar the tubules were surrounded by a continuous intact basement membrane composed of type IV collagen, whereas in tubular carcinoma basement membranes are almost entirely absent.
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PMID:[Nodular sclerosing adenosis (adenosis tumor) of the breast. An immunohistologic study particularly in reference to the relationship with radial cicatrix and to the differential diagnosis with tubular carcinoma]. 264 38

Two patients developed sinonasal small-cell neoplasms that arose 22 years and 37 years, respectively, following radiotherapy for bilateral retinoblastomas. The tumors were composed of small cells with scant cytoplasm and had a few scattered Homer-Wright rosettes. Immunohistochemically, one tumor was positive for keratin (CAM 5.2 and AE1/AE3), epithelial membrane antigen, and neuron-specific enolase. The other neoplasm was immunoreactive for keratin (CAM 5.2 only) and neuron-specific enolase; it also had focal immunopositivity for S-100 protein, desmin, and muscle-specific actin. Both were negative for CEA, vimentin, melanocyte-specific antigen (HMB45), chromogranin A, synaptophysin, Leu-7, 200 kd neurofilament, and retinal S-antigen. Despite aggressive multimodal therapy, the patients died of metastatic tumor 7 months and 10 months following their initial diagnosis, respectively. Although osteosarcoma is the most frequent second cancer following bilateral retinoblastomas, some patients develop clinically aggressive sinonasal small-cell tumors that are difficult to place into conventional classifications. Both of our cases showed evidence of multidirectional differentiation; one tumor labeled with epithelial and neural markers, and the other expressed epithelial, neural, and myogenous antigens.
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PMID:Unusual sinonasal small-cell neoplasms following radiotherapy for bilateral retinoblastomas. 267 54

The clinical and pathologic features of 13 cases of juvenile granulosa cell tumor were studied. Patients' ages ranged from 6 months to 56 years (median age, 17 years). Only one patient was postmenopausal. Three premenarchal patients had isosexual development. Five of seven postmenarchal patients had menstrual abnormalities, and two patients demonstrated virilization. Ascites was present in two patients. All patients had unilateral stage I tumors, ranging from 2.5 to 24.5 cm in greatest dimension (mean greatest dimension, 12.2 cm). Characteristic histologic features included nodular architecture, follicle formation, abundant interstitial and intrafollicular acid mucopolysaccharide-rich fluid, irregular microcysts, individual cell necrosis, and high mitotic activity (mean activity, 11 mitotic figures per ten high-power fields). The interstitial mucinous fluid consisted predominantly of hyaluronic acid. Immunohistochemical staining in five cases showed prominent positivity for vimentin (four cases), isolated cytokeratin AE1/3-positive cells (two cases), and nonreactivity for carcinoembryonic antigen and milk fat globule-2. Ultrastructurally, epithelial cells that resembled granulosa cells of the nonneoplastic preovulatory follicle and occasional cells with steroidogenic organelles were also found. Follow-up of ten patients revealed no tumor recurrences from six months to 33 years (mean, 9.5 years) after operation.
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PMID:Juvenile granulosa cell tumors of the ovary. 291 Feb 25

Immunoreactivity for endocrine peptides (serotonin, gastrin, somatostatin, insulin, corticotropin, calcitonin, neurotensin, vasoactive intestinal peptide, and bombesin), cytoskeletal proteins (high and low molecular weight keratins), and tumor differentiation markers (chromogranin, neuron-specific enolase, carcinoembryonic antigen, S100 protein, and Grimelius stain) was sought on nine cervical and one vaginal poorly differentiated small-cell carcinoids. Dense-core secretory granules were ultrastructurally identified in all cases (seven of ten) in which tissue was available for electron microscopy. Immunoreactivity for endocrine secretory products was rarely noted, and only in a minority cell population (serotonin in two of ten). The majority of the tumors exhibited immunoreactivity for low molecular weight keratin (AE1/AE3 in eight of ten; CAM 5.2 in seven of nine), and three of ten tumors focally expressed high molecular weight keratin. Among the markers of neuroendocrine differentiation, neurospecific enolase was more frequently expressed (ten of ten) than chromogranin (five of ten) or argyrophilia (three of ten). Carcinoembryonic antigen was present in eight of ten tumors. S100 protein was absent in all cases. In summary, poorly differentiated small-cell carcinoids of the lower female genital tract, similarly to other small-cell endocrine tumors, occasionally exhibit focal glandular and squamoid differentiation, and only relatively infrequently or focally express immunohistochemically detectable endocrine secretory products, chromogranin, and argyrophilia.
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PMID:Endocrine and tumor differentiation markers in poorly differentiated small-cell carcinoids of the cervix and vagina. 302 70


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