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)

Metastatic prostate carcinomas in autopsy cases from three populations 49 cases of indigenous Japanese, 29 cases of Japanese Americans and 14 from whites in Hawaii) were compared in terms of their clinicopathological, immunohistochemical (tenascin and ras p21) and lectin binding (Helix Pomatia antigen, HPA) properties. Only the clinicopathological features were analyzed in the cases of whites in Hawaii. The results indicate that poorly differentiated carcinoma is less common, whereas distant metastasis is more frequent, in indigenous Japanese. Some of the Japanese-American cases with poorly differentiated carcinomas did not show any distant metastases. HPA and ras p21 expression are more common, but tenascin is less common in indigenous Japanese. HPA expression is more common in cases with metastasis, especially with metastasis to the bone and other organs, than nonmetastatic cases. Prostatic cancer cases in indigenous Japanese were more aggressive biologically than those in Japanese Americans, but no phenotypic differences were seen relevant to the presence or absence of bone metastases.
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PMID:Comparative study of prostatic carcinoma bone metastasis among Japanese in Japan and Japanese Americans and whites in Hawaii. 128 3

A human prostate cancer model was established by inoculating a prostate specific antigen (PSA)-producing LNCaP cell line with either prostate or bone fibroblasts. Alternatively, this human prostate cancer model can also be established by inoculating LNCaP cells with growth factor(s) (GFs) and extracellular matrix (ECM) immobilized on Gelfoam. The resulting LNCaP tumors were used to evaluate PSA production and excretion in athymic hosts. This model was also employed to examine the biochemical nature of mesenchymal cell-derived growth-promoting protein(s) and to assess the efficacy of potential chemotherapeutic agents. Because of the propensity of human prostate cancer to metastasize to the bone, this study defined a 1.0 M NaCl-eluted fraction, MS1, from the conditioned medium of a bone stromal cell line (MS) by heparin-affinity column chromatography. The growth-promoting activity was assayed both in vivo (e.g., tumor formation) and in vitro (e.g., soft agar colony formation). We found that the growth-promoting activity was trypsin- and heat-sensitive, and partially degraded by acid and dithiothreitol. Immunochemical studies indicated that the polyclonal antibody raised against MS1 blocked the growth-promoting effect elicited by the bone-conditioned media. This growth-promoting factor was found to be immunochemically dissimilar to KGF, HGF, and bFGF. However, addition of bFGF, HGF and NGF, but not aFGF, TGF beta, IGF1, IGF2, PDGF, EGF, TGF alpha and KGF, stimulated anchorage-independent growth of prostate cells, a condition closely parallel to tumor formation in vivo. We found that the MS1 fraction also contained fibronectin and tenascin but not laminin or collagen IV.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human prostate cancer model: roles of growth factors and extracellular matrices. 128 80

Tenascin is a fibroblast product and extracellular matrix protein probably excerting a fibronectin-antagonizing role. Tenascin is broadly distributed interstitially during embryogenesis but restricted to a small range of structures in normal adult tissues. Using tenascin antibodies and an indirect immunoperoxidase method, normal colon, colitis, colon adenomas, and colorectal carcinomas were examined for tissue distribution of tenascin. Normal mucosa displayed a sparce meshwork of microfibrillar tenascin in the lamina propria. The basement membrane was tenascin negative at the bottom of the crypt and developed into a positive band steadily broadening towards the mucosal surface. In colitis, this polarity was effaced; the basement membrane was a broad tenascin-positive band nearly throughout while interstitial tenascin was moderately increased. Loss of polarity in tenascin content of the basement membrane was a constant feature of adenomas, inconsistently paralleled by structural alterations in surface qualities and continuity of tenascin pattern of the basement membrane. These were most pronounced in carcinomas, where this interface was often discontinuous and had a rough surface; in addition, interstitial tenascin was considerably increased. In carcinomas, the rough surface aspect of the tenascin pattern of the basement membrane was correlated with presence of lymph node metastases (P = 0.04). It is concluded that alterations in tenascin pattern and content reflect complex disturbances in the interaction of inflamed/neoplastic colon epithelium and underlying matrix, leading to an organoid induction of tenascin in the inflammatory context and to induction together with structural abnormalities in neoplasia.
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PMID:Altered content and distribution of tenascin in colitis, colon adenoma, and colorectal carcinoma. 137 2

The cellular origin of estrogen-induced kidney tumors in male Syrian hamsters has been repeatedly the subject of controversy. Several authors have proposed that the tumors arise from proximal tubules, from a combination of tubular and interstitial stromal cells, or solely from interstitial cells. Because of the model character of this tumor for hormone-associated cancer, it was further investigated in this study with respect to morphology, enzyme and intermediate filament pattern, the expression of alpha-smooth muscle actin and the extracellular matrix proteins fibronectin and tenascin. These analyses were carried out with early and late tumors as well as metastases to determine possible changes in expression of biochemical parameters during the development and progression of this neoplasm. The enzyme histochemical and intermediate filament patterns were usually the same as those described previously for proliferative foci and early tumors, i.e. highly elevated activities of glucose-6-phosphate dehydrogenase, adenylate cyclase and alkaline phosphatase, a lack of glucose-6-phosphatase and gamma-glutamyltransferase and coexpression of vimentin and desmin, alpha-smooth muscle actin could not be detected in early lesions. In five of 24 advanced tumors inclusions of kidney tubules were found which showed various degrees of alteration in their morphology and enzyme histochemical pattern, but were often directly connected with tubular segments of normal appearance outside the tumor. Like the normal tubules, the enclosed tubular segments were strongly positive for cytokeratin but never expressed vimentin or desmin. Among the 24 tumors studied, two contained cysts which expressed cytokeratin and sometimes also vimentin but not desmin. The enzyme histochemistry of the cells lining the cysts was similar to that of the surrounding tumor mass, except adenylate cyclase was lacking and alkaline phosphatase was not uniformly distributed. In tumors containing cytokeratin-positive cysts, there often were cytokeratin-positive, vimentin-negative and desmin-negative tumor formations in close contact to these cysts. With the exception of cyst formation, the pattern of metastases were identical to that of the primary tumors. All large tumors and the main component of the metastases expressed vimentin, desmin and fibronectin. Mesothelia surrounding metastatic tumor complexes were positive for vimentin, desmin, alpha-smooth muscle actin, fibronectin, cytokeratin and tenascin. It was concluded from these and previous observations on early stages of tumor development that the estrogen-induced hamster kidney tumor originates from mesenchymal interstitial cells (probably pericytes) which may rarely acquire an epithelial phenotype by metaplastic transformation during tumor progression.
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PMID:Changes in the cellular phenotype and extracellular matrix during progression of estrogen-induced mesenchymal kidney tumors in Syrian hamsters. 171 81

We have studied expression of tenascin (TN) in colonic carcinoma cells from 81 patients with colonic carcinoma without (20) and with (61) lymphogenous metastases, in order to assess whether TN plays a role in local invasiveness and metastasis of tumors. In metastatic colonic carcinoma tissues from 52 cases, moderate, partial expression of TN was observed in the primary foci but no TN expression was observed in tissues from 9 others. However, in every case of nonmetastatic colonic carcinoma, very strong TN expression was observed in the tissues. Furthermore, the presence of dense TN accumulation correlated well with the prognoses (1-year survival) of colonic cancer patients (p less than 0.01). Weak TN expression was observed in 24/61 of the metastatic lymph nodes examined. In 2 patients with metastatic colonic carcinoma, the colonic cancer cells produced TN. TN may, therefore, play a role in limiting or preventing local tumor invasion rather than preventing metastasis and is a useful marker for predicting the prognoses of patients with colonic cancer.
Invasion Metastasis 1991
PMID:Reduced tenascin expression in colonic carcinoma with lymphogenous metastasis. 172 10

Ten patients with intracranial malignancies were studied by radioimmunoscintigraphy with I-131 BC-2 MoAb. Sensitivity and specificity of radioimmunoimaging were determined and compared with the results obtained with computed X-ray tomography and magnetic resonance imaging. BC-2 MoAb is a murine IgG1 anti-tenascin, which is not expressed by adult normal brain and has been found in large amount in gliomas and/or cerebral metastases, as well as other human tumors. Gamma-camera images obtained at 1 to 4 days exhibited increasing uptake of BC-2 in eight tumors, with varying degrees of contrast with the surrounding normal brain. Two lesions resulted negative to RIS: a meningioma and an oligodendroglioma. Specific tumor uptake of I-131 BC-2 was determined, by external gamma imaging, and ranged from 0.002 up to 0.007 percent of injected dose. Nonspecific uptake in the tumor was determined injecting 99m-Tc-FO23C5 (an isotype-matched control IgG1) in four patients and it was lower than 0.0001% ID. I-131 BC-2 tumor/nontumor ratios, measured using the geometric mean on digital images, ranged from 3 to 7.5:1. This study demonstrates that the tumor uptake of BC-2 in patients with glioma was due to specific processes.
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PMID:Human gliomas radioimmunoimaging with 131-I BC-2 murine IgG: preliminary report. 209 14

Tenascin is a large extracellular matrix glycoprotein which is widely distributed in normal, hyperplastic and neoplastic tissues. Its function is unknown but it has been associated with the epithelial-stromal interactions, such as cell adhesion and movement which take place, e.g. in morphogenesis, cellular proliferation and neoplasia. In this study, we investigated tenascin expression in 70 benign, dysplastic and malignant melanocytic tumors by using immunohistochemistry and monoclonal anti-tenascin 143DB7C8 antibody on paraffin sections. In all types of benign nevi, both intradermal, compound and junctional, there was a moderate expression of tenascin at the dermoepidermal junction and in the papillary dermis. In dysplastic nevi, the fibrotic areas in the papillary dermis also showed a moderate staining for tenascin. Invasive malignant melanomas showed the strongest expression of tenascin. In addition to the staining at the dermo-epidermal junction and in the papillary dermis, there was a variable expression of tenascin in the reticular dermis. Intracytoplasmic tenascin was detected both in primary melanomas and melanoma metastases. In conclusion, we have shown that tenascin expression is moderately increased in benign and dysplastic melanocytic tumors and greatly increased in malignant melanomas and melanoma metastases. The function of tenascin may be related to the cellular-stromal interactions and it is possibly associated with the proliferation and spread of the melanocytic tumors.
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PMID:Increased tenascin expression in melanocytic tumors. 753 53

The immunohistochemical expression of tenascin was examined in the normal adult mucosa of the stomach, primary tumours and lymph node metastases of gastric cancer patients. In normal gastric tissue tenascin was expressed in the muscularis mucosae, muscularis propria and vessel walls, however it was not expressed in either the mucosal connective tissue or the stromal tissue in the submucosal layer. In gastric cancer, tenascin was expressed in 35 of 85 primary tumours, and in 8 of 25 metastases in lymph nodes. Tenascin was located in the fibrous stroma surrounding foci of cancer. The expression of tenascin in the primary tumour did not correlate with the depth of invasion, lymph node metastasis or prognosis. Tenascin appears during the process of either malignant transformation or tumour progression in gastric cancer, and the positive expression of tenascin may be useful as a stromal marker for the early detection of gastric cancer.
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PMID:Immunohistochemical expression of tenascin in normal stomach tissue, gastric carcinomas and gastric carcinoma in lymph nodes. 882 73

Tenascin serum levels were evaluated in 118 patients with primary colorectal carcinoma and in a control group of 51 healthy persons in a double-sided sandwich ELISA. The data were correlated with post-operative TNM-staging. Patients with colorectal carcinomas had significantly higher serum levels of tenascin than the control group. At the 95% level of specificity, sensitivity was 25%. Tumor grading obviously had no influence on the level of tenascin in serum. With increasing pT-category, tenascin levels increased as well. In patients with distant metastatic disease, serum tenascin levels were significantly higher than in patients without distant metastases. These data suggest that, in colorectal carcinoma, the preoperative level of serum tenasin reflects the total tumor burden and correlates with metastatic disease. Our observation warrants a prospective study of the relevance of tenascin serum levels with regard to prognosis and as an indicator of relapse.
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PMID:Significance of tenascin serum level as tumor marker in primary colorectal carcinoma. 754 44

Tenascin, a large glycoprotein of the extracellular matrix, is involved in cell proliferation, differentiation, and migration during embryogenesis. In adult tissue, it is expressed only in certain areas. However, it gains importance again in proliferative processes such as wound healing and especially in tumor development. We examined paraffin-embedded specimens of 25 patients with a squamous cell carcinoma of the esophagus, 5 patients with an adenocarcinoma of the small intestine, 4 patients with a carcinoid tumor of the small intestine, and 49 patients with an adenocarcinoma of the colorectum. Immunohistochemical staining was performed by the use of a monoclonal antibody against human tenascin and the avidin-biotin-complex technique. Amino-Ethylcarbazol served as a chromogen. We investigated the distribution of tenascin in tumors, normal tissue, and lymph node metastases and compared it to tumor grading and TNM-classification. We found a uniform pattern of tenascin expression in all tumors and lymph node metastases examined in the gastrointestinal tract. One pattern was characterized by an immunoreaction near the basement membrane in well-differentiated areas and the other showed a diffuse, network-like expression in poorly differentiated areas with abundant stroma. There was a more intensive staining of the surrounding stroma near tumor cells invading into the submucosa or muscularis propria. It was even possible to detect small early carcinomas as well as small tumor cell populations in and around the lymph nodes by a strong immunostaining of the surrounding stroma. But we could not find any correlation of the tenascin expression patterns in comparison to the tumor grading and TNM-classification.
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PMID:Expression of tenascin in tumors of the esophagus, small intestine and colorectum. An immunohistochemical study. 854 91


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