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)

The level of transglutaminase (TGase) expressed in various tumor cell lines was investigated. We found that each cell line could be categorized into three distinct groups, that is, (i) cell lines with low or negligible TGase activity, (ii) cell lines with significant or high TGase activity and immunoreactive to a monoclonal antibody against tissue type TGase, and (iii) cell lines with significant or high TGase activity but not immunoreactive to the antibody. Results reported here argue against the former proposal that tissue-type TGase is expressed at a lower level in malignant cells compared to the level in normal cells.
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PMID:Tissue-type transglutaminase is not a tumor-related marker. 872 Jan 45

The highly metastatic human melanoma cell line BLM was transfected with the E1A or E1A + E1B regions of adenovirus 5 (Ad5). A series of progression markers, correlated with the malignant phenotype of parental BLM (including calcyclin, thymosin beta 10, plasminogen activator inhibitors types 1 and 2, urokinase type and tissue type plasminogen activators, vimentin, tissue type transglutaminase, and interleukin-6), was collectively repressed in the transfectants, whereas several control genes were not affected or even induced. The apparently coordinate repression of a set of markers by the same regulator gene, Ad5 E1A in this case, suggests the existence of one pathway under the control of a main switch and predicts that one or more as yet unidentified cellular master genes normally exert this function. A reduced oncogenicity was observed after subcutaneous inoculation of the E1A transfectants into nude mice and provides additional evidence in support of a tumor suppressor function of Ad5 E1A.
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PMID:Simultaneous suppression of progression marker genes in the highly malignant human melanoma cell line BLM after transfection with the adenovirus-5 E1A gene. 878 Jun 94

Multinucleated giant stromal cells (MGSC) have been described in a variety of lesions of various anatomical sites. They are generally believed to be derived from fibroblasts or myofibroblasts. Their size and bizarre appearance may lead to an erroneous interpretation of infiltrating malignant cells, but they are regarded as reactive in nature. MGSC also seem to participate in a neoplastic process and form a part of tumors called giant cell fibroblastomas (GCF). In GCF, multinucleated giant cells are sparsely scattered throughout the tumor, which is composed of loosely arranged spindle cells. Thus far, no tumor composed of MGSC entirely, to the best of the authors' knowledge, has been reported. This study involved an 80-year-old female with an omental tumor, which is believed to represent the first case of tumor of MGSC. The patient developed abdominal pain; a large abdominal tumor measuring 18 x 15 x 5 cm by computerized tomography was found located between the left lobe of the liver, the transverse colon, and the greater curvature of the stomach. Although the tumor was adherent to the above organs and infiltrating the omentum, it was resectable. Grossly, the tumor was highly vascular and the surface was shaggy with no recognizable capsule. The cut surfaces were red to tan with frequent cystic spaces containing bloody material. Microscopically, the tumor cells were large and multinucleated (2-6 nuclei) with prominent nucleoli. The cytoplasm was abundant and stained amphophilic. These tumor cells formed moderately cellular sheets filling the spaces between the varying sized vessels. There was prominent vascularity throughout the tumor. DNA study by image analysis revealed aneuploidy peaks. On immunohistochemistry, the tumor cells were strongly positive for vimentin, moderately positive for actin along the periphery of the cytoplasm, and negative for cytokeratin, EMA, myoglobin, S-100, CEA, Factor XIIIa, HMB-45, and HAM56 and KP-1. Ultrastructurally, the cytoplasm contained rich profiles of RER with scattered lysosomes. The cell borders were slightly irregular with occasional subplasmalemmal densities facing loosely arranged collagenous stroma. The light microscopic, immunohistochemical, and electron microscopic features of tumor cells were remarkably similar to MGSC. The tumor size and gross appearance suggested a malignancy, but it was a diploid tumor and the patient remains disease free 5 years after a complete resection.
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PMID:Multinucleated giant stromal tumor of the omentum: report of a case with immunohistochemical and ultrastructural investigation. 878 15

9-cis retinoic acid (9-cis RA) is a retinoid receptor pan-agonist that binds with high affinity to both retinoic acid receptors (RARs) and retinoid X receptors (RXRs). Using a variety of in vivo and in vitro cancer models, we present experimental data that 9-cis RA has activity as a potential chemotherapeutic agent. Treatment of the human promyelocytic leukemia cell line HL-60 with 9-cis RA decreases cell proliferation, increases cell differentiation, and increases apoptosis. Induction of apoptosis correlates with an increase in tissue transglutaminase (type II) activity. In vivo, 9-cis RA induces complete tumor regression of an early passage human lip squamous cell carcinoma xenograft. Finally, 9-cis RA inhibits the anchorage-independent growth of the human breast cancer cell lines MCF-7 and LY2 (an antiestrogen-resistant MCF-7 variant). Transient co-transfection assays indicate that 9-cis RA inhibits estrogen receptor transcription of an ERE-tk-LUC reporter through RAR or RXR receptors. These data suggest that retinoid receptors can antagonize estrogen-dependent transcription and provides one possible mechanism for the inhibition of cell growth by 9-cis RA in breast cancer cell lines. In summary, these findings present evidence that 9-cis RA has a wide range of activities in human cancer models.
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PMID:The efficacy of 9-cis retinoic acid in experimental models of cancer. 882 26

An 11-year-old hispanic female was referred for evaluation of multiple asymptomatic papules which had slowly developed since age two. The patient had no significant medical history and no family members, including an older sibling, were similarly affected. Physical examination revealed multiple 2-6 mm flesh-colored to erythematous papules over the posterior scalp, trunk, and extremities, predominantly in a midline distribution. No lentigines, blue nevi, or evidence of endocrine ab-normalities were noted. Echocardiogram was normal with no evidence of myxoma. Six cutaneous biopsies showed myxomas, as evidenced by well-circumscribed dermal tumors composed of stellate, dendritic cells embedded in a mucinous stroma. Special stains and electron microscopy confirmed the H&E finding. Immunoperoxidase staining for Factor XIIIa was positive in the dendritic tumor cells, suggesting a relationship with dermal dendrocytes. This patient represents a case of multiple cutaneous myxomas without other components of Carney's complex of myxomas, spotty pigmentation, endocrine overactivity, and a variety of uncommon tumors. A long-term follow-up is indicated since some of the above cited elements of the syndrome could appear over time.
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PMID:Multiple cutaneous myxomas. Report of a case without other elements of Carney's complex. 883 75

Tissue transglutaminase (tTG) is postulated to play a role in apoptosis, cell adhesion, metastasis, and extracellular matrix (ECM) assembly. In this study, the distribution and expression of tissue transglutaminase was investigated in normal human mammary tissue and in intraductal and invasive human breast cancer by immunohistochemistry and in situ hybridization. Frozen and formalin-fixed paraffin-embedded sections of normal, intraductal, and invasive human breast carcinoma were examined with an avidin-biotin complex immunoperoxidase method for tTG antigen and by in situ hybridization to determine the cell types expressing tTG mRNA. The expression of tTG in normal and malignant mammary epithelium in culture was evaluated by quantitative immunoblot analysis. Low-level expression of tTG was found in normal tissues with the antigen located in the ECM surrounding the ducts and in the endothelium. In intraductal cancer, there was a marked increased expression of the tTG antigen, and the increased staining was found in the ECM and was also localized in a distinct pattern at the boundary between the in situ tumor cells and the normal tissue. Further immunohistochemical analysis revealed that the cells in this boundary also stained for the endothelial cell markers CD31, CD34, and von Willebrand factor. In invasive tumors, the tTG antigen was no longer localized to the normal tissue/tumor boundary but dispersed around the tumor cells. In situ hybridization studies revealed three distinct compartments of tTG synthesis: (a) tumor cells, (b) endothelial cells, and (c) stromal cells. In addition, normal and malignant epithelial cells in culture expressed variable amounts of tTG, and the expression of tTG in these epithelial cells was at least 17-fold less than endothelial cells. The up-regulation of tTG in intraductal and invasive human breast cancer and its localization to the ECM and neovasculature suggest that tTG may regulate tumor growth and metastasis.
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PMID:Tissue transglutaminase expression in human breast cancer. 894 Dec 10

The histologic and immunohistochemical features of a case of adult solitary cutaneous myofibroma are reported. The lesion consisted of interlacing bundles of spindle cells arranged around small vessels with hemangiopericytomatous appearance. Neoplastic cells were positive for vimentin and actin. Desmin, cytokeratins and Factor XIIIa were negative. Scattered Langerhans cells positive for S-100 protein and CD1a antigen, usually not reported within this type of neoplasm, were also present.
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PMID:Adult solitary cutaneous myofibroma: a case report. 895 May 77

We report on eight cases of a distinct variant of cutaneous schwannoma characterized by prominent Verocay body formation (75-100% of the tumor bulk) that may cause considerable diagnostic difficulties. Like ordinary cutaneous schwannomas, these lesions preferred the head and neck region of young adults without sexual predilection and were clinically interpreted as cyst, basal cell carcinoma, or nevus. Histological examination revealed well-circumscribed nodules. Three of them consisted exclusively of nodular or ribbon-like Verocay bodies. A variable admixture of Antoni A or B type of differentiation (< 25%) was seen in five other cases. The following patterns were seen: fascicular spindle-shaped, onion-like epithelioid, myxoid-hypocellular, and degenerated ("ancient") with prominent fibrosis/hyalinosis and occasional bizarre giant cells. Immunohistochemically, the lesions were positive for S-100 protein (and vimentin) but negative for a broad panel of neurogenic and intermediate filament markers. The capsule showed focal labeling for EMA and--when it was markedly thickened--also for SMA. Labeling with E9, an anti-metallothionein marker indicative of cell activity, was negative, underscoring the slow growth potential of these lesions. No recurrence was seen in the six patients with follow-up information. The differential diagnosis includes other lesions with prominent palisading. (Amianthoid) myofibroblastoma and palisading leiomyoma are consistently positive for SMA and desmin, respectively. Palisading cutaneous fibrous histiocytoma and myofibroblastic dermatofibroma are variably positive for Factor XIIIa, SMA, and E9 and/or NK1C3 (CD57). Palisaded encapsulated neuromas are primarilly differentiated by the presence of nerve fibers with myelin sheaths.
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PMID:Verocay body--prominent cutaneous schwannoma. 1002 39

Pharmacologically safe compounds that can inhibit the proliferation of tumor cells have potential as anticancer agents. Curcumin, a diferuloylmethane, is a major active component of the food flavor turmeric (Curcuma longa) that exhibits anticarcinogenic properties in vivo. In vitro, it suppressed c-jun/Ap-1 and NF-kappaB activation and type 1 human immunodeficiency virus long-terminal repeat-directed gene expression. We examined the antiproliferative effects of curcumin against several breast tumor cell lines, including hormone-dependent and -independent and multidrug-resistant (MDR) lines. Cell growth inhibition was monitored by [3H]thymidine incorporation, Trypan blue exclusion, crystal violet dye uptake and flow cytometry. All the cell lines tested, including the MDR-positive ones, were highly sensitive to curcumin. The growth inhibitory effect of curcumin was time- and dose-dependent, and correlated with its inhibition of ornithine decarboxylase activity. Curcumin preferentially arrested cells in the G2/S phase of the cell cycle. Curcumin-induced cell death was neither due to apoptosis nor to any significant change in the expression of apoptosis-related genes, including Bcl-2, p53, cyclin B and transglutaminase. Overall our results suggest that curcumin is a potent antiproliferative agent for breast tumor cells and may have potential as an anticancer agent.
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PMID:Antiproliferative effect of curcumin (diferuloylmethane) against human breast tumor cell lines. 921 11

An isolated perfused vessel model was used to examine the mechanisms underlying the adhesive interactions between circulating tumor cells and subendothelial matrix in denuded arterioles. Arterioles ranging from 70 to 100 microm in diameter were isolated from rat mesentery, transferred to an isolated vessel chamber, cannulated on both ends with glass micropipettes, and perfused with media containing 10(6) hamster melanoma (RPMI 1856) cells/ml. In a second group of arterioles, the endothelium was denuded by running 2 ml of air through the vessel lumen. Since the tumor cells did not adhere to the vessel wall when perfused at physiologically relevant shear rates, perfusate flow was stopped and the tumor cells were allowed to settle onto the vessel wall for 20 min. After counting the number of tumor cells that settled onto the arteriolar wall, perfusate flow was re-initiated and unattached cells were washed away. The number of cells remaining adherent were counted and the percentage of adherent cells (relative to the total number of cells that settled on to the vessel wall during the period of no-flow) were calculated and compared among different groups. We observed that tumor cells are much more adhesive to denuded arterioles than to intact arterioles. To determine the mechanisms responsible for the adhesive interactions that become established and stabilized during the period of flow reduction, denuded arterioles were treated with fibronectin antiserum or Arg-Gly-Asp (RGD) peptides. Both treatments significantly reduced tumor cell adhesion to denuded arterioles. In subsequent studies, melanoma cells were treated with a transglutaminase inhibitor, monodansylcadaverine (MDC), which reduced the ability of adherent tumor cells to withstand the anti-adhesive effects of a subsequent increase in perfusate flow rate after the period of no-flow. Our data suggest that tumor cells adhere to fibronectin in the subendothelial matrix in denuded arterioles by an RGD-dependent mechanism. Moreover, our observations are consistent with the concept that a transglutaminase-catalysed reaction acts to stabilize the adhesive interactions between subendothelial matrix components and melanoma cells during the period of flow stasis such that the cells are able to withstand subsequent substantial increases in wall shear rate and remain adherent.
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PMID:Melanoma cell adhesion to injured arterioles: mechanisms of stabilized tethering. 921 31


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