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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glutamate dehydrogenase activity was found to be present at a high level in neoplastic cytosol and microsomes, 3.45 and 9.90 nmoles NADH/min mg protein, respectively. This remains in accordance with the high rate of RNA and protein synthesis in the neoplastic process.
Mol Biol Rep 1979 Dec 31
PMID:Glutamate dehydrogenase activity in subcellular fractions of mouse fibrosarcoma. 53 Feb 74

Previous studies have shown that in the breast there are multiple forms of the enzyme oestradiol dehydrogenase (E2DH), responsible for the interconversion of oestrone (E1) to oestradiol (E2). We have now re-examined oestrogen metabolism in the breast cancer cell lines (T47D and MCF-7) and have shown that steroids previously shown to inhibit the conversion of E1 to E2 in normal breast tissue failed to do so when added to growing monolayers of these malignant cells. In contrast to earlier estimates in normal breast tissues, the apparent Km for this conversion in monolayers of these malignant cells is shown here to be considerably lower, at around 50 nM. Cell free studies on these cell lines have revealed the presence of a high affinity (for E1) form of this enzyme of Mw approximately 80 kDa. The ability to detect this enzyme in soluble cell fractions appears to be critically dependent on buffer composition. Normal breast epithelial cells and adipose tissue appear to be devoid of this form of E2DH. As this form of E2DH has the highest affinity for the substrate E1 of all the forms in the breast, it is probable that this 80 kDa enzyme is responsible for the conversion of E1 to E2 in cell monolayers. If the observation holds that the 80 kDa enzyme is absent in the normal tissues, then the possibility arises that this E2DH may be linked with the neoplastic process in some breast tumours containing malignant epithelial cells of a similar type as studied here.
J Steroid Biochem Mol Biol 1992 Sep
PMID:Oestradiol synthesis from oestrone in malignant breast epithelial cells: studies on a high affinity, 80 kDa form of oestradiol dehydrogenase. 152 49

This study examines the behavior of glycogen-storing rat hepatoma (N13) in vitro using cytophotometric techniques. A significant increase in glycogen is observed in these cells after 30 min incubation in a buffered solution containing 0.1 mM glucose, that is 80 times lower than the physiological glucose concentration in rat blood. N13 hepatoma cells grow exponentially in culture using RPMI 1640 tissue culture medium supplemented with 10% fetal bovine serum. During the first day in culture these cells store a large amount of glycogen and this increase is also observed in serum-free cultures. In more prolonged cultures the amount of glycogen per cell gradually becomes lower, although the culturing conditions are maintained. Similar variations of protein are also observed during the initial period of culture. DNA distribution does not show significant changes, although in serum-free cultures an increase in the proportion of cells in S and G2/M phases is observed. The addition of glucagon, epinephrine and cyclic AMP derivatives to serum-free cultures does not impede the storage of glycogen. Nevertheless, addition of either 2 mM N6,O2'-dibutyryl cyclic AMP or 0.1 mM 8-(4-chlorophenylthio)-cyclic AMP blocks the cell cycle at G0/G1 and glycogen content does not decrease after the first day in culture. We believe that this cell line offers an appropriated model to study glycogen metabolism and its involvement in the neoplastic process.
Virchows Arch B Cell Pathol Incl Mol Pathol 1991
PMID:Cytophotometric analysis of glycogen, protein and DNA of a glycogen-storing rat hepatoma (N13) cell line. 168 17

Oestrogens and progestins are important for both the genesis of human breast cancer and growth of those tumours once formed. Their role at different stages of the neoplastic process are reviewed and discussed within the context of a change in sensitivity of epithelial cells during either initiation or promotion stages. Evidence favours, but does not conclusively prove, the view that progestins are the predominant mitogen for normal breast epithelium whilst oestrogen assumes that function in neoplastic epithelium. Alterations in oestrogen receptor levels could provide the key for such a change. There are insufficient data on physiological progestin concentrations to judge their effect on established cancer. Models for steroidal effects on cell proliferation and oestrogen and progestin receptor regulation that are based on endometrial data are not appropriate for breast.
J Steroid Biochem Mol Biol 1991 Nov
PMID:A discussion of the roles of oestrogen and progestin in human mammary carcinogenesis. 195 71

The histologic and ultrastructural features of hepatic hemangiopericytoma from a medaka (Oryzias latipes) exposed for 48 hr to 400 mg/liter of diethylnitrosamine at 14 days of age are described. The predominant histologic pattern was of spindle-shaped cells forming numerous whorls around central capillaries, vacuolated areas, or necrotic debris. The predominant cell type was a spindle-shaped cell with oval nuclei, elongated cell processes, and abundant organelles converging upon normal appearing capillaries. Occasionally, however, they converged upon cells swollen with cytoplasmic filaments and/or containing large fenestrated or debris-filled cytoplasmic vacuoles. These features were reminiscent of endothelial cells undergoing intracellular canalization seen in angiogenesis or neovascularization. Individual capillaries were also seen in the mass independent of whorls. It was not clear, as is the case in man, if capillary formation was an integral part of the neoplastic process or a reactive response. Although the liver is an unusual location for hemangiopericytoma in man, many of the cellular features in the fish tumor were similar to the human tumor. The ultrastructural characterization of tumor cells in fish carcinogenesis correlated with histologic patterns of growth will expand our understanding of how fish cells respond when transformed, and augment the development and use of aquatic bioassays for carcinogenesis research.
Exp Mol Pathol 1991 Apr
PMID:Ultrastructure of hepatic hemangiopericytoma in the medaka (Oryzias latipes). 202 37

The phosphoprotein plastin was originally identified as an abundant transformation-induced polypeptide of chemically transformed neoplastic human fibroblasts. This abundant protein is normally expressed only in leukocytes, suggesting that it may play a role in hemopoietic cell differentiation. Protein microsequencing of plastin purified from leukemic T lymphocytes by high-resolution two-dimensional gel electrophoresis produced eight internal oligopeptide sequences. An oligodeoxynucleotide probe corresponding to one of the oligopeptides was used to clone cDNAs from transformed human fibroblasts that encoded the seven other oligopeptides predicted for human plastin. Sequencing and characterization of two cloned cDNAs revealed the existence of two distinct, but closely related, isoforms of plastin--l-plastin, which is expressed in leukocytes and transformed fibroblasts, and t-plastin, which is expressed in normal cells of solid tissues and transformed fibroblasts. The leukocyte isoform l-plastin is expressed in a diverse variety of human tumor cell lines, suggesting that it may be involved in the neoplastic process of some solid human tumors.
Mol Cell Biol 1988 Nov
PMID:Molecular cloning and characterization of plastin, a human leukocyte protein expressed in transformed human fibroblasts. 321 Nov 25

Histogenetic features of lung tumours were studied in Syrian hamsters that had been induced with 6.8 mg N-nitrosomethyl-n-heptylamine/animal by gavage once a week for 35 weeks. At intervals from experimental week 2 until week 46, pulmonary tissues from hamsters were examined by light and electron microscopy. This report describes early hyperplastic lesions associated with terminal bronchioles and the progression of these lesions to bronchioloalveolar tumours. Using immunohistochemical and ultrastructural colloidal gold labelling techniques, hamster Clara cell antigen was found to be localized in Clara cell granules and smooth endoplasmic reticulum of normal cells, in dysplastic Clara cells migrating through basement membrane defects or from the open end of terminal bronchioles, and in hyperplastic peribronchiolar cell foci. The latter progressed to bronchioloalveolar tumours growing out along alveolar basement membranes in a characteristic lace-like, lepidic pattern. Tumours were composed of secretory (Clara), ciliated, mucous, and undifferentiated cells, as well as trapped, non-neoplastic alveolar type II cells. Hyperplastic neuroendocrine cell foci lining airways were immunoreactive for chromogranin, but these cells did not participate in the pre-neoplastic or neoplastic process. It is suggested that bronchioloalveolar carcinomas in hamsters are derived from bronchiolar secretory (Clara) cells growing along alveolar walls, differentiating into other bronchiolar cell types and entrapping resident alveolar type II cells. Due to the migratory capacity of Clara cells, it is also possible for tumours composed of bronchiolar cells to develop at the lung periphery.
Virchows Arch B Cell Pathol Incl Mol Pathol 1993
PMID:Clara cell antigen in normal and migratory dysplastic Clara cells, and bronchioloalveolar carcinoma of Syrian hamsters induced by N-nitrosomethyl-n-heptylamine. 824 77

Several studies have implicated the extracellular matrix-degrading metalloproteinases (MMPs) as essential agents in tumor cell invasion and metastasis. In the present study, we have investigated the patterns of expression of a number of MMPs and their specific tissue inhibitors (TIMP-1 and TIMP-2) in human colonic tissue samples that represent various stages of progression from adenomas showing different degrees of dysplasia to adenocarcinomas. We assessed levels of mRNA by Northern blot analysis and the results were measured semiquantitatively by densitometry. In total, we analyzed nine adenomas of varying size and with varying degrees of dysplasia, three adenomas with adenocarcinoma (malignant polyps), and five adenocarcinomas. Although expression of MMP and TIMP mRNA was highly intercorrelated, transcripts for stromelysin 3 and TIMP-2 (high) showed the strongest relation to the neoplastic process. Detection of stromelysin 3 mRNA accompanied a diagnosis of severe dysplasia or malignancy, whereas levels of TIMP-2 (high) mRNA transcripts permitted finer distinctions on the neoplastic continuum. These data indicate changes within extracellular matrix acquired during the process of malignant transformation of human sporadic colorectal neoplasia.
Diagn Mol Pathol 1993 Jun
PMID:Expression pattern of metalloproteinases and their inhibitors changes with the progression of human sporadic colorectal neoplasia. 826 81

Epidemiological studies of heritable cancer have demonstrated that cancer predisposition is a dominant trait; these studies have also predicted the recessive outcome of the neoplastic process. Biochemical studies of dominantly heritable cancer have demonstrated the relevance of systemic effects. The systemic effects are presumably due to a dominant mutation at the "initiator locus." Collectively they define cancer initiation at the cellular level (as described in this review). Molecular biological studies have demonstrated that cancer progression and the appearance of clinical cancer occur through an accumulation of recessive mutations at critical loci. We must continue to try to define not only the inherited and acquired gene defects that initiate the neoplastic state but also the subsequent genetic alterations and biomarkers involved in tumor progression. These genetic defects are already proving useful in diagnosis and prognostication. The hope is that these biomarkers may be useful for designing specific differentiation therapy.
Mol Carcinog 1993
PMID:Heritable colorectal cancer and cancer genes: systemic expressions. 835 89

Aggressive fibromatosis (also called deep fibromatosis or desmoid tumor) is a proliferation of cytologically benign-appearing fibrocytes, often resulting in significant functional loss. The nature of the lesion is controversial: some evidence suggests that it is a reactive process, whereas other evidence supports a neoplastic etiology. The pattern of X chromosome inactivation, using a technique based on polymerase chain reaction (PCR) amplification of a hypervariable CAG repeat region flanking Hhal restriction sites of the human androgen receptor gene, was determined in four cases in which cryopreserved tumor and adjacent normal tissue were available. All four tumors demonstrated a monoclonal pattern, while the adjacent normal tissues demonstrated a polyclonal pattern. This demonstrates that aggressive fibromatosis is proliferation of cells derived from a single clone with a growth advantage, and thus is likely a neoplastic process.
Diagn Mol Pathol 1997 Apr
PMID:Aggressive fibromatosis (desmoid tumor) is a monoclonal disorder. 909 48


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