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Query: UMLS:C0027651 (
tumor
)
685,946
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Prostatic carcinoma accounts for about 1% of all cancers that metastasize to the skin. The regions most frequently involved are the genital region, the head and the trunk. Clinically the lesions present as nodules; less often diffuse infiltrates, red macules and papules or tumors of an angiomatous appearance occur. Histopathological examination of skin biopsy specimens can reveal gland-like, epithelial or anaplastic differentiation of
tumor
cells. Prostatic origin can be proven by the immunohistological demonstration of acid prostatic
phosphatase
or prostatic specific antigen in paraffin-embedded specimens taken for routine histological examination.
...
PMID:[Skin metastases in prostatic cancer. Immunohistologic indications of the primary tumor]. 246 19
We investigated whether monoclonal antibodies (MoAbs) reactive against both acidic and basic cytokeratins alone were sufficient to detect minimal numbers of contaminating epithelial tumor cells in the bone marrow of breast cancer patients. Monoclonal anti-cytokeratin antibodies (AE1 and AE3) were used to stain 14 breast carcinomas by the avidin-biotin-peroxidase technique. Nine tumors (64.3%) showed high reactivity and five (35.7%) showed low or moderate reactivity. Nine MoAbs that proved to be unreactive to light density bone marrow cells by immunoalkaline
phosphatase
histochemistry were screened for reactivity to breast carcinomas having only low or moderate positivity to cytokeratin antibodies. Three of nine MoAbs showed high percentages of positivity and were selected to supplement the anti-cytokeratin antibodies for immunohistochemical detection of minimal marrow disease in breast cancer patients. A MoAb cocktail was prepared, further tested for reactivity to another five breast carcinomas, and compared with cytokeratin staining alone. The cocktail labeled 100% of carcinoma cells in all the examined specimens. To determine the sensitivity of this panel for detecting minimal numbers of contaminating
tumor
cells in bone marrow, in vitro mixing experiments were performed. T47D breast carcinoma cells were mixed with bone marrow mononuclear cells at ratios from one
tumor
cell per 10 bone marrow cells up to one
tumor
cell per 1 x 10(6) marrow cells, and cytospin preparations were subsequently stained with the MoAb cocktail by the immunoalkaline
phosphatase
method. Our approach could detect one
tumor
cell in 1 x 10(5) hematopoietic cells.
...
PMID:A monoclonal antibody cocktail for detection of micrometastatic tumor cells in the bone marrow of breast cancer patients. 247 64
Immunocytochemical studies were performed on fine needle aspirates of the liver in a patient with hepatocellular carcinoma. A panel of commercially available antibodies was used to study the aspirated cells by immunoalkaline
phosphatase
and immunoperoxidase methods. The malignant cells in the aspirates, which were positively stained by the immunoperoxidase method for alphafetoprotein and by both methods for epithelial membrane antigen, were most probably hepatocellular in origin. Some cells were shown by the immunoalkaline
phosphatase
method to possess leukocyte-common antigen (LCA) and antigens of colonic and ovarian tissues. These findings were further investigated, and it was found that the
tumor
cells indeed had LCA as well as levamisole-resistant alkaline phosphatase activity. Although the immunoalkaline
phosphatase
methods are useful immunodiagnostic techniques applicable to fine needle aspirates, the endogenous enzyme activity present in some nonhematopoietic
tumor
cells is a cause for caution in the use of these methods in aspirates from nonhematopoietic
tumor
tissues.
...
PMID:Endogenous phosphatase activity in tumor cells in a liver aspirate. A potential problem for immunocytodiagnosis using immunoalkaline phosphatase methods. 247 87
Several forms of protein kinase C with molecular masses of 74-, 77-, and 80-kDa were detected in subcellular fractions of human breast cancer MDA-MB-231 cells which express the alpha-type protein kinase C. Several lines of evidence indicated that the 74-kDa is the precursor of the 77- and 80-kDa protein kinase C forms. (i) Pulse-labeling experiments revealed that protein kinase C is synthesized on membranes as a 74-kDa protein that can be chased into the 77- and the 80-kDa protein kinase C forms. (ii) The primary translation product of protein kinase C displayed an apparent molecular size of 74-kDa as determined by in vitro translation of poly(A)+ RNA from MDA-MB-231 cells. (iii) Incubation with serine/threonine-specific protein phosphatases (potato acid phosphatase and
phosphatase
1 or 2A) resulted in the complete dephosphorylation of the 77-kDa to the 74-kDa protein kinase C form. Protein kinase C appears to be synthesized in membranes as an unphosphorylated and presumably inactive 74-kDa form that is converted into the active 77- and 80-kDa protein kinase C by post-translational modification involving at least two phosphorylation steps. The first phosphorylation is probably achieved by a specific, yet unidentified, "protein kinase C kinase" since the 74-kDa protein kinase C species did not undergo autophosphorylation and was neither a substrate for the purified protein kinase C, S6 kinase, phosphorylase kinase, casein kinase II, nor for the catalytic subunit of cAMP-dependent protein kinase. Except for phosphorylase kinase and the catalytic subunit of the cAMP-dependent protein kinase, phosphorylation of the 77-kDa protein kinase C form with purified protein kinase C (autophosphorylation), S6 kinase or casein kinase II shifted the molecular mass of the 77-kDa protein kinase C to 80-kDa. Prolonged exposure of MDA-MB-231 cells to phorbol 12-myristate 13-acetate not only leads to a complete down-regulation of protein kinase C activity but also to an accumulation of 74-kDa protein kinase C due to a retarded conversion of the 74-kDa into the 77- and 80-kDa protein kinase C forms in these cells. Our data indicate that
tumor
promoters additionally interfere with the posttranslational processing that converts the 74-kDa protein kinase C precursor into the 77- and 80-kDa forms of the enzyme.
...
PMID:Biosynthesis and posttranslational modifications of protein kinase C in human breast cancer cells. 247 38
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.
...
PMID:A detailed immunohistochemical analysis of cerebellar hemangioblastoma: an undifferentiated mesenchymal tumor. 247 46
The function of the A element (nucleotides 5107 to 5130) of the polyomavirus enhancer is augumented in NIH 3T3 cells by a
tumor
-promoting phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA). One of its targets is an AP1 consensus sequence motif recognized by a nuclear factor, PEBP1. In Ha-ras-transformed NIH 3T3 cells, however, A element function was not enhanced by TPA treatment, and at the same time PEBP1 was not detected in the nuclear extract by a mobility shift assay. PEBP1 was not detected in either the extract from NIH 3T3 cells treated in vivo with a protein kinase inhibitor, staurosporine, or the extract from NIH 3T3 cells after treatment in vitro with
phosphatase
. These results suggest that PEBP1 is required to be properly phosphorylated for DNA binding and that it is underphosphorylated, possibly due to the downregulation of protein kinase C in Ha-ras-transformed cells. In addition, we observed that PEBP2, which bound to the A element adjacent to PEBP1, was converted to apparently related PEBP3 when conditions favored underphosphorylation.
...
PMID:Loss of responsiveness of an AP1-related factor, PEBP1, to 12-O-tetradecanoylphorbol-13-acetate after transformation of NIH 3T3 cells by the Ha-ras oncogene. 254 91
Critical parameters in the quantitation of altered hepatic foci (AHF) developing during multistage hepatocarcinogenesis in the rat include: 1) the enumeration of AHF induced by test agents as well as those AHF occurring spontaneously in livers of untreated animals; 2) the volume percentage or fraction of the liver occupied by all AHF as a reflection of the total number of altered cells within the liver and the degree of
tumor
promotion which has occurred; and 3) the phenotype of individual AHF as determined by multiple markers with serial sections. These parameters, especially the number of AHF, should be corrected by the presence of spontaneous AHF which increase with the age of the animal, more so in males than females. While accurate estimation of the background level of spontaneous AHF can be important in demonstrating that a carcinogenic agent does not possess the ability to increase the numbers of AHF above the background level, a better method to distinguish the effectiveness and relative potencies of agents as initiators or promoters is reviewed. The relative effectiveness of four different markers--gamma-glutamyltranspeptidase (GGT), a placental form of glutathione S-transferase (GST), canalicular ATPase, and glucose 6-
phosphatase
(G6Pase)--was described for the chemicals C.I. Solvent Yellow 14 and chlorendic acid as promoting agents in males and females. C.I. Solvent Yellow 14 is a more effective promoting agent in females than males, and AHF exhibit extremely low numbers scored by GGT. On the other hand, the numbers of AHF present in livers of male rats promoted by this agent are more than twice those seen in livers of female animals, possibly owing to the effectiveness of this agent as an initiator in the male but not the female. Very few AHF, especially in the male, are scored by GGT during chlorendic acid promotion. The distribution of phenotypes with these markers also differs in the spontaneous AHF appearing in the livers of animals fed 0.05% phenobarbital on either a crude NIH-07 or AIN-76 purified diet. Such studies emphasize the extreme dependence of the promoting stage of hepatocarcinogenesis on environmental factors of sex, diet, and the molecular nature of the promoting agent itself. The hallmark of the final stage of progression in the development of hepatocellular carcinomas is aneuploidy, which may be reflected by phenotypic heterogeneity within individual AHF, termed foci-in-foci. The implications of such quantitative analyses during hepatocarcinogenesis induced by specific agents in relation to the specific action of the agent at one or more of the stages of hepatocarcinogenesis are discussed.
...
PMID:Critical parameters in the quantitation of the stages of initiation, promotion, and progression in one model of hepatocarcinogenesis in the rat. 269 39
In a prospective study 60 patients suffering from histologically confirmed renal cell carcinoma were examined on paraneoplastic alterations. The following parameters were determined: Stauffer-syndrome (BSG, total protein with serum electrophoresis, alcaline
phosphatase
, gamma-GT, Quick values), total and ionized calcium, parathormone, calcitonin, hemoglobin, thrombocytes, LDH, IgE and arterial blood pressure. Compared to the findings obtained by other authors, we saw paraneoplastic syndromes only rarely. There was no correlation found to the stage of the
tumor
or to prognosis. In only four out of 60 patients paraneoplastic led to the diagnosis "renal carcinoma". With the exception of BGS, which was raised in 75% of the patients, paraneoplastic parameters are not suitable for the screening or the early diagnosis of renal carcinomas.
...
PMID:[Paraneoplastic syndrome in kidney cancer]. 271 55
An experimental model was designed to study the role of both diethylstilbesterol (DES) and phenobarbitone (PB) singly or in combination, in diethylnitrosamine (DEN) induced hepatic
neoplasia
. Experimental and control rats were injected DEN (200 mg/kg) or saline, ip. Acute morphological changes were studied at days 1, 2 and 3; and at weekly intervals for 3 wk. Four weeks after DEN pretreatment the experimental and control rats were randomized into various groups and fed DES (T1), PB (T2) or a combination of both DES and PB (T3). Five rats from each experimental group were sacrificed at 10, 20 and 30 wk. Group T3 showed gross nodules with a mean nodule score of 20.5 mm at 20 wk. Nodule score in T1, T2 and T3 at 30 wk were 7, 9 and 34.5 mm respectively. The sequential morphological lesions encountered were clear cell and acidophilic foci; acidophilic, basophilic and mixed nodules. Haemorrhage within the nodules was frequent when DES was administered either alone or in combination with PB. Oval cell proliferation and cholangiocellular lesions were produced in all experimental groups. Foci and nodules generally showed loss of glucose-6
phosphatase
, adenosine triphosphatase and invariable presence of gamma-glutamyl transpeptidase and glycogen. A combination of DES and PB as promoter yielded earliest and highest nodule score. This suggests that DES and PB acted synergestically as promoters or that PB caused enzyme induction thereby enhanced the promotive effect of DES.
...
PMID:Synergistic promoter effect of diethylstilbesterol & phenobarbitone in diethylnitrosamine induced hepatic neoplasia in rats. 272 21
Frozen sections of 30 breast carcinomas were stained for progesterone receptors (PRs) using a rat monoclonal primary antibody and an alkaline phosphatase-antialkaline
phosphatase
technique. The micro-TICAS image analysis system was used for evaluation of the staining, with the results obtained by image analysis compared with the results of biochemical assays for PR. Strong positive/negative concordance (90%) was observed between the immunohistochemical and biochemical assays. However, the numerical values of the positive cases in the two assays did not correlate well, possibly because the biochemical assay does not take
tumor
cellularity into account. Three PR distribution patterns, designated A, B and C, were identified by image analysis among the breast tumors. In the type A pattern,
tumor
cell nuclei were diffusely and uniformly labeled. In type B, both clearly negative as well as distinctly positive cells were present. In type C tumors, a broad range of labeling reactions (from negative to intensely positive) was observed. These results imply (1) that the PR content of human breast carcinoma may be accurately and objectively assessed by the image analysis of immunohistochemically stained frozen sections, (2) that image analysis may provide a more accurate estimate of the cellular content of PR than do biochemical assays and (3) that PR distribution patterns obtained through image analysis permit the consistent appraisal of intratumoral heterogeneity of PR expression, which is potentially of prognostic importance.
...
PMID:Assessment of hormone receptors in breast carcinoma by immunocytochemistry and image analysis. I. Progesterone receptors. 280 42
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