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)

Tissue polypeptide antigen (TPpA) in the cerebrospinal fluid (CSF) was measured in 59 consecutive breast cancer patients with suspected central nervous system (CNS) metastases. Subsequently, we determined that 13 patients had parenchymal brain metastases, 10 had leptomeningeal carcinomatosis, and 36 had no CNS involvement. The concentration of TPpA, which is a nonspecific marker for cell proliferation, was significantly higher in patients with CNS metastases than in those without it (P less than .0001; Mann-Whitney test). A tentative cutoff value for CNS metastases was set at 95 U/L TPpA; the upper limit of values indicating absence of CNS metastases was 89 U/L. Given these cutoff points, the sensitivity of TPpA as a marker for CNS metastases was 74% and the specificity was 100%; the predictive values of positive and negative tests were 100% and 86%, respectively. In 16 patients with CNS metastases, no correlation was found between TPpA activity in corresponding CSF and blood samples (correlation coefficient, Spearman's rho = .4; P greater than .1). In three patients treated for leptomeningeal carcinomatosis, the measurements of CSF TPpA showed correlation between the presence of tumor cells in the CSF and neurological clinical function. TPpA concentrations decreased in parallel with the clinical response and increased prior to CNS disease progression. As a marker for CNS metastases, the level of TPpA in the CSF in breast cancer patients appears to be superior to the level of protein, lactate dehydrogenase, or glucose, which showed very low sensitivity (41%, 47%, and 8%, respectively). For quantitative evaluation of treatment for leptomeningeal carcinomatosis, the TPpA level appears to be valuable and superior to CSF cytology, because tumor cells are not always present in CSF samples from patients with this condition.
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PMID:Tissue polypeptide antigen activity in cerebrospinal fluid: a marker of central nervous system metastases of breast cancer. 204 Oct 52

Paraneoplastic syndromes are caused by factors produced by cancer cells that often act at a distance from both the primary site and its metastases. The most extensively characterized syndromes caused by cancer are those produced by polypeptide hormones, such as adrenocorticotropic hormone, and those produced by antibodies directed against tumor antigens that cross-react with neural tissue, such as in the Eaton-Lambert myasthenic syndrome. These syndromes develop in a minority of cancer patients, and are diagnoses of exclusion. Lung cancer, particularly small cell lung cancer, is the most common malignancy causing paraneoplastic syndromes. A large number of paraneoplastic syndromes have been described. This review focuses on the increased understanding of some of the well-documented syndromes that has occurred through recent advances principally in molecular biology and immunology.
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PMID:Paraneoplastic syndromes in thoracic malignancies. 206 93

Desmosomes are adhesive junctions of epithelial cells. Their expression may be altered or lost in carcinomas resulting in reduced cellular adhesiveness. The desmosomes of colorectal carcinomas have been studied by fluorescent antibody staining, immunoblotting and electromicroscopy. A series of 58 malignant specimens, comprised of primary tumours and metastases, were desmosome positive. There was no indication of a comparative reduction in desmosome expression that might give rise to reduced adhesiveness of tumour cells, although loss of polarised junctional distribution in poorly differentiated tumours might have such a consequence. Western blotting analysis of colorectal cancers and cultured carcinoma cells identified desmosomal polypeptides dp1 + 2, dg1 and dg2 + 3 with similar relative molecular weights to normal homologues. In addition, a polypeptide of 140,000 was recognised only in malignant epithelium by anti-dg2 + 3 antiserum. The significance of this polypeptide is not understood. Tumours and uninvolved epithelium were exposed to low extracellular [Ca2+] to test whether tumour desmosomes were of reduced stability. This caused much cellular degradation in tumours but some viable cell clumps possessed desmosomes resistant to disruption by low [Ca2+]. Desmosomes may thus have a positive role in metastasis by maintaining intercellular adhesion between metastasising cells.
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PMID:A study of desmosomes in colorectal carcinoma. 212 14

The effect of an octapeptide analogue of somatostatin, octreotide, on tumor blood flow was evaluated with angiography in eight patients with hepatic endocrine tumors; one patient had primary intrahepatic gastrinoma, two patients had hepatic metastases from gastrinomas, two patients had VIPomas (vasoactive intestinal polypeptide-secreting tumor), and three patients had carcinoid tumors. Octreotide caused a marked decrease in tumor blood flow in two patients with gastrinomas and two with VIPomas. One patient could not be evaluated due to the lack of a tumor blush on a control angiogram. In patients with carcinoid tumors, octreotide caused a slight reduction in blood flow through the tumors in two patients, while there was no change in one patient. Octreotide markedly decreased gastrin and gastric acid secretion in two of three patients with gastrinomas, lowered VIP and stopped the diarrhea in patients with VIPomas, and controlled symptoms in two of three patients with carcinoid tumors. The vasoactive effect of octreotide on hepatic endocrine tumors may be a direct action on tumor blood supply or secondary to inhibition of the endocrine tumor cell secretion and consequent decreased blood flow.
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PMID:Effect of somatostatin analogue (octreotide) on blood flow to endocrine tumors metastatic to the liver: angiographic evaluation. 217 Oct 15

The definitive treatment of a pancreatic tumour secreting vasoactive intestinal polypeptide is surgical removal of the tumour, but when curative resection is not possible symptomatic treatment of the endocrine hyperfunction is important. Streptozotozin, although relative effective for palliation, may involve unpleasant side effects. A review of the literature and a case report with long-term use of subcutaneous somatostatin analogue SMS 201-995 in an elderly woman presenting with severe watery diarrhoea due to a pancreative vipoma is presented. Good symptomatic improvement was achieved with no side effects apart from tachyphylaxy to some extent over a period of 12 months. It is suggested that there is a use for subcutaneous SMS 201-995 in elderly patients with inoperable pancreatic gut hormone producing tumours with metastasis and in those in whom surgery would involve a high operative risk. Two cases are presented, where SMS 201-995 resulted in shrinkage of tumour and metastases.
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PMID:[The somatostatin analog SMS 201-995 in long-term treatment of vipoma]. 217 34

The fibroblast growth factors (FGFs) are a family of polypeptide growth regulators. The prototypes of this family are acidic and basic FGF. Unusual among their characteristics are a high affinity for the glycosaminoglycan heparin and the lack of a signal sequence for secretion. Other members of the FGF family include a number of oncogene products that also display heparin affinity but do possess signal sequences. Results from early tissue culture studies were consistent with the prediction that acidic and basic FGF would not be secreted. Investigators found that virtually no FGF was secreted into conditioned media, instead it remained cell-associated and was deposited into the basement membrane. More recently, however, a number of studies have indicated that a small amount of FGF is 'released' from cells where it is postulated to act as an autocrine regulator. Acidic and basic FGF have been localized in basement membranes both in vivo and in vitro. The mode of release to this site is also unclear but may be secondary to the mechanisms cited above with soluble FGF becoming bound to heparan sulfate molecules in the extracellular matrix. A number of observations have indicated that matrix-bound FGF is biologically active in vitro. There are no data to indicate whether the same is true for FGF bound to basement membranes in vivo. In addition to its apparent sequestration in the basement membrane, FGF has also been localized to the surface of a variety of normal and tumor cell types. In particular, endothelial cells have been shown to possess two classes of FGF-binding sites: low abundance, high-affinity receptors that mediate the biological activity as well as high abundance, low affinity binding sites. The physiologic relevance of FGF binding to these low affinity sites is not clear. The possibility of locally high concentrations of heparin released by mast cells, as well as the presence of heparan sulfate-degrading enzymes, suggests that this glycosaminoglycan bound FGF might be released from these binding sites under some circumstances. Cell surface binding of FGF has also been demonstrated in vivo; in rabbits plasma levels of the growth factor were shown to be dramatically elevated following intravenous heparinization. Since the FGFs were first noted to lack a signal sequence, cell injury has been suspected to be the most likely route for FGF release in vivo. A number of studies using different models of cell injury, including endotoxins and irradiation, have revealed that damaged cells do release FGF.(ABSTRACT TRUNCATED AT 400 WORDS)
Cancer Metastasis Rev 1990 Nov
PMID:Modes of FGF release in vivo and in vitro. 229 37

The nuclear DNA content of 17 pancreatic neuroendocrine tumors was measured from paraffin-embedded tissue with flow cytometry. The tumors were classified by immunostaining with antisera for synaptophysin, insulin, gastrin, glucagon, pancreatic polypeptide, somatostatin, and vasoactive intestinal polypeptide. Eight (47%) of the 17 tumors were aneuploid, and two (12%) were multiploid (had two aneuploid stemlines of cells). Seven of the eight insulinomas, one of the four gastrinomas, and two of the four nonspecified neuroendocrine tumors had an abnormal nuclear DNA content. The DNA indices of the aneuploid and multiploid cases ranged from 1.13 to 1.93, and three cases had a DNA index greater than 1.50. During the follow-up for up to 16 years (mean, 7 years), one patient with diploid nonspecified tumor died of the disease, another patient with a multiploid gastrinoma had metastatic disease develop, and a third patient with a multiploid nonspecified tumor was alive with the disease. The authors conclude that many neuroendocrine tumors of the pancreas have an abnormal nuclear DNA content as measured by DNA flow cytometry. DNA multiploid pancreatic neuroendocrine tumors may be associated with a less favorable clinical course, but this needs to be confirmed in additional studies.
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PMID:DNA ploidy in pancreatic neuroendocrine tumors. 234 35

Serum levels of tissue polypeptide antigen (TPA) were measured in 233 patients at the time of initial diagnosis of nasopharyngeal carcinoma (NPC). Staging of NPC was done using Ho's recommendations together with computerised tomography (CT) of skull findings. The upper limit of normal serum TPA levels in our population was noted to be 112 U/1. In 126 patients with N0 and N1 lymph node staging, the mean level of TPA was 90 U/1 +/- 9 (standard error of mean, sem), while in 107 patients with N2 and N3 nodal disease the mean was 193 U/1 +/- 25.6 (p less than 0.001). Similarly, in 162 patients with T1 and T2 disease, the average TPA level was 119 +/- 13.4 while in 71 patients with T3 disease, the mean TPA was 179 U/1 +/- 29.8 (p less than 0.03). Of 200 patients without metastases, the mean TPA level was 112 +/- 12 U/l whereas in 33 patients with known metastases in liver, lung, bone or brain, the mean TPA level was 290 +/- 51 (p less than 0.001) with liver metastases producing the highest levels. The present study indicates rising values of TPA with advancing nodal and tumour stage in NPC, with high values in metastatic disease. There is a highly significant correlation between nodal stage and TPA levels. TPA is a useful marker in the staging and follow-up of NPC patients.
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PMID:Significance of tissue polypeptide antigen (TPA) levels in nasopharyngeal cancer. 234 88

Three monoclonal IgG 2a antibodies were produced after immunization of mice with dispersed cells from a human mid-gut carcinoid tumor. Acetone-fixed cryosections of 57 primary and metastatic mid-gut carcinoid tumors as well as 2 hind-gut (rectal) carcinoids showed a conspicuous immunoreaction while a thymic carcinoid was essentially unstained with the antibodies. The 3 antibodies yielded a similar pattern of immunostaining. The immunoreaction comprised more than 95% of the carcinoid tumor cells, and it was more uniform and intense in primary tumors than in mesenteric, hepatic, and ovarian metastases of the mid-gut carcinoid tumors. Immunofluorescence studies on suspended carcinoid tumor cells showed that the antibodies bound to the surface membrane of the cells. The antibodies immunostained enterocytes of the small and large bowel, intestinal metaplasia of the stomach mucosa as well as colorectal adenocarcinomas. Endocrine pancreatic tumors producing vasoactive intestinal polypeptide, gastrin, somatostatin, and/or pancreatic polypeptide as well as the epithelium of pancreatic ducts were also stained with the antibodies, whereas a large number of other normal and abnormal human tissues, including benign and malignant insulinomas, were unreactive. The findings indicate that the antibodies recognize differentiation antigens on the carcinoid tumor cell surface preserved also on endocrine and nonendocrine cells of the normal bowel mucosa. The restricted tissue reactivity of the antibodies suggests that they may constitute useful tools in the histological characterization of carcinoid tumors. Further studies may reveal if they are applicable for immunolocalization and perhaps even immunotherapy of these neoplasms.
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PMID:Monoclonal antibodies raised against mid-gut carcinoid tumor cells. 236 42

The serum levels of carcino-embryonic antigen, tissue polypeptide antigen (TPA), breast carcinoma antigen 15-3 and mucin-like carcinoma-associated antigen were measured pre-operatively in 99 patients with breast cancer receiving no adjuvant hormonal or chemotherapy and in 64 patients with benign breast tumours. Using the 95th percentile of the marker levels in patients with benign breast tumours as the cut-off level, marker levels in patients with breast cancer were related to prognosis. In the follow-up period of 6-36 months (mean = 17.9 months), 20 out of the 99 patients developed metastases. Only 4 out of these 20 patients had elevated pre-operative levels of one or more of the markers. One out of these 4 patients was misclassified having metastatic disease at the time of the operation. On the other hand, in a total of 28 patients the pre-operative levels of one or more markers were noted to be elevated; 26 of the patients remained disease-free at the time of follow-up.
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PMID:Pre-operative tumour marker levels in patients with breast cancer and their prognosis. 237 96


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