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)

Analysis of carcinoembryonic antigen (CE)-reactive glycoproteins from liver metastasis of primary colon and breast tumors and from primary breast tumors has been carried out by affinity chromatography on concanavalin A (Con A)-Sepharose. Three CEA-reactive glycoproteins from colon tumors (liver metastasis) with different binding capacity to Con A have been separated and further purified by gel filtration. Of the 3 CEA-reactive glycoproteins, 1 of them did not bind to Con A. Both Con A-binding and nonbinding CEA-reactive glycoproteins were immunologically indistinguishable when tested with a reference goat anti-CEA (ACE, 67-70; Dr. C.W. Todd and Dr. M.L. Egan), as well as with a variety of rabbit anti-CEA and anti-CEA (nonbinding) prepared in this laboratory. Carbohydrate analysis showed that mannose content of different purified CEA preparations or nonbinding CEA did not differ appreciably. N-Acetylglucosamine content of purified CEA preparations, however, varied considerably, suggesting that this sugar may impart the specificity of binding of CEA to Con A. The purified CEA preparations differed in their ability to inhibit the binding of 125l-labeled CEA to goat anti-CEA. One of the purified CEA preparations had 3- to 8-fold greater inhibitory capacity when compared to other preparations and shared a partial identity with a glycoprotein present in the extracts of fetal colon. The glycoprotein extracts of primary breast tumors did not contain a CEA that was immunologically identical to CEA present in colon tumors, whereas the liver metastasis of primary breast tumors showed several CEA-reactive glycoproteins as judged by radioimmunoassay. However, these CEA-reactive glycoproteins did not have any antigenic relationship with CEA from colon tumors when tested by double diffusion and immunoelectrophoresis. In conclusion, when Con A affinity chromatography of tumor glycoproteins is carried out under defined conditions and with the use of appropriate antisera, it is possible to delineate the presence or absence of CEA in tumors of nonentodermal origin.
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PMID:Immunochemical studies on carcinoembryonic antigen-reactive glycoproteins from carcinomas of the colon and breast separated by concanavalin A affinity chromatography. 97 8

Optimum cutoff levels for plasma des-gamma-carboxy (abnormal) prothrombin (DCP) and serum alpha-fetoprotein (AFP) were determined by analyzing receiver operating characteristic (ROC) curves to discriminate between hepatocellular carcinoma (HCC) and benign hepatic conditions. Plasma DCP levels in 200 patients with HCC and 197 control patients with benign liver diseases were measured by an enzyme immunoassay with anti-DCP monoclonal antibodies, while serum AFP levels for both groups were measured by radioimmunoassay. From ROC curves and tangential lines with a slope of 1.0, the cutoff levels of DCP and AFP were determined to be 0.11 AU/ml and 150 ng/ml, respectively. Lowered cutoff levels of DCP did not improve the sensitivity, in contrast to the increased sensitivity obtained by lowering the specificity of AFP. The sensitivities and specificities determined in this study were close to the currently used values of 0.1 AU/ml for DCP and 200 ng/ml for AFP, justifying these cutoff levels for the differentiation of benign and malignant liver diseases.
Tumour Biol 1992
PMID:Determination of optimum cutoff levels of plasma des-gamma-carboxy prothrombin and serum alpha-fetoprotein for the diagnosis of hepatocellular carcinoma using receiver operating characteristic curves. 128 27

The effect of menaquinone-4 (MK-4, vitamin K2) was studied on des-gamma-carboxy prothrombin (DCP or PIVKA-II) levels in three subjects with vitamin K deficiency and five patients with hepatocellular carcinoma (HCC) with positive DCP. The half-life of DCP in HCC patients after intravenous MK-4 administration (50 mg daily for 14 days) was determined to be 60 hours, identical to that found in vitamin K-deficient subjects who received MK-4. When a single dose of MK-4 (10 mg) was given intravenously to three patients with HCC and elevated DCP, the levels decreased with a reduction rate identical to that in vitamin K-deficient subjects for the first 1 to 3 days, followed by an increase reaching the previous level in 7 to 10 days. Changes in plasma coagulant activity were compared between subjects with vitamin K deficiency and those with HCC before and after a single dose of MK-4 (10 mg). The activity increased in DCP-positive patients with HCC as in vitamin K-deficient subjects who received the same single dose of MK-4. The increase was greater in HCC patients with higher DCP levels. These results suggest that the level of plasma DCP in patients with HCC responded to vitamin K with the same sensitivity as that in vitamin K-deficient subjects. When patients with HCC underwent effective tumor therapy (resection or arterial embolization), the reduction rate (slope of DCP decline) was found to be identical to that in vitamin K-deficient subjects given with MK-4. In patients with less effective therapy, the reduction rate was smaller, or there was an increase in DCP. These observations strongly suggest that sequential measurements of the DCP reduction rate after treatment for HCC are useful for assessing therapeutic effects.
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PMID:Changes of plasma des-gamma-carboxy prothrombin levels in patients with hepatocellular carcinoma in response to vitamin K. 130 8

A biological cancer marker is a molecule, synthetized from a neoplastic tissue, which is present in the tumor and can be detected in measurable amounts in circulating blood. The natural history, prognosis, heterogeneity of each tumor and the histology of bronchial cancers clearly show the difficulty to establish the role of markers in the management of these tumors, especially for the initial assessment of extension. The analysis of the literature shows that studies on this subject are rare. The use of an isolate marker is not sufficient for a positive diagnosis of non-small-cell bronchial cancer. The use of several markers produces better results. However, no model is accurate enough to formally influence the diagnosis of operability. No isolate or associated marker allows differentiating between small-cell and non-small-cell bronchial cancers. The most interesting two markers finally seem to be ACE and CA 125. All other markers must not be used as a routine during the assessment of non-small-cell bronchial cancers. However, these markers are still important for therapeutic follow-up. Even though they are not predictive of chemosensitivity, and even though their decrease is not regarded as an objective criterion of response, their variations are linked with the response to chemotherapy, and their persistent normalization after surgery is compatible with apparent complete remission. The ACE and CA 125 assays can therefore be used as a reference, in case of initial positive findings, for the subsequent follow-up of the patient.
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PMID:[The role of tumor markers in the pre-therapeutic staging of non-small cell bronchial cancer]. 133 77

Two cases of intracranial germinoma with different clinical expression, are described. The clinical symptomatology, the diagnosis and the treatment of this tumor are discussed. The symptoms depend on the localization of the tumor: in the suprasellar germinoma endocrinologic manifestations prevail while the symptoms in germinomas which are located in the pineal region, are mainly due to increased intracranial pressure. The diagnosis is suggested by the findings on CT-scan and MRI of the brain, but for the definitive diagnosis, pathologic examination of the tumor remains necessary. Blood HCG and alpha-fetoprotein are useful markers for follow-up; the value of angiotensin converting enzyme (ACE) as a marker, is still unclear. The ideal treatment of germinoma consists of surgical removal, postoperative chemotherapy and, afterwards, local radiotherapy. On the whole, the prognosis of this tumor is good.
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PMID:[Intracranial germinoma in children]. 144 May 52

The effect of kininase II inhibitor, enalapril, on the delivery of monoclonal antibody A7 to the targeted tumor was investigated using athymic mice bearing human colon cancer, SW1116. Enalapril alone, which enhances tumor vascular permeability through the kinin-generating cascade, did not increase the uptake of 125I-labeled A7 (125I-A7) in SW1116 due to the systemic hypotension induced by its inhibitory effect on angiotensin converting enzyme. However, with combined angiotensin II (AT-II) and enalapril treatment, a 2-fold increase in the accumulation of 125I-A7 was seen when compared to A7 alone. This marked increase was presumably due to increased tumor vascular permeability induced by enalapril combined with the absence of hypotension due to the actions of AT-II. This approach might be useful in radioimmunodetection and immunotargeting chemotherapy using monoclonal antibody.
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PMID:Enhanced tumor localization of monoclonal antibody by treatment with kininase II inhibitor and angiotensin II. 158 84

The activities of alanyl aminopeptidase (AAP), arginyl aminopeptidase (RAP), alpha-glutamyl aminopeptidase (EAP) and angiotensin I-converting enzyme (ACE) were investigated in primary human lung tumors of different histological types and in matched lung parenchyma. In contrast to the studied aminopeptidases whose activity differences between tumor and lung tissues were infrequently significant, the activity of ACE was decreased highly significantly in the majority of lung tumors.
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PMID:Aminopeptidases and angiotensin I-converting enzyme activities in primary human lung tumors and lung parenchyma. 168 70

To date, one hundred and ten cases of malignant neoplasms arising from untreated bladder exstrophy have been reported. We describe another case of uncorrected bladder exstrophy with invasive adenocarcinoma and in situ squamous carcinoma discovered in a 51 year old woman. Postoperative radiotherapy was performed after cystectomy with nephroureterectomy and hysterectomy. The neoplastic samples were investigated by mucin histochemistry and immunocytochemistry. The epithelium lining the tumor villi and the surrounding mucosae was colonic with mucin histochemistry and reacted to anti KL1, EMA and ACE antibodies. These features were those of colonic and vesical adenocarcinomas. Although early vesical reconstruction is the best oncologic prevention, patients with bladder exstrophy run the risk of sigmoid adenocarcinoma after cystectomy and urinary diversion including ureterosigmoidostomy.
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PMID:[Invasive adenocarcinoma with epidermoid carcinoma on the site of bladder exstrophy. Histochemical and immunocytochemical study]. 178 47

This analysis of IMG has focused on the long-term natural history and current approaches to therapy of this disorder. It seems clear that IMG is intrinsically a relatively benign disease, particularly in certain populations. Risk factors for an unfavorable course can often be identified at the discovery of disease. For example older age at onset, male sex, very heavy proteinuria (greater than 10 g/d), sustained hypertension, impaired renal function, and significant chronic tubulointerstitial lesions in the initial renal biopsy all portend an unfavorable outcome. Contrariwise, patients lacking these prognostic features usually do quite well with a high likelihood of spontaneous complete or partial remissions and stable renal function. Once a complete remission has occurred, whether spontaneous or therapy induced, the long-term evolution of the disorder is quite favorable. Some patients may present with what appears to be "idiopathic" MGN, only to later demonstrate underlying disease, such as neoplasia, chronic viral infection, or systemic lupus erythematosus. Glucocorticoids alone, particularly when administered orally, do not seem to have significant beneficial effects over the long term; however, high-dose intravenous methylprednisolone may at times reverse declining renal function in patients with severe nephrotic syndrome. A small subset of patients may display a remitting and relapsing course following treatment with oral glucocorticoids, resembling to some extent patients with minimal change disease. Combination of alkylating agents, either cyclophosphamide or chlorambucil with glucocorticoids is very likely beneficial for the group of patients having an intrinsically unfavorable prognosis or for patients who demonstrate progressive renal insufficiency. At the present time it is not known whether regimens that involve long-term therapy with oral cyclophosphamide combined with glucocorticoids are superior to, equivalent to, or inferior to regimens that involve the cyclical use of intravenous methyl-prednisolone oral prednisone, and oral chlorambucil. Very long-term use of cyclophosphamide, in excess of 12 months, is probably associated with unacceptable long-term risks, particularly the emergence of neoplasia. Long-term follow-up, more than 10 years, will be required to establish the magnitude of the oncogenic potential of existing shorter term regimens of cyclophosphamide-glucocorticoid combinations and for cyclical regimens using chlorambucil. Further data is required to establish the role of cyclosporine, nonsteroidal antiinflammatory agents and intravenous immunoglobulins in the treatment of patients with IMG. ACE inhibitors, sometimes combined with nonsteroidal antiinflammatory agents, may have some usefulness in patients with heavy proteinuria and declining but not advanced renal failure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The therapy of idiopathic membranous glomerulonephritis. 203 23

Hypertension and cardiomyopathy are prominent findings in humans and rats harboring pheochromocytomas, tumors that can secrete enormous quantities of catecholamines. We have previously found that alpha- and beta-adrenergic receptor antagonists may ameliorate the hypertension and cardiomyopathy found in New England Deaconess Hospital rats implanted with pheochromocytoma. The present studies were designed to determine the possible action of the angiotensin converting enzyme inhibitor captopril on these changes in rats harboring pheochromocytomas. Rats were implanted with transplantable pheochromocytomas and treated with captopril dissolved in the drinking water (1 mg/ml) for 4-6 weeks. Systolic blood pressure was monitored by using the tail-cuff technique. In the rats with pheochromocytoma, blood pressure progressively increased to 184 +/- 3 mm Hg after the tumor was implanted. However, in rats with pheochromocytoma treated with captopril in the drinking water before the development of hypertension, blood pressure did not increase (137 +/- 3 mm Hg). In rats with pheochromocytoma with established hypertension, captopril normalized the systolic blood pressure. Plasma norepinephrine was markedly elevated to a similar extent in both groups compared with unimplanted control rats. Plasma renin activities were slightly lower in rats with pheochromocytoma compared with unimplanted control rats. Treatment with captopril of rats with pheochromocytoma did not modify contraction of isolated rings of thoracic aorta exposed in vitro to either phenylephrine or angiotensin II. Treatment with captopril markedly attenuated the cardiomyopathy induced by pheochromocytoma. These results demonstrate that captopril prevents the development of hypertension despite markedly elevated concentrations of catecholamines. In addition, captopril attenuates catecholamine-induced cardiomyopathy in pheochromocytoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril improves hypertension and cardiomyopathy in rats with pheochromocytoma. 215 6


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