Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0005684 (bladder cancer)
 16,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma determinations for TPA and CEA resulted in a sensitivity of 90% and 19-42%, respectively, for urothelial bladder cancer. By immunohistochemical staining TPA was positive in 100% and CEA in about 80% of the cases. The CEA staining in cancer tissue seemed to correlate with the WHO grade. Because TPA resulted in strong positive staining and high sensitivity in the plasma, contrary to CEA, showing less positive staining and a lower sensitivity, there seemed to be a good correlation between staining and plasma sensitivity for both markers.
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PMID:Comparison between tissue antigen analysis and plasma determinations for TPA and CEA in transitional cell carcinomas and in tumorfree urothelium of the urinary bladder. 245 97

Tumour markers are often circulating tumour-associated indicators of tumour development. As such they are not suitable for tumour screening and localization, but valuable as adjuncts for medical follow-up care of tumour patients, where their serum level alterations may anticipate the clinical detection of tumour behaviour by a lead time of 1 to 6 months before other methods. The following tumour may be controlled by established markers: endocrine tumours by NSE, calcitonin, parathormone, 5-HIAA, catecholamines/metabolites etc.; head-neck tumours: SCC, CEA; thyroid carcinoma: TG, calcitonin; lung cancer: CEA, NSE, SCC; liver cancer: AFP (PLC), CA 19-9 (cholangiocell.), CEA (secondary): biliary tract and pancreatic cancer: CA 19-9; colorectal carcinoma: CEA, CA 19-9; squamous cell carcinoma (ENT, oesophagus, anal): SCC; breast cancer: CEA and CA 15-3; ovarian cancer: CA 125 (epithelial), CA 19-9 (mucinous); germ cell tumours (ovary including trophoblastic tumours/testes): AFP and HCG; prostatic cancer: PAP and PSA; bladder cancer: TPA.
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PMID:[Clinical relevance of tumor markers]. 267 6

Urine-Tissue Polypeptide Antigen (U-TPA) was measured in 81 patients with a previously diagnosed bladder carcinoma. U-TPA was elevated in 74% of the patients with invasive bladder cancer as compared to only 15% of the patients with superficial tumors. Only one patient without a tumor recurrence had an elevated U-TPA level (4%). The results were compared with cytological grading and flow-DNA measurements in a multivariate analysis with T-category as the result variable. U-TPA and grade showed each, independently, a significant relation (P much less than 0.001) to T-category whereas the result of the DNA measurements did not explain the variation in T-category when U-TPA and grade were already in the equation. For diagnostic purposes U-TPA seems to be of limited value but may serve as an indicator of tumor recurrence in bladder cancer patients.
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PMID:Urine-TPA (tissue polypeptide antigen), flow cytometry and cytology as markers for tumor invasiveness in urinary bladder carcinoma. 281 27

Prostaglandins play a potential key role in the pathogenesis of urinary bladder cancer. Bradykinin and TPA increases in prostaglandin (PG)E2 levels were compared in primary cultures of human urothelial cells. Increased PGE2 levels were dependent upon the dose of TPA and were not apparent until 30-60 min after addition of TPA, with larger increases occurring between 60 and 120 min. Stimulation was inhibited by cycloheximide. Addition of arachidonic acid to TPA-stimulated cells increased PGE2 to a level similar to that seen in arachidonic acid-stimulated controls, and this level was not altered by cycloheximide. In contrast to TPA, the bradykinin-increased PGE2 levels were maximal at 5 min (the earliest time-point assessed) and were not inhibited by cycloheximide. Increases in PGE2 levels by both TPA and bradykinin required calcium. Excessive stimulation by TPA resulted in a desensitization to subsequent stimulation by TPA, but not bradykinin. Combination of TPA with bradykinin produced at least an additive effect on PGE2 levels. Both agonists increased the release of [3H]arachidonic acid over a time-course similar to their PGE2 response. Bradykinin and TPA appear to increase PGE2 levels by enhancing arachidonic acid availability through separate phospholipase pathways. Thus, human urothelial cells exhibit similar, but yet distinct profiles for prostaglandin stimulation by TPA and bradykinin.
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PMID:Characteristics of bradykinin and TPA increases in the PGE2 levels of human urothelial cells. 313 27

The evolution of a fully malignant tumor is a multistep process resulting from the action of multiple factors, both environmental and endogenous, and involves alterations in the function of multiple cellular genes. Chemical carcinogens that initiate this process appear to do so by damaging cellular DNA. In addition to producing simple point mutations, this damage appears to induce the synthesis of a transacting factor that can induce asynchronous DNA replication. This response may result in gene amplification and/or gene rearrangement. This phenomenon may also play a role in synergistic interactions between chemicals and viruses in the causation of certain cancers. The primary target of the tumor promoters TPA, teleocidin, and aplysiatoxin appears to be cell membranes. All three of these agents act, at least in part by, enhancing the activity of the phospholipid-dependent enzyme PKC. We have proposed a stereochemical model to explain the interaction of these amphiphilic compounds with the PKC system. We have found that TPA and teleocidin markedly enhance the transformation of C3H10T1/2 mouse fibroblasts when these cells are transfected with the cloned H-ras human bladder cancer oncogene. Thus, tumor promoters can act synergistically with an activated oncogene to enhance cell transformation. Furthermore, carcinogen-transformed rodent cells display aberrations in the expression of various endogenous retrovirus-related sequences. Activation of some of these sequences may lead to insertion mutations and further aberrations in gene expression. These findings are discussed in terms of a multistep model that involves progressive changes in cellular oncogenes and aberrations in the function of DNA transcription enhancer sequences. It will be of interest to determine to what extent these concepts apply to the etiology of cancers of the respiratory tract.
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PMID:Mechanisms of multistage chemical carcinogenesis and their relevance to respiratory tract cancer. 315 53

Tumor recurrences were observed 70 times in 715 cystoscopies performed in 253 patients. The sensitivity of microhematuria to detect a tumor recurrence was 61%, the specificity 84%. The sensitivity of microhematuria increased to 90% in Tis and T2 tumors. Urine cytology showed a specificity of 100% and a sensitivity of only 43%. The specificity and sensitivity of TPA was only 58% and 41%, respectively, the latter increased to 80% in Tis. 60 patients with proven tumor recurrence showed an increase of neopterin with higher tumor stage. In tumors of stage T2 and Tis serum neopterin was raised in 90% and urine neopterin in 75%. Based on these results cystoscopy, exfoliative urinary cytology and urine analysis are obligatory in the follow-up of patients with superficial bladder cancer. Because of the low specificity (29-41%) TPA and neopterin are not suitable for follow-up.
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PMID:[Value of microhematuria, urine cytology, TPA and neopterin in the after care of patients with bladder tumors]. 343 83

The evolution of a fully malignant tumor is a multistep process resulting from the action of multiple factors, both environmental and endogenous, and involves alterations in the function of multiple cellular genes. Chemical carcinogens that initiate this process appear to do so by damaging cellular DNA. In addition to producing simple point mutations, this damage appears to induce the synthesis of a trans acting factor that can induce asynchronous DNA replication. This response may result in gene amplification and/or gene rearrangement. This phenomenon may also play a role in synergistic interactions between chemicals and viruses in the causation of certain cancers. The primary target of the tumor promoters TPA, teleocidin, and aplysiatoxin appears to be the cell membrane. All three of these agents act, at least in part, by enhancing the activity of the phospholipid-dependent enzyme protein kinase C. We have proposed a stereochemical model to explain the interaction of these amphiphilic compounds with the PKC system. We have found that TPA and teleocidin markedly enhance the transformation of C3H 10T1/2 mouse fibroblasts when these cells are transfected with the cloned H-ras human bladder cancer oncogene. Thus, tumor promoters can act synergistically with an activated oncogene to enhance cell transformation. Furthermore, carcinogen-transformed rodent cells display aberrations in the expression of various endogenous retrovirus-related sequences. Activation of some of these sequences may lead to insertion mutations and further aberrations in gene expression. Thus, multistage carcinogenesis may involve both changes in cellular oncogenes and aberrations in the function of DNA sequences that control gene transcription.
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PMID:Cell culture studies on the mechanism of action of chemical carcinogens and tumor promoters. 406 3

Carcinogenesis is a multistep process resulting from a complex interaction between multiple factors, both environmental and exogenous. In contract to initiating agents that act by damaging cellular DNA, the primary targets of the phorbol ester tumor promoters are membrane-associated receptors. We have proposed a stereochemical model to explain the interaction of these amphiphilic molecules, and of teleocidin and aplysiatoxin, with this receptor system. The model is consistent with evidence that a complex between protein kinase C and phospholipid is the actual receptor for these compounds. Recent data we have obtained with a compound present in tung oil, 12-O-hexadecanoyl-16-hydroxyphorbol-13-acetate (HHPA), and twelve of its congener's (provided by Y. Ito et al.) are also consistent with our stereochemical model. We have studied phorbol ester receptors in a wide variety of tissue culture cell types. Our data, together with other findings, provide evidence for considerable receptor heterogeneity and this may relate to the pleiotropic effects of these compounds. We have found a case of "masked" receptors in a rat liver cell line and shown that it is due to a cell-associated esterase. Normal human melanocyte cultures contain phorbol ester receptors and this is of particular interest since these cells actually require these or related compounds for optimal growth (in collaboration with M. Eisinger). The receptor studies provide clues to how tumor promoters can, via inductive mechanisms, produce alterations in the structure and function of cell membranes. It is not known, however, how in the multistep carcinogenic process promoters enhance the eventual outgrowth of permanently altered tumor cells. We have found that TPA and teleocidin produce a marked enhancement of transformation of C3H 10T1/2 cells induced by transfection with h-ras human bladder cancer oncogene. These and other results are discussed in terms of the role of alterations in cellular oncogenes and transcriptional enhancer sequences during multistage carcinogenesis.
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PMID:Molecular mechanisms of tumor promotion and multistage carcinogenesis. 609 83

We measured the serum TPA level in 260 patients with benign urogenital diseases, 189 patients with urogenital cancer and 72 healthy blood donors by using a radio-immunoassay kit in order to evaluate its usefulness as an indicator for the presence of cancer. TPA value (mean +/- 2SD) in healthy blood donors was in the range of 36.8-110.8 units per liter, so that values higher than 110 U/L were considered to be abnormal. Significantly higher serum TPA levels were observed in patients with non-treated cancers, compared to healthy blood donors. But elevated serum TPA levels were also observed in the patients with benign diseases, especially in cases of benign prostatic hyperplasia with urinary tract infection. Consequently, it is considered that the serum TPA test is very useful for detecting urogenital diseases, but not for screening urogenital cancer. In cases of urogenital cancer, serum TPA levels elevated significantly by recurrence or recrudescence of the disease. Therefore, a good correlation was established between serum TPA and the efficiency of a given therapy in patients with prostatic cancer and bladder cancer.
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PMID:[Serum tissue polypeptide antigen (TPA) in patients with urogenital cancer]. 650 5

Serum tissue polypeptide antigen (S-TPA) levels in 22 patients with bladder cancer were determined using a radioimmunoassay kit by the two-antibody technique to evaluate the usefulness of this parameter as an index of the presence of cancer. As S-TPA values (mean +/- SD) in 72 Japanese normal blood donors (37 male and 35 female) were in the range of 32.4-97.2 units per liter, values higher than 97.2 u/l were considered positive. We found a remarkably increased level of S-TPA in 14 out of 18 (77.8%) patients with untreated cancer and a slightly increased level of S-TPA in 3 out of 4 patients whose tumors had been removed. Elevated S-TPA levels in patients who had tumors remaining were suggested to correlate with histological stage and grade of tumors, type of growth and size of tumors, although not to correlate with number of tumors and whether tumor occurrence was initial or recurrent. Simultaneous urinary cytological examination and measurement of plasma CEA in the same patients gave the positive ratio of 7/16 (43.8%) and 0/14 (0%), respectively. It is possible that S-TPA may be one of the most useful tumor markers in the screening of cancer, diagnosis of histological characteristics, monitoring of cancer therapy and detection of recurrence.
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PMID:[Tissue polypeptide antigen (TPA) in urological malignancies. I. S-TPA in bladder cancer patients]. 667 10


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