Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sialyltransferase activity was measured in plasma samples using desialated fetuin as the acceptor and cytidine 5'-phosphate-sialic acid as donor. The data show an increased enzyme level in 56 of 65 cancer patients studied, as compared with normal control values. The enzyme was not significantly elevated during lacation or in liver cirrhosis, but it was elevated in rheumtoid arthritis. Of the patients with cancer, 35 showed plasma enzyme levels above any value encountered in rheumatoid arthritis plasmas. The determinants of enzyme level in cancer appear to be complex: monitoring of plasma sialytransferase may be of value in measuring tumor progression, metatastatic involvement, or success of therapeutic programs.
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PMID:Elevated plasma sialyltransferase in the cancer patient. 116 8

Total serum testosterone, serum testosterone binding globulin and free androgen index were determined before and during treatment in 14 patients with previously untreated disseminated prostatic cancer. Six patients received estramustine phosphate and six other patients underwent orchiectomy. Two further patients received estramustine phosphate because of tumor progression one and two years after orchiectomy. The result of the study indicates that estramustine phosphate is significantly more effective than orchiectomy in eliciting low levels of free androgens. This complete androgen ablation is produced by a depression of total testosterone and a concomitant increase of total serum testosterone binding globulin which yields a free androgen index an average 4.6 times lower in estramustine phosphate treated patients than in patients who underwent orchiectomy.
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PMID:Effect of estramustine phosphate on free androgens. A comparative study of the effect of orchiectomy and estramustine phosphate on free androgens in patients with prostatic cancer. 209 2

To facilitate understanding of the mechanisms underlying pulmonary diseases, including lung cancer and cystic fibrosis, we have transformed and characterized cultures of human tracheal epithelial cells. Cells were transfected by calcium phosphate precipitation with a plasmid containing a replication-defective simian virus 40 (SV40) genome. Colonies of cells with enhanced growth potential were isolated and analyzed for transformation- and epithelial-specific characteristics. Precrisis cells were observed to express the SV40 large tumor antigen, produce cytokeratins, have microvilli, and form tight junctions. After crisis, cells continued to express the SV40 large tumor antigen as well as epithelial-specific cytokeratins and to display the apical membrane microvilli. Apical membrane Cl channels were opened in postcrisis cells exposed to 50 microM forskolin. These channels showed electrical properties similar to those observed in primary cultures. The postcrisis cells have been in culture for greater than 250 generations and are potentially "immortal." In addition to providing a useful in vitro model for the study of ion transport by human airway epithelial cells, the cells can be used to examine stages of neoplastic progression.
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PMID:Characterization of human tracheal epithelial cells transformed by an origin-defective simian virus 40. 245 4

In vivo effects of DL-alpha-difluoromethylornithine (DFMO) on the metabolism of polyamines and nucleotide phosphates were monitored in P388/S leukemia cells grown intraperitoneally in BDF1 inbred male mice. Inhibiting the ornithine decarboxylase (ODC) activity DFMO depleted putrescine and spermidine to 30-50 and 50-60%, respectively, and increased spermine to 25-60% compared with the controls, when given as 2% solution in drinking water of the tumor-bearing animals. DFMO treatment caused a parallel 56% elevation of total nucleotide content in tumor cells with distinct and significant increase of some nucleotide phosphates. The most pronounced alterations were shown in the intracellular UTP (202%), CTP (103%), ADP (92%) and ATP (71%) concentrations. Changes in polyamine and nucleotide phosphate metabolisms were dependent on tumor progression. A possible explanation of the metabolic events induced by DFMO is discussed.
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PMID:In vivo effects of DL-alpha-difluoromethylornithine on the polyamine and nucleotide phosphate metabolism in P388/S leukemia cells. 308 89

In a prospective multicenter study, 244 men with highly or moderately differentiated prostatic cancer in stage I, II or III (VACURG) were consecutively randomized to three groups of treatment: Group A (77 patients) received polyestradiol phosphate (Estradurin, Leo) 80 mg i.m. every fourth week + ethinyl estradiol (Etivex, Leo) 150 micrograms daily, group B (72 patients) estramustine phosphate (Estracyt, Leo) 280 mg twice daily, and group C (76 patients) no therapy. Only men without current or previous other malignancy and without cardiovascular disease were admitted to the study. After 4 1/2 years 125 of the 244 patients had left the study, 9 because of cancer progression (stage IV, VACURG). The most serious complications were cardiovascular, including ischemic heart disease, cardiac decompensation, cerebral ischemia and venous thromboembolism, which occurred in 24 patients from group A and 9 from group B as compared to only one patient in group C. The subgroup superficial or deep venous thrombosis comprised 11 group A and 2 group B patients. Estrogens (E + e) offered as palliative treatment to patients with non-generalized prostatic carcinoma is burdened with a high incidence of serious cardiovascular complications.
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PMID:Cardiovascular complications of estrogen therapy for nondisseminated prostatic carcinoma. A preliminary report from a randomized multicenter study. 352 68

The number of approaches available for the management of metastasizing prostatic carcinoma is overwhelming. If due attention is paid to prognostic factors, however, patients can be effectively treated in the urological practice. Once the condition has been diagnosed the first-line treatment carried out should be orchiectomy. Adjuvant drug therapies with such agents as progestogens and estrogens seem to be of little value. Data are not yet available from prospective studies performed to assess the value of complete androgen blockade. In addition, there is so far only experimental evidence that the effect of endocrine therapy is enhanced by an initial adjuvant chemotherapy in untreated prostatic carcinoma, and this should be investigated in randomized clinical trials. In the case of tumor progression estrogens or antiandrogens can be administered to relieve the symptoms; good effects have been achieved especially with estramustine phosphate. Further progression demands chemotherapy, which should be selected with reference to Berry's parameters. There is no agent or combination generally accepted as the chemotherapeutic agent of choice.
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PMID:[Advanced prostate cancer--a therapeutic dilemma?]. 357 64

Hexamethylmelamine, methotrexate, and 5-fluorouracil (HMF) is a second-line chemotherapy for patients with ovarian carcinoma refractory to platinum-based regimens. Two of 15 patients with tumor progression treated with HMF alone had objective complete responses while one had a 12-month disease-free interval (DFI). Among 8 patients treated with HMF and either intraperitoneal chromic phosphate and/or alternating platinum-based chemotherapy following second-look surgery which documented persistent carcinoma, 3 have experienced disease-free intervals of 19, 27, and 42 months. However, no one has been cured or had a long-term remission after HMF therapy alone.
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PMID:Hexamethylmelamine, methotrexate and 5-fluorouracil (HMF) for progressive ovarian carcinoma during therapy with cis-platinum, cyclophosphamide +/- doxorubicin. 393 41

Decimal dilutions containing 5 X 10(5) to 5 X 10(1) cells were inoculated s.c. into nude mice and the course of tumor development was recorded. The highest concentration of cells produced rapidly growing poorly differentiated sarcomas within 2-3 weeks of their inoculation. Upon explantation the resultant tumors yielded cells which multiplied on plastic almost as rapidly as did their progenitors used to initiate the tumors, and had as high a colony forming efficiency in agar as long as tryptose phosphate broth was omitted from the agar medium. Tumors initiated by the lower concentrations of cells were disproportionately delayed in their appearance and tended to increase in size at a low rate. At least one tumor regressed and one which apparently regressed appeared again at a later time. These changes are characteristically described under the rubric of tumor regression. Host reactive cells such as neutrophils, eosinophils, macrophages, and fibroblasts were observed in some tumors. One of the tumors was a low grade hemangiosarcoma, another a well-differentiated fibrosarcoma, and the rest poorly differentiated sarcomas. Cells from two tumors initiated by 500 and 5000 cells multiplied slowly in early passages in culture, particularly when seeded at low densities at which they appeared to sustain cumulative damage even when multiplying. In later passages, the "low dose" tumor cells gained the capacity to multiply in culture after seeding at low densities, but it took up to 50 cell generations to reach this capacity. The loss of growth capacity on plastic of cells from the low dose tumors and its subsequent restoration by passaging in culture may provide a quantitative method for analyzing the type of cellular change which underlies tumor progression.
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PMID:Dynamics of tumor growth and cellular adaptation after inoculation into nude mice of varying numbers of transformed 3T3 cells and of readaptation to culture of the tumor cells. 394 78

Vitamin B6 metabolism has been investigated in several highly and well-differentiated Morris hepatomas. Comparisons have been made with two poorly differentiated Morris hepatomas, with host livers obtained from tumor-bearing animals, and with fetal, neonatal, and adult rat liver. The pyridoxal phosphate content and the activities of pyridoxine kinase and pyridoxine phosphate oxidase of all Morris hepatomas examined were significantly less than those in adult host or control livers and generally fell in the range determined for fetal and neonatal liver. A similar pattern was not evident for the activity of pyridoxine phosphate phosphatase. Relative to control and host livers, the activity in hepatomas of the pyridoxal phosphate (PLP)-dependent enzyme, ornithine decarboxylase, was generally elevated. Dexamethasone, at a dose which caused an elevation in the activity of PLP-dependent tumor tyrosine aminotransferase, had no effect on PLP metabolism. The data indicate that tumor progression in the Morris hepatoma spectrum in relation to vitamin b6 metabolism falls into an onco-developmental pattern characterized by a diminished amount of tissue PLP and a diminished capability to metabolize precursor vitamer forms to PLP.
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PMID:Vitamin B6 metabolism in liver and liver-derived tumors. 612 59

Fischer rats, in whom superficial transitional cell cancers of the urinary bladder were induced by the carcinogen N-[4-(5- nitrofuryl )-2-thiazolyl] formamide, were inoculated intraperitoneally with either phosphate buffered saline, indomethacin (a prostaglandin synthetase inhibitor), poly I:C (an interferon inducer), or indomethacin together with poly I:C. While indomethacin alone appeared to have a significant albeit variable inhibitory effect on tumor size, poly I:C had a far more pronounced significant inhibitory effect. The combination of poly I:C and indomethacin together, however, led to the greatest inhibition in tumor growth, and in some instances, to tumor regression. Splenic lymphocytes from the same animals demonstrated enhanced natural cytotoxicity after treatment with poly I:C. Surprisingly, levels of natural cytotoxicity seen in animals treated with indomethacin and poly I:C together were lower than those seen with poly I:C alone. No enhancement of cytotoxicity could be demonstrated in vitro in lymphocytes from indomethacin-treated animals. Macrophages were also treated in this system under identical conditions. However, the activity of macrophages alone and of macrophages and lymphocytes together did not appear to be modified either by indomethacin alone or by the combination of prostaglandin synthetase inhibition and interferon induction together, the combination of which in vivo was suggested to be most effective in controlling tumor progression. Further studies to determine timing of these interactions and doses of immune response modifiers in order to characterize mechanisms possibly at work in modifying tumor growth in this system therefore seem highly indicated.
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PMID:Indomethacin and poly I:C in the inhibition of carcinogen-induced bladder cancer in an experimental animal model. 620 90


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