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)

Patients with poorly differentiated prostatic carcinoma and skeletal metastases were randomized to treatment with 2.6-cis-diphenylhexamethylcyclotetrasiloxane (2.6-cis) and estramustine-17-phosphate (estramustine). Parallel with the clinical study a group of non-randomized patients were treated with 2.6-cis. Cytological regression of the tumor could be registered in half of the estramustine group but not in the 2.6-cis group. There were no drug-related changes in blood chemistry, kidney function tests, hematology or liver enzymes. There was in increase in acid and alkaline phosphatase in both groups but more pronounced in the 2.6-cis group. In both groups follicle-stimulating and luteinizing hormone values were depressed. Testicular and penis atrophy was observed in the 2.6-cis group. Relief of pain and marked improvement of conditions occurred in the majority of the cases in both groups. In general, no tumor regression was observed during administration of 300 mg. 2.6-cis daily for at least 3 months. Some tumor regression was noted during 600 mg. estramustine therapy daily.
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PMID:Clinical experimental randomized study of 2.6-cis-diphenylhexamethylcyclotetrasiloxane and estramustine-17-phosphate in the treatment of prostatic carcinoma. 73 10

Six pyridine-2-carboxaldehyde, one pyridine N-oxide 2-carboxaldehyde, and five diketone thiophosphoric hydrazones, three thiophosphoric hydrazides, and two cupric chelates were synthesized. The chelates and nine of the hydrazones were tested against Ehrlich ascites carcinoma. Seven of these latter agents were administered concurrently with either cupric and/or ferrous salts to mice bearing this tumor. The greatest activity was found with the chelate, cimethyl pyridine-2-carboxyaldehyde phosphorothioic hydrazone-copper (1:1). The hydrazone portion of this chelate also formed a ligand-copper (2:1) complex. Although all of the hydrazones but one were inactive when evaluated alone, the concurrent injection of cupric ion increased survival times by an avoli alkaline phosphatase was found to be inhibited by two thiosemicarbazones in a manner similar to that previously reported by these agents against alkaline phosphatase derived from Sarcoma 180-6-thiopurine resistant ascites cells. None of the 14 hydrazides or hydrazones tested against E. coli enzyme displayed significant inhibition.
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PMID:Phosphorus-nitrogen compounds. 20. Thiophosphorus hydrazones. 78 82

A spontaneous papillary adenocarcinoma was found in the lung of an A/St female mouse 20 months of age, and its transplantable line forming bone and chondroid tissue was established. The basic patterns changed from papillary adenocarcinoma to anaplastic carcinoma or a fibrosarcoma-like pattern through tubular adenocarcinoma. Osseous tissue appeared in the 1st transplant generation and increased with serial transplantations. In the 5th transplant generation, abundant osseous tissue was seen, a fibrosarcoma-like pattern became predominant and chondroid tissue appeared. Morphologically, the fibrosarcoma-like pattern was proved to be epithelial in nature. Marked alkaline phosphatase activity was demonstrated in the spindle-shaped tumor cells, and the activity obviously elevated in the serum of hosts bearing tumors which included more spindle-shaped cells and osseous tissues than chondroid ones. It is presumed that the osseous and chondroid tissues formed by carcinoma cells did not result from metaplasia in the strict sense of the word but rather from pseudometaplasia or metamorphosis.
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PMID:A transplantable pulmonary tumor line in mouse forming bone and chondroid tissue. 80 91

Squamous cell carcinomas were induced in the hamster cheek pouch with 9,10-dimethyl-1,2-benzanthracene. The process of carcinogenesis was inhibited by phenylphosphate, an inducer of alkaline phosphatase. Orthophosphate and l-phenylalanine, which inhibit alkaline phosphatase, had a promoting effect on tumor formation. The results are in accordance with those of previous studies on the effect of inducers of alkaline phosphatase on chemical carcinogenesis. The effect of the studied substances on carcinogenesis was apparently unrelated to the presence of phenyl or phosphate groups or of steroid rings. The tumor inhibition or promotion seemed to be related to the potential of the tested substances to induce or inhibit alkaline phosphatase activity.
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PMID:Chemical carcinogenesis in the hamster cheek pouch. Influence of inhibitors and inducers of alkaline phosphatase. 81 3

Metronidazole (0.6 mg/gm) was injected intraperitoneally at 12 hour intervals for 10 days into C3H/HeJ mice with established C3HBA mammary adenocarcinomas. Tumor growth, total white cell count and body weight were decreased by 3 days. Heart rate and rectal temperature were depressed most following the initial injections but were less depressed by 10 days. Hemoglobin and hematocrit were not changed. Plasma assays of total protein, uric acid, bilirubin, alkaline phosphatase and calcium were not affected. It was not possible to separate the tumors treated with metronidazole from control tumors, based on cellular differences. Blood vessels in most of the tumors in the drug treated animals were larger and appeared engorged with blood.
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PMID:Effect of metronidazole on the C3H/HeJ mouse and growth of the C3HBA mammary adenocarcinoma. 85 27

The cellular localization and isoenzyme pattern of alkaline phosphatase in five cell lines derived from human bladder carcinomas (T24, RT4, RT112, J82, EJ) shown not to be HeLa cells has been established. RT112 cells had a high level of alkaline phosphatase. RT4 had a moderate amount of alkaline phosphatase but in the other three lines, levels were extremely low. Prednisolone caused a small (2 to 3-fold) increase in total alkaline phosphatase in T24 and RT112 lines only. Electrophoretic separation of isoenzymes showed that RT112 and RT4 cells (derived from more highly differentiated tumor types) had three heat stable bands equivalent to placental alkaline phosphatase and three slower bands of a modified placental type. Prednisolone increased only the former. In T24 cells the enzyme resembled the liver-type alkaline phosphatase in electrophoretic mobility and sensitivity to heat denaturation. Cytochemical studies confirmed the presence of cell surface-associated extramembraneous placental type enzyme in RT112 cells. All five cell lines had small deposits of intramembraneous alkaline phosphatase in the plasma membrane and deposits associated tith the mitochondrial membranes and the endoplasmic reticulum that were not completely inhibited by phenylalanine or Levamisole.
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PMID:Alkaline phosphatase activity in human bladder tumor cell lines. 87 May 58

In a study of 30 patients with hypernephromas, 23 patients manifested systemic effects of the tumor, and in 5 of these, the systemic effects were the presenting feature that led to the diagnosis. In contrast to this, only 17 patients had urologic complaints, and no single patient in this study had the classic triad of hematurial, loin pain, and mass. Weight loss (52 per cent), pyrexia, and elevated sedimentation rate (36 per cent) were seen most frequently. Anemia was seen in 25 per cent of patients. Other features seen in this group wer abnormalities in liver function, elevated alkaline phosphatase, hypertension, erythrocytosis, and hypercalcemia. In the majority of instances, removal of tumor was associated with remission of these effects. The effects were classified as those of a general toxic nature, those due to normal or abnormal production of hormones, and those due to production of abnormal substances by tumor cells. The evaluation of these effects was useful in making an early diagnosis and in follow-up care.
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PMID:Systemic effects of hypernephroma. 89 63

Lactic dehydrogenase (LDH), glutamic-oxalacetic transaminase (GOT), and acid and alkaline phosphatase activities in bone marrow and in cubital vein serum were compared. For patients without cancer, marrow serum LDH attained levels four times as high, and GOT and alkaline phosphatase, levels twice as high as those normal for cubital vein serum; levels of acid phosphatase were the same for both sources. For patients with cancer, significant increase of enzyme levels over reference levels depends on the tumor origin and on the presence and localization of metastases. Marrow enzyme levels may become elevated with or without concurrent elevation in cubital vein serum. Concurrent elevations were found with colonic carcinoma and lymphoid leukemia, and noncurrent elevations, with prostatic cancer, myeloid leukemia, and myeloma. A nonconcurrent elevation of marrow enzymes indicates that the origin of the enzyme is in the marrow, whereas with concurrent elevation, the source of the enzyme may be another organ.
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PMID:Enzymes in peripheral and bone marrow serum in patients with cancer. 98 36

The two oncotrophoblast proteins, Regan isoenzyme (placental-type alkaline phosphatase) and human chorionic gonadotrophin, are readily studied oncodevelopmantal gene products in human cancer patients and in three experimental model systems. The latter consists of (a) HeLa sublines TCRC-1 and TCRC-2, which produce Regan and non-Regan isoenzymes, (b) HEp-2 and FL amnion cell lines as models for the reciprocal expression of developmental genes, and (c) modulation in vivo of developmental gene expression in HeLa cells. In the case of the third model, for example, HeLa TCRC-1 cells grow in immunosuppressed rats to form a tumor nodule, which expresses a new oncoamnion (FL) isoenzyme, while the Regan isoenzyme disappears. Return of the tumor cells to cell culture medium results in a disappearance of the oncoamnion (FL) species and the reappearance of Regan isoenzyme. This interesting model is expected to bridge the interpretation of experiments done in cell culture with observations made on tumors of cancer patients. Most helpful in interpretation of all these studies has been a chronology of early development. It appears that the counterparts of a number of tumor proteins appear as early as gametogenesis and as late as 10 weeks of gestation.
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PMID:Regulatory controls of oncotrophoblast proteins and developmental alkaline phosphatases in cancer cells. 98 46

Alkaline phosphatase (E.C.3.1.3.1.) has been used as a marker for embryonal carcinoma cells which constitute the multipotential stem cells of the mouse teratoma. Studies by other investigators based on kinetics of thermal inactivation and L-phenylalanine inhibition have shown that the alkaline phosphatase of the teratoma differs from the mouse intestinal and liver isozymes, but resembles the isozymes of kidney and placenta. Since functional characterization of nonpurified enzymes is not the most accurate means for distinguishing different molecular forms of an enzyme, we have partially purified the enzymes from the ascitic (embryoid body) and solid tumor forms of the OTT-6050 teratoma line, and utilized the technique of electrophoresis in polyacrylamide gels to compare the teratoma enzyme with isozymes from kidney and placenta. Covalent 32PO4-labeling of the alkaline phosphatases and polyacrylamide gel electrophoresis in sodium dodecylsulfate was also used to compare the subunit molecular weights of the enzymes. The results indicate that the mouse teratoma enzyme is distinct from the kidney and placental isozymes. Since histochemical studies have localized the enzyme to the stem cell population of the teratoma, the results imply that stem cell alkaline phosphatase is a distinct isozyme. The embryoid bodies contain a second alkaline phosphatase which may correspond to the placental isozyme. This enzyme may be attributed to the outer cell layer of embryoid bodies of the ascitic tumor, since this cell type histochemically demonstrates alkaline phosphatase activity.
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PMID:Characterization of two different alkaline phosphatases in mouse teratoma: partial purification, electrophoretic, and histochemical studies. 98 56


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