Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Optimal schedules of benzaldehyde (50-100 mg kg-1 intraperitoneally) on day 1 or on several days after inoculation of 10(5) P388 leukemia cells to DBA 2J mice increased survival by 70-100%. No significant prolongation of survival was observed between the various schedules of benzaldehyde treatment. Significantly longer survival was observed on day 30 after benzaldehyde treatment with 100 mg kg-1 on day 1 or 50 mg kg-1 on days 1-4 as compared to untreated controls, but no cure was achieved with any schedule and dose of benzaldehyde. No or minimal activity of benzaldehyde on L1210 and L5178Y leukemias, Ehrlich adenocarcinoma and Yoshida sarcoma was observed.
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PMID:Therapy of P388 leukemia with benzaldehyde. 322 39

P-30 Protein is a novel protein, of molecular weight approximately 15 KD, obtained from the extract of a vertebrate tissue showing in vivo antitumour activity. Cytostatic and cytotoxic effects of this product in its purified form (P-30 Protein) or in partially purified extracts (Pannon) were studied in vitro on human leukaemic HL-60, human submaxillary carcinoma A-253, human colon adenocarcinoma Colo 320 CM and murine erythroleukaemia (Friend leukaemia) cell lines. Of these cells, HL-60, A-253 and Colo 320 CM were sensitive and Friend leukaemia resistant to this agent. The effects were time- and concentration-dependent. During the initial 24-48 h of treatment, a slowdown in cell proliferation was apparent but cell death was not extensive. After 24-48 h, there was a reduction in the proportion of cells in S phase of the cell cycle and the cells became preferentially arrested in G1 phase. The G1 cells showed high heterogeneity with respect to RNA content and some cells were characterized by very low RNA content. Progressive cell death occurred in cultures maintained with Pannon for up to 7 d in proportion to its concentration. Reductions of 50 and 90% in clonogenicity of A-253 cells were observed during their growth in the presence of 0.13 and 1.5 micrograms/ml of this protein, respectively. Exponentially growing cells were more sensitive to Pannon compared with cells from confluent cultures. Colonies of A-253 cells growing in the presence of Pannon were much smaller in size compared with control colonies, indicating that the rate of proliferation of clonogens is reduced by this agent. It appears that P-30 Protein induces cytostatic effects via modulation of cell transition to quiescence or differentiation. The mechanism of its cytotoxic activity is unclear.
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PMID:Cytostatic and cytotoxic effects of Pannon (P-30 Protein), a novel anticancer agent. 322 65

The antitumour efficacy of batracylin was investigated in vivo against murine tumours. The drug displayed an original spectrum of activity. It was totally inactive against L1210 leukaemia and B16 melanoma, while it was marginally active against ascitic P388 leukaemia. However, the tumour growth of the subcutaneously (s.c.) implanted colon 38 adenocarcinoma (Co 38) was completely inhibited in 80-90% of the mice. Therapeutic efficacy was retained upon oral administration and the drug was able to induce tumour regression in the advanced Co 38 disease. These data justify the selection of batracylin for toxicological studies and possible clinical investigations.
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PMID:A new antitumour agent, batracylin, selected by a preclinical solid tumour model. 322 19

Mice and rats of various ages (3, 10-12, and 18-19 months) were inoculated with the transplantation tumours murine melanoma B16 (B16), mammary adenocarcinoma 755 (Ca-755), leukemia P388 (P388), and rat rhabdomyosarcoma RA-2 (RA-2). Subcutaneous (sc) growth of B16 was not markedly affected by the age of the syngeneic host whereas intravenously (iv) inoculated 12 months old C57BL/6 mice developed more pulmonary metastases than animals 3 months of age. Median survival time (MST) of 18 months old mice bearing Ca-755 was significantly shorter than that of younger individuals. In contrast, old rats that had been injected RA-2 iv survived longer than controls. Survival of DBA/2 mice inoculated intraperitoneally (ip) with P388 cells was not influenced by the age of the host. The antineoplastic activity of ambazone and, to a less extent, of 5-fluorouracil against P388 was drastically lower in 12 months old mice than in 3 months old tumour bearers. Likewise a graduate loss of antineoplastic activity of ambazone against Ca-755 was observed with increasing age of the mice, whereas the effect of ambazone and 5-fluorouracil against RA-2 did not depend on the age of the rats. It is suggested that tumour-host interactions as well as pharmacokinetics of a given drug may underlie age-related changes.
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PMID:Carcinogenesis and aging. VIII. Effect of host age on tumour growth, metastatic potential, and chemotherapeutic sensitivity to 1.4-benzoquinone-guanylhydrazonethiosemicarbazone (ambazone) and 5-fluorouracil in mice and rats. 322 59

Certain derivatives of phenolselenonic acid, namely ammonium, calcium, potassium, and sodium 3-acetoxy-4-methoxybenzolselenonates as well as the corresponding derivatives of 3-hydroxy-4-methoxybenzolselenonic acid were studied. These compounds were tested for anticarcinogenic activity against urethane-induced pulmonary adenomas and for antitumoral activity against some transplanted tumours such as leukemia L 1210, mammary adenocarcinoma Ca 755 and Walker carcinosarcoma 256. These compounds were found to produce more intensive anticarcinogenic action than antitumoral one. The results showed that ammonium 3-acetoxy-4-methoxybenzolselenonate given before the injection of urethane or together with urethane exert a significant influence on adenomas, while calcium 3-hydroxy-4-methoxybenzolselenonate inhibited the formation of adenomas at various stages of their development.
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PMID:[Anticarcinogenic and antitumor properties of selenium-containing phenol derivatives]. 324 98

Monoclonal antibodies (MAbs) were generated by immunizing mice with the mesothelioma cell line SPC111 and selected by indirect immunofluorescence on viable cells. Indirect immunofluorescence staining and radioimmunoassays demonstrated selective binding of the antibodies ME1 and ME2 with the surface membrane of mesothelioma, but not with lung adenocarcinoma cell lines. Lung small-cell carcinoma cell lines were unreactive, while staining was seen in a proportion of lung squamous-cell carcinoma cell lines. The antibodies were unreactive with other cell lines, including breast, colon, ovarian, and renal-cell carcinoma, leukemia, and lung fibroblast. The antibodies stained normal mesothelial cells, but were unreactive with normal bronchial epithelial cells in primary cultures, or peripheral blood cells. Immunohistochemical staining of cryostat sections of tumor tissues confirmed the ability of the antibodies to distinguish between mesothelioma and lung adenocarcinoma. All 12 mesothelioma tissues, but none of 9 lung adenocarcinomas or large-cell carcinomas, stained with the MAbs. Staining of malignant mesothelioma tissues was very homogeneous. Some lung squamous-cell carcinomas and breast carcinomas were stained focally by both, and some ovarian carcinomas by one antibody. Solid-phase radioimmunoassays demonstrated antigen sensitivity to chymotrypsin digestion and binding competition between the antibodies. The antibodies ME1 and ME2 identify a surface membrane antigen with preferential expression on normal and malignant mesothelial cells. They distinguish malignant mesothelioma from lung adenocarcinoma on cryostat sections and promise to be useful tools in biological studies of mesothelial cells.
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PMID:Monoclonal antibodies against mesothelial membrane antigen discriminate between malignant mesothelioma and lung adenocarcinoma. 327 35

A series of 1-amino-substituted 4-methyl-5H-pyrido[4,3-b]indoles that are structurally related to ellipticines by deletion of a ring have been synthesized in order to evaluate their DNA affinity, their in vitro cytotoxicity on L1210 cultured cells, and their in vivo antitumor activity. Among 24 derivatives that have been prepared and studied for the structure-activity relationship in this new class of antineoplastic agents, those that have a NH(CH2)3N(R)2 side chain (R = CH3 or C2H5) at their 1-position, a 4-methyl group, and an 8-OH substituent, either with a 5-NH or with a 5-NCH3 group, show the most potent cytotoxicities on L1210 cultured cells and in vivo antitumor properties in P388 and L1210 leukemia systems. In vivo antineoplastic activity of the most potent products was confirmed in P388 and L1210 leukemia systems. In vivo antineoplastic activity of the most potent products was confirmed on other mouse experimental tumors from the standard NCI screening:B16 melanoma and C38 adenocarcinoma.
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PMID:1-Amino-substituted 4-methyl-5H-pyrido[4,3-b]indoles (gamma-carbolines) as tricyclic analogues of ellipticines: a new class of antineoplastic agents. 333 9

Modification effect of sodium salts and ethers of linolenic, arachidonic and alpha-linolenic acids on the growth of transplantable mouse tumors was examined. Polyunsaturated fatty acids (PUFA) enhanced the growth of mammary adenocarcinoma Ca-755, whereas the opposite effect was observed in mice with leukemia L-1210 and sarcoma 180. No differences in the growth of melanoma B-16 and Lewis lung carcinoma were noted in control and experimental animals. Modification effect of PUFA was significantly suppressed by prostaglandin inhibitor indomethacin and to a lesser extent by antioxidant alpha-tocopherol.
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PMID:[Nature of the modifying action of polyunsaturated fatty acids on the growth of transplantable tumors of different types]. 335 34

The cytotoxic effects of ketoconazole, an antifungal agent known to have some activity against human prostate cancer, adrenal cancer, and male metastatic breast cancer, were evaluated using colony-growth and clonogenic assays in eight malignant cell lines. The cytotoxicity of ketoconazole showed a dose- and time-dependent pattern, with the following concentrations inhibiting 90% of the growing colonies (IC90): MCF 7 (human breast cancer) 7.25 micrograms/ml, T 47 D (human breast cancer) 9.0 micrograms/ml, MiaPaCa (human pancreatic carcinoma) 10.0 micrograms/ml, COLO 357 (human pancreatic carcinoma), 9.5 micrograms/ml, HCT 8 (human colonic adenocarcinoma) 27.1 micrograms/ml, DU 145 (human prostatic cancer) 40.0 micrograms/ml, AR 42 J (rat pancreatic carcinoma) 9.0 micrograms/ml, and L1210 (murine leukemia) 8.6 micrograms/ml. Since a concentration of 10 micrograms/ml can be achieved in humans, the use of ketoconazole in human malignancies might be worthy of clinical evaluation.
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PMID:Cytotoxicity of ketoconazole in malignant cell lines. 337 Jul 40

Con A acceptor glycoproteins from the human Molt 4 (T cell leukaemia) and HeLa (endocervical adenocarcinoma) cell lines were purified by affinity chromatography and used for the preparation of rat antisera. Cross-absorption analysis showed that each antiserum contained antibodies which recognised cell surface antigens preferentially expressed by the donor cell line. Molt 4-associated antigens were fully expressed on T cell tumour lines and normal thymocytes, but not on non T cell tumour lines, peripheral blood lymphocytes or other blood cells. Immunofluorescence studies showed that the antigens were preferentially expressed on a sub-population of immature thymocytes. HeLa-associated antigens were only fully expressed on one other epithelial tumour cell in a panel of 17 cell lines. Immunofluorescence studies showed that the HeLa-associated antigens were expressed on normal endocervical adenoepithelium but not on ectocervical, endometrial or intestinal epithelia. Thus purified Con A acceptor glycoproteins of cultured tumour cell lines are potent immunogens for the generation of antibodies recognising lineage-associated differentiation antigens. These antigens should be useful in tumour classification and in the study of normal differentiation.
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PMID:Specificity of antibodies to the purified Con A acceptor glycoproteins of cultured tumour cells. 351 35


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