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)

The biochemical basis for natural resistance to 1-beta-D-arabinofuranosylcytosine (ara-C) was investigated in the intact cells of 4 rat ascites hepatomas, AH-66F, AH-60C, AH-109A, and AH-66, whose sensitivity to ara-C was different in that decreasing order. The initial rapid uptake of ara-C, mediated by the facilitated diffusion, was similar in all the cell lines tested but the subsequent slow uptake due to phosphorylation of ara-C was inversely correlated with their drug resistance. The capacity for drug phosphorylation was slightly higher in AH-66F and much lower in AH-60C, AH-109A, and AH-66 than in the host bone marrow. In contrast, mouse leukemia L-1210, one of the tumors sensitive to ara-C, phosphorylated the drug about 7 times faster than AH-66F and 4 times faster than the host bone marrow. More than 95% of phosphorylated ara-C was the triphosphate, the active form. Deamination of ara-C was not observed in any tumor or bone marrow. It is concluded that the low capacity for nucleotide formation is related to the natural resistance of rat ascites hepatomas to ara-C.
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PMID:Mechanism of natural resistance of rat ascites hepatomas to 1-beta-D-arabinofuranosylcytosine. 71 Aug 5

Fractionation of Simaba multiflora A. Juss. guided by bioassay has resulted in the isolation of a new antileukemic quassinoid 6alpha-senecioyloxychaparrinone (2) and the previously reported quassinoid chaparrinone (3). The structure of the former has been established by spectral and chemical methods. Compound 2 has high anti-neoplastic activity against several mouse leukemia systems (P-388, L-1210 and in solid-tumor B-16 melanoma). This demonstrates for the first time that the presence of a C-15 ester function is not required for antineoplastic activity in the quassinoids.
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PMID:Plant antitumor agents. XVI. 6alpha-Senecioyloxy-chaparrinone, a new antileukemic quassinoid from Simaba multiflora. 73 40

Carcinogenic effect of a single oral administration of 300 or 200 mg/kg body weight of 1-butyl-1-nitrosourea (BNU) and continuous oral administration of 400 ppm solution of BNU in the drinking water for 5, 10, 15, and 20 weeks to female SD rats was studied. In addition, the number of spleen cells capable of forming plaques (PFC) against primary immunization with sheep red blood cells was investigated in various stages of the animal experiments. With a single oral administration of BNU, tumors developed in 31/50 (62%) rats between the 25th and 75th week. They were most frequently seen in the mammary gland (40%), followed by the stomach (10%), kidneys (8%), and ovary (8%). Leukemia was found in 8%. No dose-effect relationship was observed in these 2 experimental groups. On the other hand, tumors developed in 67/77 (88%) of the rats that received BNU in their drinking water. The incidence of tumors was highest in leukemia (61%), followed by mammary tumors (26%), intestinal tumors (12%), and ear duct tumors (8%). There was a dose-effect relationship among the 4 groups in the latent period and target organs for tumor development. Although the PFC count of the rats receiving BNU for 5 weeks recovered gradually to about 50% of the control level at the end of the 25th experimental week, it remained less than 10% of the control level for the whole experimental period in those receiving BNU longer than 10 weeks. Therefore, it was apparent that the tumors developed, proliferated, and finally killed the host rats in highly immunosuppressive state.
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PMID:Carcinogenic effect of 1-butyl-1-nitrosourea on female Sprague-Dawley rats. 77 31

Female Sprague-Dawley rats, 36 days old, were pretreated for 2 weeks either with 100 ppm 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) or 250 ppm S-(1,2-dicarbeth-oxyethyl)OO-dimethyldithiophosphate (Malathion) in the diet. From day 50 they were given, via stomach tube, 21 consecutive daily doses of 0.714 mg 7,12-dimethylbenz[a]anthracene (DMBA). Pesticide diets and observation of the animals for mammary tumors continued until necropsy, 230 days after the start of DMBA administration. DDT-treated rats had a significantly lower mammary tumor incidence, prolonged tumor latency period, and fewer tumors per rat than did the control group. Animals given Malathion (an organophosphate pesticide) had a higher mammary tumor incidence, shortened latency period, more tumors per rat, and more actively growing tumors than did the control group (DMBA only). Leukemia incidence in rats surviving to necropsy (230 days after the start of DMBA administration) was 11/20 for control, 2/29 for DDT, and 8/12 for Malathion-treated rats. Leukemia was primarily myelogenous. DDT may inhibit DMBA-induced mammary tumors and leukemia by stimulating hepatic metabolism and excretion of DMBA so that less carcinogen is available to peripheral tissues. Malathion may potentiate DMBA induction of mammary tumors and leukemia by inhibiting the same enzyme systems induced by DDT.
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PMID:Protection by 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) against mammary tumors and leukemia during prolonged feeding of 7,12-dimethylbenz(a)anthracene to female rats. 80 43

The tests on AKR and C57BL mice of different age were conducted using experimental models of transplanted Gross leukemia (the first passage), Pujman leukemia and spontaneous AKR mouse leukemia. An inverse relationship between the ability of mice to produce humoral antibodies and their susceptibility to transplantation of singeneic leukemic cells and the incidence of spontaneous leukemia has been established. The differences in the ability of the animals to develop immune response to a heterologous antigen were connected with the physiological processes of the aging organism. The data obtained indicated that the failure of one of the links of immunity did not always result in a higher risk of tumor development.
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PMID:[Relationship between the development of experimental leukemia and animals' capacity for a humoral immune response]. 99 Apr 63

The concept that type-C RNA viruses serve as determinants of chemically induced cancer would be supported if immunization against such viruses reduced the incidence of methylcholanthrene-induced sarcomas. A formalin vaccine was employed which was able to protect mice against the development of virus-induced Rauscher leukemia: 8/12 vaccinated mice survived versus 1/12 controls. When mice so immunized were challenged with near-threshold doses of chemical carcinogen, sarcoma incidence and death latency did not differ between vaccinated and control groups: within 10 months, a 320 mug dose of methylcholanthrene induced 100% sarcomas in both groups, while a 64 mug dose induced 62% and 65% tumors in vaccinated and control mice respectively. Thus, a relevant postulate of the oncogene hypothesis could not be supported by these studies. Formalin treatment neutralizes the oncogenic effect of mouse leukemia viruses yiwlding preparations that are immunogenic and can be successfully used as vaccines to protect against virus-induced leukemia (5). The finding of murine leukemia viruses in chemically induced tumors (1, 2) poses the question of whether these viruses are present in the tumors as passengers, or whether they are etiologically involved in the process of tumor induction. An approach to answering this question would be to challenge with chemical carcinogens mice which have been vaccinated with leukemia virus. If the virus were somehow involved in tumor induction, antiviral immunization might conceivably interfere with chemical carcinogenesis. Whitmire and Huebner (9) have reported that mice immunized with formalin-treated leukemia viruses, become resistant to sarcomagenesis by methylcholanthrene. Repetition of this experiment by Gericke and Chandra (6) gave non-significant differences between experimental and control groups. The present paper deals with the effect of immunization against Rauscher leukemia virus upon tumor induction by near-threshold doses of methylcholanthrene.
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PMID:Effect of a Rauscher leukemia virus vaccine upon chemical oncogenesis in the mouse. 102 Oct 12

The incidence of spontaneously occurring neoplasms was observed over 10 years in a colony of germfree F344 rats (78 males and 102 females) representing 10 generations of inbredding. Leukemia was the most common neoplasm (25.6% of males, 36% of females) followed by mammary tumors (11.5% of males, 19.6% of females). Various other tumors developed in 9% of the males and 5% of the females. The overall incidence of spontaneous tumors was comparable to that reported for conventional rats of different strains. This was particularly true of leukemia for which the most data were available. However, for unknown reasons, significantly fewer solid tumors were observed in germfree than in conventional male rats.
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PMID:Occurrence of spontaneous tumors in the germfree F344 rat. 106 60

Leukemia patients in remission were immunized with RAJI lymphoid tissue culture cell lines. Four of 7 patients developed antibody to the immunizing cell as well as to allogeneic leukemia cells. Sera from 3 patients were tested against autochthonous tumor cells either frozen or obtained at the time of disease relapse. Patient's sera were cytotoxic to their own leukemia cells; however, this cytotoxicity was lost at the time of relapse.
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PMID:Human antisera detecting leukemia-associated antigens on autochthonous tumor cells. 111 20

Of four lactones studied in the systems Sa-180, EAC and L-1210, two compounds: alatolide, (ALA) and eupatoriopicrin (EUPP), according to the criteria of CCNSC, showed high cytostatic activity, and ursiniolide A (URSA) "moderate" cytostatic activity against at least one type of transplantable tumor. Two compounds were selected for further confirmatory investigation: EUPP, which gave 92% inhibition of EAC and 60% increase in survival of animals bearing Leukemia L-1210; and ALA, which gave 96% inhibition of growth of EAC.
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PMID:Sesquiterpene lactones XVII. Cytostatic and pharmacological activity. 122 Jun 38

A heterologous antiserum against a Nitrosomethylurea--induced mouse leukemia prevented the outgrowth of syngeneically transplanted leukemia cells in neonatally thymectomized mice. After subcutaneous challenge with 50 000 leukemia-ascites cells thymectomized CBA mice at the age of 8 weeks were given 5 intraperitoneal injections each of 0,1 ml of the heterologous serum. While the antileukemic serum protected 9 out of 11 mice all of the 11 mice treated with normal rabbit serum developed a tumor. The absence of the thymus was confirmed by macroscopic control and by the absence of antibodies against the injected rabbit serum. With regard to previous findings showing a cooperation of heterologous antibodies with host cells as responsible for the antileukemic effect this result indicates that the effector cells are thymus-independent.
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PMID:[On the mode of action of heterologous antileukemic sera. Growth of syngeneically transplanted leukemia cells on serum treated neonatally thymectomized mice (author's transl)]. 122 57


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