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 effects of Fluosol-DA, an oxygen-carrying perfluorochemical emulsion, and carbogen breathing alone or in combination on the antitumor activity of cyclophosphamide (CTX) in vivo were investigated. The addition of 12 ml/kg Fluosol-DA immediately prior to CTX treatment exerted no effect on the antitumor effect of CTX on the RIF-1 tumor in C3H mice. On the other hand, carbogen breathing alone for 8 h significantly enhanced the antitumor effect of CTX, with a dose-modification factor of 1.29 +/- 0.07. The combination of Fluosol-DA and carbogen breathing further increased the effect of CTX, with a dose-modification factor of 1.63 +/- 0.05. There was no significant difference in animal lethality within the treatment groups. It was concluded that Fluosol-DA in combination with carbogen breathing may be useful for the enhancement of CTX chemotherapy of human neoplasms.
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PMID:The influence of Fluosol-DA and carbogen breathing on the antitumor effects of cyclophosphamide in vivo. 251 38

The effects of schedule and sequence on the survival of EMT6 tumor cell and bone marrow (CFU-GM) obtained after treatment using combinations of cyclophosphamide (CTX) and thiotEPA or melphalan (L-PAM) were examined and analyzed by isobologram methodology. On a single-injection schedule, when CTX and thio-tEPA were given simultaneously or thiotEPA was given prior to CTX, the result was slightly greater than additive tumor-cell kill. However, when CTX preceded thiotEPA by 4 h, there was less than additive cell kill. When the interval between the administration of the two drugs was 8 h, both sequences of the drugs produced greater than additive tumor-cell kill. Simultaneous administration of CTX and thiotEPA on a multiple-injection schedule resulted in sub-additive tumor-cell kill. On the multiple-injection schedule, extending the interval between injections of CTX and thiotEPA to 4 and 8 h resulted in increasing tumor-cell kill. With the 4- and 8-h intervals, no significant sequence-dependent difference in tumor-cell kill was obtained. The results of CTX and L-PAM combinations paralleled those of CTX and thiotEPA. Bone marrow (CFU-GM) survival was used as a representative normal tissue with which to compare tumor-cell survival after each treatment to obtain a measure of therapeutic effect. The trends for the ratios of bone marrow: tumor cell survival were the same for the treatment sequences of CTX with thiotEPA or L-PAM; however, greater magnitudes of differential tumor-cell kill were obtained with CTX L-PAM combinations. Using this measure, the greatest therapeutic effectiveness was seen with single-dose L-PAM or thio-tEPA followed 4 h later by CTX and with CTX given as a single or as multiple doses followed 8 h later by L-PAM or thiotEPA. Such data from tumor-model systems may be useful in the development of more effective alkylating agent regimens for use in the clinic.
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PMID:Influence of scheduling on two-drug combinations of alkylating agents in vivo. 251 39

A pilot phase II study of a hybrid chemotherapy for SCLC has been conducted between October 1986 and March 1988. Dose and schedule of the regimen were as follows: CTX, 700 mg/m2, on day 1; ADM 30 mg/m2, on day 1; VCR, 1.4 mg/m2, on day 1 (CAV); and CDDP, 60 mg/m2, on day 8; VP-16, 100 mg/m2, on days 8 and 9 (PVP). Courses were repeated q. 4 weeks up to 6 cycles. Patients with LD received chest irradiation at a dose of 50 Gy when maximal response was achieved. Thirty-six patients were fully evaluated for tumor response and toxicity. All 18 patients with LD responded to the regimen including 11 CRs (61%); there were 7 CRs (39%) and 9 PRs (50%) in patients with ED. Fourteen of the 18 patients with LD have survived for 7 to 22 months, against 12.8 months in ED patients. The major toxicity was myelosuppression, but it was well tolerated. These results indicate that hybrid chemotherapy is highly effective for SCLC, and warrants further clinical trials.
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PMID:[Pilot phase II study of hybrid chemotherapy of CAV-PVP in small cell lung cancer (SCLC)]. 254 49

Nude mice, inoculated with LAX 83 in bilateral subrenal capsules, were used in experimental therapy with 8 antitumor drugs. Treatment was initiated 2 d after tumor inoculation. All the drugs were ip to the nude mice daily for 7 d. At the daily doses VCR 0.4, MMC 2, CCNU 16, cis-DDP 2, AdM 2.5, 5-Fu 30, CTX 40 and MTX 2-6 mg/kg, the inhibition of the tumor growth were 100, 95.8, 91.3, 79.2, 65.2, 60.7, 62.3 and 0%, respectively. The results indicated that the effects of the drugs on nude mice inoculated with LAX-83 in subrenal capsule not only exhibited a good correlation to those in sc, but also shortened the period of experiment from 22 to 11 d. Furthermore, when LAX-83 was inoculated into the subrenal capsule of Swiss +/+ mice, the tumor tissues degenerated and disintegrated 2 d after the inoculation and replaced by inflammatory granuloma tissues 6 d later.
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PMID:[Effects of 8 antitumor drugs against the growth of human lung adenocarcinoma (LAX-83) transplanted under the kidney capsule of nude mice]. 261 35

A novel murine tumor resistant to cis-diamminedichloroplatinum (cisplatin, DDP) was obtained (M5/DDP) after 22 passages in which mice bearing the ovarian reticular cell sarcoma M5076 (M5) were treated with DDP. Although DDP conserved some inhibitory activity on growth of M5/DDP, it was much less effective than on M5. Treatment with DDP did not prolong the survival time of mice with M5/DDP, whereas it markedly prolonged survival of M5-bearing mice. M5 and M5/DDP tumors shared many biological and biochemical features. They were similar histologically, they metastasized reproducibly to the liver and were poorly immunogenic. Their growth rates were comparable; their DNA index, percentage of cells in S phase and intra-cellular glutathione content were also similar. In both tumors, DDP caused an accumulation of cells in S late-G2-M within 24 hr after drug treatment. However, this was efficiently reversed in M5/DDP, whereas it worsened and persisted longer in M5. Cross-resistance was observed between DDP and its analogues carboplatin and iproplatin, but tetraplatin retained marginal activity on M5/DDP tumor. Several alkylating agents tested [L-phenyalanine mustard (L-PAM); cyclophosphamide (CTX); chlorambucil (CLB); 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and dacarbazine (DTIC)] were not totally cross-resistant to DDP, but showed greater activity on M5 than on M5/DDP. Other non-alkylating anti-neoplastic drugs showed a similar degree of activity on M5 and M5/DDP. 5-Aza-2'-deoxycytidine (Aza-d-Cyd) was very effective on both tumors, etoposide (VP-16) and cytosine arabinoside (Ara-C) had no activity and Adriamycin (ADR) was weakly effective.
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PMID:Characterization of a novel mouse reticular cell sarcoma M5076 subline resistant to cisplatin. 265 42

Human ovarian carcinomas (HOC) were established s.c. and i.p. in nude mice and the biological characteristics were investigated for 4 xenografts. HOC8 and HOC18, derived respectively from a primary tumor of the ovary and a pleural effusion (from 2 different patients) were established s.c. in nude mice. HOC10 and HOC22, derived from the ascites of 2 patients, were directly established as ascites after i.p. injection in nude mice. The s.c. and i.p. growth behavior of the 4 HOC lines was investigated. HOC18, HOC8 and HOC22 cells produced progressively growing tumor after s.c. injection but HOC10 ascites would not grow s.c. The cell suspension derived from HOC18 only produced carcinomatosis upon i.p. injection, while HOC8 cells produced both ascites and carcinomatosis. The 2 ascites HOC10 and HOC22 produced ascites in nude mice, but only HOC22 formed i.p. carcinomatosis. Histopathological characteristics of the patients' primary tumors persisted in nude mice, regardless of the site of tumor implantation. DNA histograms of the xenografts closely matched the patients' tumors and remained stable at different passages. Cisplatin, adriamycin and cyclophosphamide given i.v. were tested against HOC8 and HOC18 growing s.c. and HOC22 and HOC10 growing i.p. HOC8 showed a significant response to DDP and almost no sensitivity to ADR and CTX. HOC18 showed only moderate growth delay with all 3 drugs. Mice bearing HOC10 and HOC22 ascites had a prolonged survival time after DDP and ADR treatment.
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PMID:Intraperitoneal and subcutaneous xenografts of human ovarian carcinoma in nude mice and their potential in experimental therapy. 277 13

In a series of studies designed to extend our understanding of interleukin-2 (IL-2) and to study the effect of biologic response modifiers on bone marrow, we observed that administering recombinant human (rH) IL-2 to normal mice resulted in an increase in the frequency of colony-forming units-culture (CFU-C) in bone marrow. In addition, rH IL-2 was able to accelerate host recovery from cyclophosphamide (CTX)- or radiation-induced bone marrow depression and peripheral blood leukopenia. Not only can rH IL-2 accelerate, in a dose-dependent manner, the return of bone marrow, peripheral blood cellularity, and CFU-C frequency to normal levels following cytoreduction by CTX or irradiation, but it also significantly increases CFU-C frequency to greater than normal levels. Furthermore, rH IL-2 can significantly prolong survival of animals receiving a lethal dose of irradiation or CTX. Thus, multiple mechanisms are responsible for the synergistic therapeutic activity associated with rH IL-2 and CTX. rH IL-2 does not act only as an immunomodulatory agent in the presence or absence of suppressor T cells, but also accelerates host recovery from cytoreductive agents, resulting in decreased leukopenia and perhaps resistances to secondary infection. Thus, rH IL-2 plus chemotherapy may increase therapeutic activity against neoplastic disease, not only by adding immune stimulation to the direct antitumor effect of the drug but also by allowing delivery of higher, more effective doses of chemotherapy.
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PMID:Myelostimulatory activity of recombinant human interleukin-2 in mice. 278 8

The occurrence of tumor immunity in mice bearing a growing plasmacytoma (PC) was studied by local adoptive transfer assay. Spleen cells from mice with a large PC but not with a nonpalpable or small PC retarded and often inhibited entirely the growth of homologous PC. They occasionally caused late regression of growing homologous and heterologous PC. The individual tumor-specific immune effector cells were found to be radiosensitive, non-adherent, Thy 1-positive T-cells. They were resistant to treatment of mice with high-dose cyclophosphamide (CTX). Their generation, however, was abrogated by low-dose CTX and irradiation at the early stage of their development. Spleen cells from PC-bearing mice treated with high-dose CTX were enhanced in their effector activity, suggesting the co-existence of CTX-sensitive suppressor cells. The suppressor cells could be demonstrated in spleens of mice bearing a heterologous PC and were found also to be radiosensitive, non-adherent, Thy 1-positive T-cells. Their generation was blocked by treatment of mice with CTX during the early stage of PC development. These findings provide evidence for the occurrence of immune effector T-cells in mice with a growing PC. This immunity appears to be down-regulated by CTX-sensitive suppressor cells.
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PMID:Splenic immune effector and suppressor cells in mice bearing a growing plasmacytoma. 293 18

The Dunning R3327 adenocarcinoma represents a model for studying prostate cancer in rats; early studies have indicated its utility for studying relationships between tumor growth, immunologic markers, and chemotherapy. Normal animals and those bearing the metastatic Dunning R3327 MAT-LyLu tumor were treated with 10, 30, and 100 mg/kg doses of cyclophosphamide (CTX) and their spleens assayed for leukocytic subset distributions using monoclonal antibodies. Tumor-bearing animals had significant reductions in helper T cell content as well as reduced helper/suppressor T cell ratios, compared to controls. These effects occurred rapidly following implantation and were not reversed by chemotherapy. When administered to both tumor- and non-tumor-bearing animals, CTX also depleted T cell populations. Despite reductions produced in all subsets, two administrations of CTX (30 mg/kg) were capable of retaining (in non-tumor-bearing animals) or restoring (in tumor-bearing) normal helper/suppressor T cell ratios. Such studies aid in identifying therapeutically effective dosages of cytotoxic drugs that minimize their deleterious effects on the immune system.
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PMID:Effect of cyclophosphamide on leukocytic subset distributions in rats carrying the Dunning R3327-MAT-LyLu prostatic adenocarcinoma. 295 10

A 17 cm hepatoblastoma was unresectable at initial exploration. Multiagent chemotherapy (ADR, CTX, VCR, 5FU, BLEO) incurred minimal response at 5 months. Infuse-A-Ports were placed in each hepatic artery and FUDR infused intermittently but there was no response at 6 weeks. Adriamycin and vincristine were then begun via the Infuse-A-Port, with prompt regression of the tumor mass. The intra-arterial course was continued 3 months. Repeat arteriography showed vascular distortion but exploration revealed no gross tumor. A persistent alpha-feto-protein elevation prompted repeat arteriography 4 months afterward. A 3 cm calcific tumor was removed via an extended left lobectomy. Selective hepatic arterial infusion appeared to potentiate chemotherapy after systemic chemotherapy had failed to produce sufficient cytoreduction to allow safe surgical excision. The intra-arterial chemotherapy for unresectable hepatoblastoma warrants further investigation.
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PMID:Conversion to resectability by intra-arterial infusion chemotherapy after failure of systemic chemotherapy. 300 23


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