Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The involvement of mast cells in anti-tumor resistance was studied by employing 2 strains of mast cell deficient but otherwise immunocompetent mice on a C57BL/6 (H-2b) background (W/Wv and Sl/Sld) and their respective normal +/+ littermate controls. Sensitization of control mice with irradiated semisyngeneic B16 melanoma cells (H-2b) resulted in protection against subsequent challenge with viable B16 cells, in contrast to sensitization of either W/Wv or Sl/Sld mice. The involvement of serotonin in antitumor resistance was studied by employing 2 serotonin active drugs: reserpine, that depletes mast cells of serotonin; and methysergide, a serotonin antagonist. Sensitization of BDF1 mice with irradiated B16 cells and sensitization of DBA/2 mice (H-2d) with irradiated SL2 cells (H-2d) resulted in protection against subsequent challenge with viable B16 cells and viable SL2 cells, respectively. Treatment with either reserpine or methysergide resulted in a decreased protection. Delayed-type hypersensitivity (DTH) footpad responses to allogeneic L5178Y (H-2d) tumor cells in C57BL/6 mice showed a biphasic reaction pattern, similar to that found in DTH responses to simple reactive haptens, such as picryl chloride. Moreover, the early swelling responses were also dependent on T cells and on mast cells. BDF1 mice carrying a semisyngeneic L5178Y tumor on the chest showed an early swelling response after footpad challenge but no late response, possibly indicating that selective down regulation of the late component of DTH was associated with progressive tumor growth in these animals. The biphasic patterns of DTH to both tumor cells and picryl chloride and the T cell and mast cell dependence of both antitumor resistance and DTH to tumor cells suggest that T cell-dependent activation of mast cells to allow entry of mononuclear leukocytes into sites of tumor growth is similar to the mechanism that occurs in DTH.
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PMID:A role for mast cells and the vasoactive amine serotonin in T cell-dependent immunity to tumors. 387 Dec 9

Purified splenic macrophage (M phi) from normal DBA/2J mice and mice bearing P815 tumors were examined for responsiveness to lymphokine (LK) preparations containing high concentrations of IFN-gamma. For both normal and tumor-bearing M phi, LK treatment induced morphologic changes and increased the percentage of Ia+ cells from 35 to 55%. Although neither population exhibited spontaneous cytotoxicity toward P815 targets, LK treatment induced considerable tumoricidal activity in tumor-bearing M phi (32 to 80% lysis) but only minimal activity in normal M phi (8 to 17% lysis). Subcutaneous injection of 1 X 10(6)P815 cells into DBA/2J led to progressive tumor growth and death of 100% of the recipients after 27 +/- 3 days. Injection of a 1:18 mixture of P815 with either LK-activated normal or tumor-bearing M phi caused tumor regression after 10 days, and prolonged life until 43 +/- 4 days with tumor-bearing M phi and 39 +/- 3 days with normal M phi. Untreated normal or tumor-bearing M phi were unable to cause the effect (30 +/- 2 days), and lymphocytes could not be substituted for M phi (25 +/- 3 days). In x-irradiated recipients, no effect of LK-activated M phi could be observed (control = 19 +/- 2 days; LK-activated tumor-bearing M phi = 21 +/- 3 days). In addition, administration of an admixture of LK-treated M phi and x-rayed tumor before challenge with viable P815 enabled the recipient to inhibit tumor growth and caused tumor necrosis with inflammatory cell infiltration of the tumor. These observations suggest that, in part, LK-activated M phi may interact in vivo with host-derived cellular components and enhance the immune reactivity of the host against the tumor.
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PMID:In vivo activity of lymphokine-activated macrophages in host defense against neoplasia. 392 Mar 23

The growth and spontaneous resolution of syngeneic intraocular tumors were studied in DBA/2 mice. The P91 mutant clone of P815 mastocytoma (DBA/2 origin) expresses potent tumor-specific transplantation antigens (TSTA) that elicit vigorous immune responses in the syngeneic host. P91 tumors grew transiently and underwent spontaneous resolution following intracameral transplantation in DBA/2 hosts. The spontaneous rejection of the intraocular P91 tumors was a T-cell-dependent, radiosensitive immune process since these tumors grew progressively in T-cell-deficient nude mice and sublethally x-irradiated DBA/2 hosts. Intraocular P91 tumors induced vigorous cytotoxic T-lymphocyte (CTL), antibody, and delayed-type hypersensitivity (DTH) responses in immunocompetent DBA/2 hosts. The acquisition of DTH and CTL reactivity against the TSTA on the intraocular P91 tumors coincided with the onset of spontaneous rejection and suggested a pivotal role for cellular immune mechanisms in the destruction of the primary intraocular neoplasms. Moreover, histopathologic features attending tumor regression were compatible with the DTH reaction in the mouse. Tumor regression was associated with extensive vascular margination and emigration of neutrophils among viable tumor cells at the interface of the tumor mass and uveal components. Areas of previous tumor growth were replaced by a bed of granulation tissue accompanied by a mixed inflammatory infiltrate. Although immunocompetent hosts were able to rid their eyes of tumor, all of the eyes eventually became phthisical. The present findings are consistent with the hypothesis that cellular immune processes play a major role in the spontaneous rejection of intraocular tumors.
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PMID:Spontaneous immune rejection of intraocular tumors in mice. 392 53

Groups of BDF1 and DBA mice were treated with either the cupric chelate of nitrilotriacetic acid (NTA-Cu+2) or the cuprous chelate of neocuproine (NC-Cu+1) every other day for 7 days prior to either i.p. or s.c. inoculation with 10(6) viable B16 melanoma cells, and then every other day for 15 days post-tumor inoculation. This treatment schedule was non-toxic to host mice. NC-Cu+1 acted as a tumor growth promoting factor in mice by enhancing tumorigenicity, stimulating body weight gain, inhibiting encapsulation of i.p. tumors that permitted growth as unrestrained ascites, and increasing final tumor weight over a shortened host survival period regardless of the site of tumor inoculation. Treatment with NTA-Cu+2 inhibited pigmentation in DBA mice bearing s.c. tumors, while treatment with NC-Cu+1 enhanced tumor pigmentation regardless of the site of tumor inoculation and murine strain. These results suggest that exogenous copper in the form of chelates alters the growth characteristics of a copper-requiring tumor system in both a copper-chelate- and murine-specific manner, and further suggests that the growth promoting activity of exogenous copper in the B16 melanoma system involves both enhanced copper nutrition and concomitant alteration of host reactions to tumors.
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PMID:Pharmacological perturbation of murine melanoma growth by copper chelates. 397 9

Adverse (tumor-enhancing) effects of cyclophosphamide at moderate dose (50 mg/kg) given therapeutically were confirmed on the intraperitoneally implanted Lewis lung carcinoma (LLC) in allogeneic DBA/2 and BALB/c mice. It was recently demonstrated that antitumor effects of five standard drugs (actinomycin D, adriamycin, BCNU, 5-fluorouracil and methotrexate) were abolished or diminished when cyclophosphamide (50 mg/kg) was therapeutically combined with such drugs against intraperitoneally implanted LLC both in syngeneic C56BL/6 and allogeneic DBA/2 and BALB/c mice, while the effects of three drugs (cis-diamminedichloroplatinum, 5-thioguanine and vincristine) were not affected by the cyclophosphamide therapy. It is suggested that cyclophosphamide therapy at adjusted lower doses in man might not only be effective but also have a risk to enhance tumor growth and diminish the beneficial effects of other drugs in combination chemotherapy.
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PMID:Adverse effect of cyclophosphamide at moderate dose in combination with standard drugs on intraperitoneally implanted Lewis lung carcinoma in mice. 399 89

A purified i-carrageenan prepared by means of pronase digestion and fractional precipitation with KCl was investigated for its growth-inhibitory effect on mouse leukemia L-1210 transplanted in (C57BL/6 x DBA/2)F1 (BDF1) mice. This carrageenan specimen was not growth-inhibitory on this tumor when it was administered alone in a dose of 0.1 to 10 mg/kg/d, 4 times. However, in combination, with a small amount of mitomycin C, 0.25 mg/kg/d, a remarkable tumor growth-inhibition has manifested affording a complete regression of this tumor. Acid phosphatase alpha-galactosidase and active oxygen generation activities of the peritoneal exudate cells in the carrageenan-administered mice were remarkably higher than those of the control mice. Therefore, the booster effect of this carrageenan preparation on antitumor activity of mitomycin C is assumed to be associated with the inflammatory activity of this sulfated polysaccharide.
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PMID:Growth-inhibition of leukemia L-1210 ascites tumor by combination of carrageenan and mitomycin C in vivo. 609 97

The intense clinical interest in bleomycin as an anti-tumour agent has led to different methods of administration in an attempt to administer sufficiently high concentrations of the drug to the tumor. Therefore, a study was designed to determine the distribution and the therapeutic effect of a bleomycin emulsion and aqueous bleomycin after different routes of application. The tissue distribution of radioactively labelled bleomycin emulsion and aqueous bleomycin was determined in tumor-free CF 1 and tumor-bearing (EL 4, L 1210) C 57 Bl 6 and DBA 2 mice after local (s.c., i.t.) and systemic (i.v.) injection. The distribution studies for aqueous 57Co-bleomycin showed increased activity in the injection sites and the lymph nodes draining the injection sites after s.c. and i.t. injection compared to i.v. administration of the drug. In comparison to the aqueous local administration, the application of 57Co-bleomycin emulsion resulted in a disproportional increase of the 57Co-bleomycin concentration at the injection sites and in the draining lymph nodes. To prove the therapeutic relevance of the bleomycin tissue distribution tumor-bearing (line 10) strain 2 guinea pigs were treated with different modes of bleomycin. Animals with already lymphogenously metastasized tumors have been cured by means of low i.t. doses of the bleomycin emulsion. Guinea pigs treated with i.t. administration of aqueous bleomycin need, compared to the bleomycin emulsion, five times higher doses for tumor-free survival. Intravenously treated animals died either because of progressive tumor growth or because of toxic bleomycin effects. These findings made by animal experiments favor the i.t. treatment of head and neck carcinomas with a bleomycin emulsion.
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PMID:[Animal experiments for intratumoral chemotherapy with bleomycin (author's transl)]. 616 44

The effect of trans-retinoic acid on the growth of P388 lymphoid tumors in inbred female DBA/2 mice in the presence or absence of interferon (FN) treatment was studied. This acid derivative of vitamin A enhanced local tumor growth. trans-retinoic acid also partially reversed IFN protection against tumor growth and mortality.
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PMID:Retinoic acid: enhancement of a tumor and inhibition of interferon's antitumor action. 616 81

The term "photoimmunotherapy" describes an anti-cancer treatment that combines the phototoxic effects of chemical such as hematoporphyrin and the target-seeking ability of antibodies. Hematoporphyrin was chemically coupled to monoclonal antibodies directed to the DBA/2J myosarcoma M-1. Administration of anti-M-1-hematoporphyrin conjugates i.v. to M-1 tumor-bearing animals followed by exposure to incandescent light resulted in suppression of M-1 growth. The time interval between injection and light exposure was an important parameter in terms of tumor suppression. Tumor-bearing animals maintained in the dark for 96 to 196 hr after hematoporphyrin-antibody injection followed by 4-hr light exposure demonstrated significantly lower tumor incidence and longer latency periods, in comparison to conjugate-treated animals instantly exposed to light. The growth inhibiting properties of the conjugate appeared to be M-1-specific; it had no effect on the growth of a C57BL/6J lymphoma EL4. In addition, conjugates made with a nonspecific monoclonal antibody did not have any specific anti-tumor effect on M-1 growth. Treatment with equivalent doses of hematoporphyrin or antibody had no significant inhibiting effect on tumor growth. Clearly, the homing ability of the specific monoclonal antibody-hematoporphyrin conjugate was essential for effective drug delivery and inhibition of tumor growth.
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PMID:Photoimmunotherapy: treatment of animal tumors with tumor-specific monoclonal antibody-hematoporphyrin conjugates. 618 91

Effects produced by intratumor or systemic application of FK-156 and its synthetic derivatives on the syngeneic P388-DBA/2 mouse system were investigated. Among 21 compounds tested, FK-156, FK-565, FR-46758, FR-48217, FR-46091 and FR-47920 substantially suppressed tumor growth when directly injected into a tumor mass and further experiments showed that FK-156, FK-565 and FR-46758 were effective even when administered subcutaneously into site remote from tumor. The mechanisms of growth inhibition are strongly suggested to be host mediated, because these three compounds have remarkably low cytotoxicity against P388 cells in vitro. A single dose of FK-565, however, markedly decreased body weight in healthy DBA/2 mice, whereas FK-156 and FR-46758 did not. These results indicate the superiority of FK-156 and FR-46758 as immunotherapeutic agents over FK-565 with respect to their safety for treatment of cancer. Although significant life-span prolongation could not be seen in the two-injection regimen of six compounds in either system, systemic multiple injections of FK-156 and FR-46758 provided a statistically significant increase in the median survival time of P388 tumor bearing mice.
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PMID:Antitumor effects of novel immunoactive peptides, FK-156 and its synthetic derivatives. 619 22


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