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At least 145 records · Page 8Linked to original sources
PubMed1975

In vivo cortisone sensitivity of nonspecific antitumor activity of Corynebacterium parvum-activated mouse peritoneal macrophages.

The nonspecific antitumor activity of Corynebacterium parvum-activated mouse peritoneal macrophages in vitro was inhibited by their prior treatment with cortisone acetate in vivo. Inhibition was marked (60 percent) 24 hours after cortisone injection and was still significant at 7 days, but antitumor activity was completely recovered by 9 days. This transient inhibition was sufficient to abolish the non-specific protection afforded by C. parvum in an in vivo pretreatment model.

Animals↗
PubMed1975

Control of local tumor growth with combined fractionated radiotherapeutic and chemotherapeutic regimens.

A treatment concept for the control of tumor growth utilized weekday radiotherapy and weekend chemotherapy. Mice were given sc injections of P815X2 mastocytoma cells on the lower back (day 0) and separated into the following treatment groups: 5-day/week X-irradiation, adriamycin alone at either 5 mg/kg body wt (days 6 and 13) or 2 mg/kg (days 5, 12, and 19), and combined radiotherapy and chemotherapy. Untreated controls had a mean tumor volume of 2.77 cm-3 and a mean survival time of 24 days. Adriamycin alone at 5 mg/kg resulted in an eventual tumor of 70 percent of the control value at death, whereas at 2mg/kg the tumor volume was 60 percent of control. After radiotherapy only, tumor size was 52 percent of control. Irradiation plus either 5 or 2 mg drug per kg body wt resulted in tumor volumes of 23 and 30 percent, respectively, of control values. Although no treatment regimen prolonged survival, the marked reduction in local tumor growth with combination therapy indicates that it may be a useful concept in future cancer therapy.

Animals↗
PubMed1975

Immunopotentiation with BCG: dimensions of a specific antitumor response.

The dimensions of a BCG-potentiated antitumor response against the poorly immunogenic murine mastocytoma, P815 (MA), are described for a model in which the tumor immunogen is injected into subcutaneous sites previously infected with BCG; a distantly located tumor challenge is subsequently monitored for evidence of regression. A comparison of concomitant immunity and the immunity elicited by injection of varying doses of live MA into sites previously infected with BCG revealed similar antitumor effects. The subcutaneous site was the most effective route for immunization with BCG and irradiated tumor cells. Antitumor immunity was maximally expressed at intravascular sites and in the footpad. Complete tumor suppression was limited to footpadchallenge with 10-4-10-5 MA. Not only did the iv injection of BCG and immunogen fail to elicit immunity against subcutaneous challenge, but also systemically administered immunogens abrogated antitumor immunity elicited by subcutaneous immunization. These effects were reversed by prior splenectomy. Immunity was specific for the evoking tumor immunogen, but challenge with the specific tumor did not elicit nonspecific resistance against another 3-methylcholanthrene-induced tumor. In another strain of mice, immunity potentiated by BCG against the highly antigenic tumor, Meth A, was more effective than that potentiated against the poorly immunogenic MA.

Animals↗
PubMed1975

Potentiation of the tumor-specific immune response by Corynebacterium parvum.

Strong, specific, cell-mediated antitumor immunity resulted from the sc injection into mice of Corynebacterium parvum (CP) mixed with irradiated cells from mastocytoma P815 (MA), whereas injection of irradiated MA alone was without effect. Maximum immunity was achieved with small doses of CP, and the injection sites of CP and irradiated MA did not need to be coincident but required common lymphoid drainage for immunity to result. The process was largely T-cell dependent but not dependent on the development of a specific immune response to CP; it was also demonstrable and effective in a therapy situation. No such immunity was evident after systemic administration of CP and irradiated MA. Simultaneous systemic injection of CP and irradiated MA did, however, nonspecifically reduce the enhancing effect of systemic injection of irradiated MA alone.

Adjuvants, Immunologic↗
PubMed1975

BCG immunopotentiation of an antitumor response: evidence for a cell-mediated mechanism.

BCG-immunopotentiated antitumor immunity was studied in a model in which irradiated murine tumor cells, mastocytoma P815, were injected into subcutaneous sites prepared by a prior injection of BCG; challenge in a distant foot-pad was used as an indicator of specific resistance. The onset of antitumor immunity correlated with the proliferation of lymph node cells draining the immunization sites and the development of delayed type hypersensitivity (DTH) to the tumor. Tuberculin hypersensitivity, however, was depressed during the evolution of DTH to the tumor. Antitumor immunity was transferred locally with spleen or lymph node cells that were sensitive to anti-theta sera and complement but not to anti-lg and complement. They had velocity sedimentation rates in a bovine serum albumin gradient of 3.9-5.9 mm/hour and were relatively resistant to vinblastine at the peak of the immune response. Sera from immunized mice failed to confer antitumor immunity either in vitro or on transfer in vivo.

Animals↗
PubMed1976

Altered immunologic responsiveness in mastocytoma-bearing mice.

Immune responses to sheep erythrocytes were enhanced in mice bearing small mastocytomas soon after injection of a few tumor cells. In contrast, mice with larger tumors after transfer of a greater number of mastocytoma cells and those in the later stages of tumor development after transfer of small numbers of tumor cells showed moderately suppressed immune responses. Transfer of spleen cells from mastocytoma-bearing mice to irradiated recipients resulted in more antibody-forming cells as compared to transfer of splenocytes from normal donor mice. The addition of graded numbers of mastocytoma cells to a constant amount of normal spleen cells transferred to irradiated mice also resulted in enhanced responses and increased spleen weights in the recipients. This increase, in direct proportion to the number of mastocytoma cells transferred, also occurred when Escherichia coli lipopolysaccharide (a T-cell independent antigen) was used to immunize animals given spleen cells from normal mice and mastocytoma cells. Mastocytoma cell-free homogenates or X-irradiated tumor cells also heightened immune responses in recipient mice, which indicated that viable cells were not needed for the effect. Such homogenates, as well as the tumor cells per se, stimulated increased lactate dehydrogenase (LDH) activity in the sera of recipient mice. However, tumor cells passaged in tissue culture for several months, those derived from mice bearing a mastocytoma cell line with a low LDH-stimulatory activity, or UV-irradiated mastocytoma cells with a high LDH-stimulatory activity did not induce enhanced plaque-forming cell responses.

Animals↗
PubMed1976

Treatment of solid P815x2 murine mastocytoma with adriamycin (NSC-1231127): toxity limitations.

The efficacy of adriamycin (NSC-123127), given as weekly or as 5-day-per-week doses, on the control of solid P815X2 murine mastocytomas was severely limited by hematopoietic and gastrointestinal toxicity. Although daily or weekly drug schedules both elicited dose responsiveness in terms of tumor control, no dose level of drug increased the life-span of tumor bearing animals.

Animals↗
PubMed1976

Combined-modality oncotherapy with cyclophosphamide (NSC-26271) and radiotherapy: control of murine mastocytoma.

We investigated the effects of cyclophosphamide, alone and in combination with a 1,000-R/week radiotherapy schedule, on the growth of solid P815X2 tumors in 12-week-old male DBA/2 mice. Single-dose treatments of 150 mg cyclophosphamide/kg were given to animals bearing tumors of different ages. Such treatment of young tumors resulted in proportionately greater degrees of regression and steeper regrowth curves than did treatment of older tumors. Although slopes of regrowth curves differed greatly, time to regrowth (to pretreatment size) was the same for all age classes of tumors. Graded weekly exposures of 50-250 mg/kg for 4 weeks resulted in dose-dependent increases in incidence of complete remission, duration of remission (time to regrowth), and mean animal life-spans. The combination of radiotherapy to the tumor and 75, 150, or 225 mg cyclophosphamide/kg/week resulted in better local tumor control than occurred with radiotherapy or the drug alone. However, a dose-dependent increase in radiosensitivity of the gastrointestinal mucosa included in radiotherapy fields was observed. A 3-week course of radiotherapy plus 75 mg cyclophosphamide/kg/week (which is tolerated by the mucosa) increased animal lifespans to 165% of those of controls.

Animals↗
PubMed1976

Potentiation of cytotoxic T-cell function by virus.

Inoculation of C57BL/6J mice with allogeneic P815 mastocytoma cells in the presence of simian virus 40 (SV40), a DNA tumor virus, led to an enhanced cytolytic T-cell response to P815 in vivo. Cytotoxic function was also augmented if SV40 was given subsequent to a primary immunization, even when mice were given a suboptimal dose of immunizing cells. Although SV40 increased the cell-mediated immune response to allogeneic cells, it did not enhance the antibody response to the soluble antigen dinitrophenyl bovine gamma-globulin, a helper T-cell-dependent response. Thus it appeared that SV40 had a selective adjuvant effect on lymphocyte subpopulations, since it increased cytotoxicity but not helper T-cell function.

Animals↗
PubMed1977

Antigenic changes of DBA/2J mastocytoma cells when grown in the BALB/c mouse.

A 10-day growth period of the DBA/2J strain-specific P815-X2 mastocytoma in the BALB/c mouse altered the antigenicity of the tumor cell surface. The in vivo-modified mastocytoma cells differed from mastocytoma cells grown in the original DBA/2J mice in suspectibility to lysis by immune peritoneal exudate cells, in vitro antigenic recognition by cytotoxic T-cells, and immunizing capacity in allogeneic C57BL/6 mice. Propagation of the altered tumor cells in the original host or maintenance in tissue culture for 40 hours restored complete susceptibility to lymphocyte-mediated cytotoxicity.

Animals↗
PubMed1977

Effect of hyperthermia on the functional activity of cytotoxic T-lymphocytes.

The effect of hyperthermia on the functional activity of murine cytotoxic thymus-derived lymphocytes (CTL's) has been investigated. CTL's were generated in vitro in mixed leukocyte cultures (MLC's) and assayed for cytotoxicity on 51Cr-labeled allogeneic P-815 mastocytoma cells. Exposure of MLC cells to temperatures of 43 degrees C or above rapidly inactivated CTL function. The degree of inactivation depended on temperature and time of exposure to heat. CTL function was much more sensitive to hyperthermia than was the reproductive capacity of tumor target cells (assessed by a cloning assay), and the heat sensitivity of CTL's appeared to depend on their stage of differentiation. CTL function dramatically increased when MLC cells were incubated at 37 degrees C after exposure to hyperthermia or when a total exposure to heat was split into two equal fractions separated by an interval at 37 degrees C. These latter findings were operationally analogous to the repair of potentially lethal and sublethal radiation damage, respectively, and suggested that further studies are required to assess the complex interrelationships between hyperthermia, cell-mediated immunity, and tumor cell survival.

Animals↗
PubMed1978

Tumor cell threshold required for suppression of macrophage inflammation.

In DBA/2 mice bearing transplanted, syngeneic P815 mastocytoma, macrophage accumulation was impaired in the tumor when the cancer grew intraperitoneally. By varying the number of transplanted mastocytoma cells and quantitating the macrophage response to a standardized stimulus of proteose peptone, we determined that 4-16x10(6) mastocytoma cells were required to inhibit monocyte inflammation. That interference with monocyte inflammation required a threshold number of tumor cells was consistent with an increase in tumor-associated macrophages proportional to tumor growth during early cancer. It was also consonant with a greater number of macrophages in tumors initiated with small rather than large tumor inocula. Impairment of monocyte inflammation could be passively transferred with ascitic fluid.

Animals↗
PubMed1978

Isotope-release cytotoxicity assay with the use of indium-111: advantage over chromium-51 in long-term assays.

The adaptation of indium-111-oxine (also known as 8-hydroxyquinoline) (111In Ox) chelate for long-term (18-48 hr) isotope-release assays of cell-mediated cytotoxicity (CMC) and its advantages over the use of 51 Cr are described. Labeling of DBA/2 P815 mastocytoma cells with 111InOx resulted in the incorporation of as many as a million counts per minute in 10(5) cells with no reduction in cell viability. 111InOx labeled both mouse and human tumor cells. 111InOx, like 51Cr, primarily labeled cytoplasmic constituents; up to 80% of the label existed in a releasable form. 111InOx was quantitatively released from labeled P815 in response to specifically sensitized C57BL/6 lymphocytes. The high labelling efficiency of 111InOx offered a significant advantage over 51Cr in 18- to 48-hour assays for CMC by reducing the counting error and thus making the assay more precise. Because of its higher labeling efficiency, 111InOx can be used in microcytotoxicity assays. 111InOx has the added advantage of a lower spontaneous release in culture than 51Cr. This feature of 111InOx also makes the calculation of specific isotope release more accurate than that achieved with 51Cr in long-term cytotoxic assays.

Animals↗
PubMed1979

Response of canine mast cell tumors to radiation.

Twenty-three dogs completed a fractionated course of ionizing radiation therapy for mast cell tumors. In 10 dogs the response was satisfactory, and the tumors were considered controlled 12 months after completion of the prescribed course of therapy. Treatment was considered unsatisfactory for the remaining 13 dogs due to failure to control the tumor locally, generalized metastasis, or both. A dose effect was noted in the response of the tumors to radiation. Of 6 dogs, 5 responded satisfactorily when the tumor dose was 4,000 rads or greater. When the tumor dose was less than 4,000 rads, 5 of 17 dogs responded satisfactorily. The dose calculated to control 50% of the meat cell tumors was 3,625 rads (95% confidence interval: 3,265-4,024 rads). Adverse normal tissue reactions, which consisted of moist desquamation in 10 animals and necrosis in 4, were recorded. The dose calculated to cause desquamation in 50% of the dogs was 3,750 rads (95% confidence interval: 3,348-4,200 rads).

Animals↗