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

The involvement of peritoneal macrophages in rejection of mastocytoma cells in the C57BL/6 mice was examined in comparison to similar cell responses in susceptible DBA/2 mice. By means of scanning and transmission electron microscopy it was found that macrophages constituted the major cell class responding to the mastocytoma cells in the peritoneum of both mouse strains. However, in the resistant mouse strain macrophages formed the predominant cell type during the course of tumor growth. Furthermore, tissue culture of peritoneal exudate cells from this resistant mouse strain injected with mastocytoma cells five days earlier failed to grow out tumor cells. On the other hand, macrophages decreased in number in the susceptible DBA/2 mouse strain and tumor cells did grow readily in vitro when peritoneal cells containing tumor cells and macrophages were cultured in vitro. These results indicate that macrophages constitute an important cell class in resistance of a mouse strain which is now susceptible to mastocytoma cells. The ultrastructural study provided some insight into the nature of the cell types involved and their interaction with the tumor cell.
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PMID:Involvement of peritoneal macrophages in cellular responses to mastocytoma in resistant and susceptible mice. 12 Oct 34

1-(2-Chloroethyl)-3-(beta-D-glucopyranosyl)-1-nitrosourea (GANU), a water-soluble nitrosourea, differs from 2-[3-(2-chloroethyl)-3-nitrosoureido]-D-glucopyranose (chlorozotocin) by the placement of the cytotoxic group on C-1 of glucose. Its biological and biochemical properties are compared with those of chlorozotocin. At a 10% lethal dose (10 mg/kg i.p.), GANU demonstrates minimal myelosuppression. This dose failed to depress normal bone marrow DNA synthesis, in contrast to a 96% inhibition in L1210 DNA synthesis. In L1210 cell suspension, equimolar doses of GANU and chlorozotocin produced equivalent degrees of inhibition in DNA synthesis. GANU has significant L1210 activity in BALB/c X DBA/2 F1 mice treated on Day 2 of tumor growth. A 117% increased life-span and 15% 45-day survivors are atained with 15 mg/kg i.p., a 50% lethal dose. However, in concurrent studies using randomly selected littermate groups of mice, GANU proved less active than chlorozotocin which produced a 306% increased life-span (15 mg/kg i.p.). GANU and chlorozotocin have similar in vitro alkylating activity but the in vitro carbamoylating activity of GANU is sevenfold that of chlorozotocin. On a molar basis, the lethal toxicity of GANU is twice that of chlorozotocin. The significant carbamoylating activity of GANU may contribute to its greater toxicity and therefore limit the mumoles of alkylating agent that can be administered to the tumor. These structure-activity studies further confirm that the addition of a glucose carrier to a cytotoxic nitrosourea moiety can selectively reduce bone marrow toxicity while retaining antitumor activity.
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PMID:Biological and biochemical properties of 1-(2-chloroethyl)-3-(beta-D-glucopyranosyl)-1-nitrosourea (NSC D 254157), a nitrosourea with reduced bone marrow toxicity. 13 78

Growth of various fetal tissues and transplantable tumors in syngeneic newborn and adult mice [BALB/c, DBA/2, and (CBA X C57BL/6J)F1] was compared. Fetal skin, a mixture of all fetal tissues, and tumors were transplanted. The tumors arose spontaneously [hepatomas, mammary gland adenocarcinoma (MGAC)] or resulted from malignant conversion of ectopic transplants either of fetal tissues (urinary bladder carcinoma, adenocarcinoma of small intestine, stomach sarcoma) or of adult animal tissues (ovarian carcinoma) in the syngeneic system. The growth of fetal skin transplants and teratomas, which developed after transplantation of minced tissue from 18- to 20-day and 12- to 14-day fetuses, was considerably inferior in newborn syngeneic recipients, as compared with similar transplants in adults. Inhibition of tumor growth observed in newborn animals was manifested in prolongation of latent period before tumor node appearance and in slowing of growth rate of developed tumors. One of six tumors studied (MGAC) grew at the same rate in newborn and adult recipients. It was suggested that a special type of cellular and/or humoral mechanisms controlling tumor growth exists in newborns. The activity of such factors was conceivably based on fetal tumor antigens as targets. We assumed that weakly antigenic and strongly antigenic tumors behaved differently in respect to nonimmune and immune surveillance mechanisms.
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PMID:Nonimmune and immune surveillance. I. Growth of tumors and normal fetal tissues grafted into newborn mice. 18 65

The graft-versus-host reaction (GVHR) was evoked in (C57BL/6J times C3H/6J times DBA/2J) F1 hybrids by grafting parental lymphoid cells. Groups of bothe F1 hybrids were immunized with thymocytes carrying Thy-1.1 (theta AKR) antigen and still other groups of (C57BL/6J times C3H/HeJ) F1 hybrids were immunized with thymocytes carrying the H-2-d antigen. Plaque-forming cells (PFC) producing antibodies to the Thy-1.1 antigen, lytic for AKR thymocytes, or antibodies to the H-2-d antigen, lytic for lymphoblasts carrying the H-2-d antigens, were enumerated in spleens of experimental animals. A pronounced suppression of the immune response to the Thy-1.1 antigen was found in animals suffering from GVHR. The suppression could be demonstrated in some animals as late as 180 days after the onset of GVHR. Significant, although less pronounced suppression was found when response to the H-2-d antigens was assayed. After grafting 10-3 or 10-4 DBA/2J derived lymphoma cells (L5178Y) into (C57BL/6J times DBA/2J) F1 hybrids, clinically detectable tumor growth was found earlier and more frequently in hybrids suffering from GVHR than in control animals. The results obtained lend support to the concept that immunosuppression accompanying GVHR may influence the formation and/or growth of the malignant tumors. In addition, a synergistic effect in the suppression of the responsiveness of F1 recipients was seen in some instances when a mixture of parental bone marrow and thymus cells was grafted. The results are consistent with data indicating that more than one cell type is involved in the initiation of GVHR.
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PMID:Effect of graft-versus-host reaction on the immune response to alloantigens and growth of a syngeneic tumor. 23 66

The tumor-inhibitory effect of an intralesional injection of Propionibacterium acnes was of limited duration ("finite"). Our model was the DBA/2 syngeneic mouse injected with P815 mastocytoma cells (5 X 10(5)) into each rear footpad; only the left was treated, leaving the right as a "pseudometastasis." The finite effect occurred at approximately 21 days after the first treatment. Subsequent i.p. treatments with P. acnes did not alter this effect, although they increased mean survival time. With one footpad tumor, we achieved 22% cures with complete regression and no sign of metastatic growth. A RNA fraction from P. acnes produced inhibition of tumor growth, but crude cell walls and cell walls treated with Pronase had no effect. A P. acnes cytoplasmic fraction with tumor-inhibitory activity was pelleted by high-speed centrifugation; this fraction inhibited P815 mastocytoma as fully as whole cells injected in one-fifth the dose on a nitrogen basis and did not cause a local inflammatory reaction. The activity of the pellet also differed from whole cells in that it was equally inhibitory to the pseudometastasis in the contralateral right rear footpad. The cytoplasmic fraction apparently contained at least two active components since activity was obtained at two dilution levels. Such activity was relatively stable at 5 degrees, but it was unstable at -30 degrees.
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PMID:Antitumor activity of Propionibacterium acnes (Corynebacterium parvum) and isolated cytoplasmic fractions. 40 91

DBA/2 mice were treated with four successive subcutaneous injections of rabbit anti-theta-gamma-globulin followed by the subcutaneous implantation of chemically induced mastocytoma (P-815-X2). Another series of animals received rabbit anti-thymus-gammaglobulin according to the same schedule and still another series of animals served as non-treated controls. A definite augmentation of the tumor growth, as evidenced by the dissemination of the tumor into the spleen, liver and kidney, was evident in the globulin-treated series. Such dissemination was not observed in the control animals, where the metastases were limited to the reginal lymph nodes. The studied gammaglobulins were different in two important respects; the death rate of animals and the frequency of thymic metastases were higher in the anti-theta-globulin series. These findings advocate the conclusion that anti-theta-globulin, prepared against the brain tissue, is the more specific and more potent T-lymphocyte suppressor of these two globulins studied. T-lymphocyte population seems to play an important role in host resistance against experimental neoplasia.
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PMID:The influence of anti-theta-globulin treatment on the growth of mastocytoma in mice. 41

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.
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PMID:Tumor cell threshold required for suppression of macrophage inflammation. 41 87

Ehrlich ascites tumor grows in almost any mouse host. We have found a strain of dystrophic mice to be strongly resistant to Ehrlich ascites tumor. Mice of the dystrophic strain survived injection of Ehrlich Ascites tumor cells that had just been passaged through either dystrophic mice or C57BL X DBA/2 F1, (hereafter known as BD2F1) mice. However, most of the dystrophic mice died when they were given injections of Ehrlich ascites tumor cells that had just been passaged through Swiss white mice. All Swiss white and BD2F1 mice died when they were inoculated with Ehrlich ascites tumor cells, regardless of the type of mouse through which the Ehrlich ascites tumor cells had just been passaged. In some dystrophic mice, the tumor grew to a palpabale size and then disappeared. This provided the opportunity to passage the tumor from one dystrophic mouse to another and thereby to demonstrate resistance in the dystrophic mice to tumor that had grown previously in dystrophic mice. There was no detectable difference in the rate of tumor growth in either Swiss white or BD2F1 mice.
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PMID:Resistance to Ehrlich ascites tumor in a strain of dystrophic mice. 44 11

A series of N-protected vinyl, 1,2-dihaloethyl, and cyanomethyl esters of phenylalanine was synthesized and these compounds were evaluated for antitumor activity against the growth of Ehrlich ascites carcinoma in CF1 male mice (33 mg/kg/day), Walker 256 carcinosarcoma in Sprague-Dawley male rats (2.5 mg/kg/day), and P388 lymphocytic leukemia in DBA/2 mice (20 mg/kg/day). Structure-activity relationships were evaluated and acute toxicity studies (LD50 determinations) in male CF1 mice were also carried out on selected compounds. Carbobenzoxy-L0phenylalanine vinyl ester (5), N-carbobenzoxy-L-phenylalanine 1,2-dibromoethyl ester (12), and N-carbobenzoxy-L-phenylalanine cyanomethyl ester (8) were found to be very potent inhibitors of Ehrlich ascites tumor growth at nontoxic doses cited above. Compounds 5 and 12 also tripled survival time in the Walker 256 system. LD50 values for compounds 5, 12, and 8 were greater than 2000 mg/kg (greater than 6.15 mmol/kg), 74 mg/kg (0.15 mmol/kg), and 150 mg/kg (0.44 mmol/kg), respectively.
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PMID:Antineoplastic agents. 1. N-Protected vinyl, 1,2-dihaloethyl, and cyanomethyl esters of phenylalanine. 59 22

Using 2 immunogenic (3-methylcholanthrene-induced fibrosarcomas in BALB/c x DBA/2 F1 (CD2F1) male mice, we observed initially that the rate of tumor growth might be enhanced by castration. For confirmation, tumor transplantation experiments with over 500 mice were done to compare tumor-specific transplantation immunity in castrate and in control male mice. Inbred mice bearing a 3-methylcholanthrene-induced fibrosarcoma transplant underwent surgical excision of the tumor; specific resistance to subsequent challenges with varying doses of that tumor cell line were compared in castrate and in noncastrate groups of mice. Although castration influenced the rate of tumor growth, it had no apparent effect on tumor-specific immunoresistance. Mechanisms of host-tumor immunorelationships are discussed as they might relate to endocrine therapy of prostate adenocarcinoma.
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PMID:Castration effects on tumor-specific immunity. 74 64


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