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 absorption of retina and uvea pigment is very high in infrared light of 700-1000 nm, whereas hemoglobin absorbs light of lower frequencies much better. Density-Slicing is performed by a computer receiving information from an infrared film. Pigments of nevi and melanomas are demonstratable by this method and tumor growth is possible to see as well.
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PMID:[Computer evaluation of infrared photos of the optic fundus. II. Clinical aspects (author's transl)]. 64 71

In rats, injection of nickel sulfide (5 mg) into each pole of one kidney, unlike intramuscular administration, elicits a plethoric condition a few weeks later. The resulting hematologic changes (increased hematocrit, hemoglobin, erythrocytes and circulating erythrocyte mass with normal plasma volume) indicate that the plethoric condition is due to polycythemia, which is not associated with alterations in the 2,3-diphosphoglyceric acid content of erythrocytes. Removal of the treated kidney, following the development of the polycythemia, as well as the tumor growth and expansion in the renal parenchyma, reverse the plethoric condition, suggesting that the erythropoietic changes derive from nickel-induced renal lesions. Further studies are required to elucidate the nature and mechanisms of the cellular alterations.
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PMID:Polycythemia induced in rats by intrarenal injection of nickel sulfide Ni3S2. 112 98

Polymerized bovine hemoglobin solutions (PBHS) are being actively investigated as blood substitutes. In studies analogous to those we conducted with perfluorochemical emulsions/carbogen, we have examined the effect of PBHS +/- carbogen (95% O2, 5% CO2) breathing on the antitumor efficacy of melphalan, cyclophosphamide, N,N'-bis(2-chloroethyl)-N-nitrosourea (BCNU) and cis-diamminedichloroplatinum(II) (cis-platin). The tumor growth delay of the FSaIIC fibrosarcoma treated with melphalan (10 mg/kg), cyclophosphamide (150 mg/kg), cisplatin (10 mg/kg) and BCNU (15 mg/kg) was increased about 2.2-fold, about 2.1-fold, about 1.2-fold and about 1.5-fold, respectively, when PBHS (12 mg/kg) was administered i.v. before each drug was injected i.p. The tumor growth delay produced by each drug was further increased when carbogen breathing for 6 h was allowed after administration of the drug and PBHS. In tumor cell survival experiments 24 h following drug treatment, the addition of PBHS increased the tumor cell killing of both melphalan and cyclophosphamide by about a factor of 10 at the lowest doses of each drug tested (10 mg/kg for melphalan and 100 mg/kg for cyclophosphamide) compared to the drug alone. However, at higher drug doses this effect was lost. The toxicity of each antitumor agent toward bone marrow (granulocyte/macrophage-colony-forming units) was increased 2- to 3-fold by the combined treatment. These results suggest that use of PBHS +/- carbogen breathing may add significantly to the efficacy of antitumor alkylating agents, however, the in vivo/in vitro data suggest that there will be increased bone marrow toxicity with this approach. This needs to be taken into account in the design of clinical trials.
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PMID:Effect of a bovine hemoglobin preparation on the response of the FSaIIC fibrosarcoma to chemotherapeutic alkylating agents. 173 32

Attempts to correct tumor hypoxia with oxygen-carrying solutions have used high concentrations of inspired oxygen (FiO2 100% or 95%). In the clinic, however, obtaining such high levels of FiO2 using mask ventilation in older patients or in children may be difficult. Since lower levels of FiO2 had not been previously tested, we examined the antitumor efficacy of FiO2 levels of 65, 85, and 95% breathed for 1 hr prior to and during irradiation used with the concentrated perfluorochemical emulsion F44E, the less concentrated emulsion, Fluosol-DA, or a new preparation consisting of purified bovine hemoglobin solution, PBHS. When tested in mice bearing the Lewis lung carcinoma with 2, 3, or 4 Gy daily for 5 days, daily Fluosol-DA produced only a small increase in the slope of the tumor growth delay versus irradiation alone, when used with 85% FiO2 (dose modifying factor [DMF] 1.3), but produced a DMF of 2.1 with 95% FiO2. Various concentrations of F44E (2, 4, or 8 g PFC/kg) each required a 95% FiO2 for full effect but the 8 g/kg dose had a discernable effect with an FiO2 of 65% and 85% (DMF 1.25 and 1.30, respectively). For PBHS, in contrast, a DMF of 1.6 was observed at 20% FiO2, but surprisingly this increased further to 2.1 with 95% FiO2. Further investigations of PBHS with irradiation demonstrated that daily administration of PBHS (12 ml/kg) 1 hr before single Xray fractions of 5, 10, 15, or 20 Gy with 20% FiO2 resulted in a DMF of 1.6-1.7 in the FSaIIC fibrosarcoma compared with irradiation alone when ascertained by tumor cell excision assay. These results indicate that to achieve maximum antitumor benefit with these oxygen-carrying solutions with radiation therapy, care must be taken to insure that FiO2 levels near 100% are achieved.
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PMID:Effect of oxygen level on the enhancement of tumor response to radiation by perfluorochemical emulsions or a bovine hemoglobin preparation. 191 27

Monoclonal antibody CO17-1A, which has specificity for colorectal and pancreatic carcinomas, was radiolabeled with the pure beta emitter, 90Y, by either the cyclic diethylenetriaminepentaacetic acid (DTPA) anhydride technique or by a site-specific bifunctional chelate technique using 1-(p-aminobenzyl)DTPA (p-NH2-Bz-DTPA). Female nude mice bearing SW 948 human colorectal carcinoma xenografts were given injections i.v. of 90Y-labeled monoclonal antibody CO17-1A at dosages of 100, 150, and 200 muCi/25 g body weight. Unlabeled CO17-1A (100 micrograms/25 g body weight) was coadministered. In animals receiving 90Y-CO17-1A prepared by the cyclic DTPA anhydride technique, tumor volume was unchanged from base line at a dose of 200 microCi/25 g. As the dosage of 90Y-CO17-1A increased, the rate of tumor growth decreased, but all experimental animals in this group died between 14 and 21 days. In contrast, CO17-1A radiolabeled with 90Y by the site-specific p-NH2-Bz-DTPA bifunctional chelate technique produced a maximum tumor volume reduction of 87% in the 200 microCi/25 g group by day 15, and no deaths were noted in any of the 90Y-CO17-1A-treated groups for 71 days. Dose-response curves again showed increased tumoricidal effects with increased dosages of 90Y-CO17-1A. S-2-(3-Aminopropylamino)ethylphosphorothioic acid, commonly known as WR-2721, is a radioprotective drug which has been shown to protect against bone marrow depression in irradiated humans. No protection was observed when WR-2721 was used as an adjunct to treatment with 90Y-CO17-1A prepared by either the cyclic DTPA anhydride technique or the site-specific p-NH2-Bz-DTPA technique. When the site-specific p-NH2-Bz-DTPA technique was used, the reduction in WBC and hemoglobin levels correlated with increasing bone marrow toxicity at higher doses. We conclude that CO17-1A labeled with 90Y via the site-specific p-NH2-Bz-DTPA technique has potential for radioimmunotherapy of human colorectal carcinoma.
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PMID:Radioimmunotherapy of human colorectal carcinoma xenografts using 90Y-labeled monoclonal antibody CO17-1A prepared by two bifunctional chelate techniques. 216 41

The cancer chemotherapeutic efficacy of 3,4-dihydroxybenzylamine (DHBA), a dopamine analog with reduced neurotoxic effects, was evaluated in strain A mice bearing transplantable Ehrlich's ascites carcinoma. The analog was administered intraperitoneally on day 1 post-transplantation at dose schedules of 50, 100 and 200 mg/kg/day for 7 consecutive days. The results demonstrated a significant inhibition of tumor growth and prolongation of the survival time of EAC tumor bearing mice following DHBA treatment. Diminished activity of the growth-related respiratory enzyme succinate dehydrogenase along with the stimulated activity of the lysosomal enzyme beta-glucuronidase in the DHBA-treated tumor cells indicated inhibition of tumor growth as well as active lysis of the tumor cells. Tumor inhibition was accompanied by marked improvements in hemoglobin concentration. RBC count and bone marrow cellularity. The results demonstrated that DHBA did not adversely affect hematological profile of the host while it inhibited the growth of Ehrlich's ascites carcinoma.
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PMID:Tumor inhibition and hematological improvements by dopamine analog 3,4-dihydroxybenzylamine in mice bearing transplantable carcinoma. 223

The in vivo differentiation-inducing activity of a purified human erythroid differentiation factor (EDF) toward mouse erythroleukemic cells (MEL cells) was examined. BDF1 mice with diffusion chambers implanted in the peritoneal cavity were treated with continuous i.p. administration of EDF. MEL cells within a diffusion chamber differentiated into hemoglobin-positive cells when treated with EDF, the percentage of the positive cells being 32.3 +/- 28.3 on day 5 as compared to 0.2 +/- 0.3 in the controls. The anti-tumor activity of EDF was also examined in a nude mouse MEL solid tumor model. Daily intra-tumor treatment with EDF for 10 days resulted in 73% suppression of tumor growth on day 25. A histological study revealed that EDF-treated solid tumor cells became hemoglobin-positive, indicating the anti-tumor activity of EDF through induction of differentiation in vivo. EDF could induce in vitro the differentiation of human erythroleukemic cell lines K562 and HEL, as well as the murine cell line. These results indicate the possibility of differentiation therapy for erythroleukemia using EDF.
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PMID:Differentiation-inducing and growth-inhibitory activities of erythroid differentiation factor (EDF/activin A) toward mouse erythroleukemic cells in vivo. 232 49

A severe anemia develops in recipient C57L/J mice after syngeneic transplantation of the BW7756 murine hepatoma. The tumor undergoes an exponential growth spurt in the 14-21 days post-implantation, accompanied by a parallel increase in serum alpha-fetoprotein levels and a significant decrease of hemoglobin concentration and hematocrit extending to the 28th day. Concomitant with the decreased hematocrit, the blood volume displayed a 10% increase. The blood cell population was generally one of reticulocytosis and leukocytosis. Mild icteric plasma was observed and both "cold" and "warm" antibodies were detected in the sera of tumor-bearing mice. An elevation of IgM was observed by day 7, followed by a depletion of IgG1 and IgG2 throughout the tumor growth period. When RBCs of tumor-bearing mice were compared to those of normal mice, the same degree of osmotic fragility was found. However, the lifespan of the transfused RBC was shorter in tumor-bearing mice than in normal mice (half-life: 2 days vs. 4 days). The data suggest a type of auto-immune hemolytic anemia which is analogous to various hematopoietic disturbances described for murine hosts bearing solid tumors distal to hematopoietic sites.
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PMID:Characterization of murine hepatoma BW7756. III. Hematological profile of a tumor-associated anemia. 240 35

The mechanism of tumor-induced hematological alterations at the level of pluripotent hematopoietic stem cells (CFU-S) was investigated in mice bearing transplantable ascites tumor, Sarcoma 180. Tumor growth for 10 days caused neutrophilic leukocytosis and decline in hemoglobin and RBC values in the peripheral blood, and significant reduction (p less than 0.05) in the concentration as well as absolute number of CFU-S in the femoral marrow but an increment in the spleen. Intraperitoneal administration of cell-free ascitic fluid caused similar alterations of CFU-S in normal mice, but heat-killed tumor cells failed to elicit such response. Tumor cell-conditioned medium when injected into normal mice caused CFU-S alterations in a pattern similar to that of tumor-bearing animals. It is concluded that alterations of CFU-S following tumor transplantation is attributable to tumor growth rather than the presence of dead or necrotic cells in the tumor inoculum. It is likely that tumor cells elaborate some factor(s) which mediate such changes.
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PMID:Colony-forming ability of pluripotent hematopoietic stem cells in mice following tumor transplantation. 342 12

Lewis lung carcinoma (LLC) of C57BL/6 mice, a transplantable tumor widely metastatic by 6-7 days post implant (PI), caused hematopoietic alterations such as progressive anemia (hemoglobin: day 1 PI, 11.0 g/dl; day 19 PI, 7.8 g/dl), neutrophilia (neutrophils: day 1 PI, 2 X 10(3)/microliter; day 19 PI, 22 X 10(3)/microliter), and marrow and splenic myeloid hyperplasia (marrow myeloid-to-erythroid ratio: day 1 PI, 1:1; day 7 PI, 3:1). Accompanying these changes were an increased concentration of marrow granulocyte-macrophage colony-forming units (culture) (GM-CFUC) (day 3 PI, LLC 185 +/- 27% of control; day 19 PI, LLC 265 +/- 10% of control) and accelerated cycling of these myeloid progenitors [day 3 PI, LLC 45.3 +/- 6.5% GM-CFUC in cycle vs. sham (media) injected 17.5 +/- 10.5%; day 7 PI, LLC 52.2 +/- 2.5% vs. sham (media) injected 29.8 +/- 9.8%; day 11 PI, LLC 56.2 +/- 4.4% vs. sham (media) injected 22.2 +/- 14%]. This study questioned whether enhanced hematopoiesis was a result of progressive tumor growth or whether the injection of tumor cells could evoke the response. By use of groups of C57BL/6 mice given an injection of live LLC cells, x-irradiated killed LLC cells, or media, the hematopoietic response to live LLC cells versus dead LLC cells could be dissected. A biphasic colony-stimulating activity (CSA) response in the sera of tumor bearers was found to account for the myelopoietic changes. The first wave of CSA from days 1 to 3 PI stimulated 168 +/- 3.7% more GM-CFUC than control sera and was likely released by dead cells of the tumor inoculum; the second wave from day 7 onward stimulated 220 +/- 7.6% more colonies and was a result of the enlarging tumor mass. Tumor growth was necessary for GM-CFUC proliferation, and the declining growth fraction at day 19 in LLC-bearing mice suggested that hematopoietic exhaustion was a consequence of tumor growth.
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PMID:Early hematopoietic events during tumor growth in mice. 348 12


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