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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of combination of local hyperthermia and radiation on tumor growth and metastases was studied using Lewis lung carcinoma. Tumors growing intramuscularly in the right hind legs of C57BL/6 mice were irradiated at 10 Gy of radiation dose and immersed in a water bath. Time and number of development of metastases were determined according to size and number of lung colonies at 19 days after tumor implantation. Local hyperthermia at 42.8, 43.3 or 43.5 degrees C for 30 min immediately after or before irradiation enhanced the growth delay of tumor with irradiation or with hyperthermia alone. Development of metastases several days after heating was also inhibited by the combination of heating and irradiation. These effects were diminished with hyperthermia applied 3 hr or more after irradiation. Promotion of metastases around the time of heating by severe hyperthermia with above 43.3 degrees C alone was not inhibited by combination with radiation, regardless of their sequence. Radiation had no effect on the number of metastases developed by the heating. However, irradiation 48 hr or more before severe heating reduced the number of metastases developed by the heating.
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PMID:[Influence of local hyperthermia combined with radiation on tumor growth and lung metastases of transplantable Lewis lung carcinoma growing in hind legs]. 279 49

Adult sarcoma-bearing mice were used to demonstrate whether hypoglycemia was the immediate cause of death in experimental animals with rapidly growing tumors without metastases. This kind of tumor model is representative of the majority of animal models used in experimental cancer research. Tumor-bearing animals died with severe hypoglycemia under all experimental conditions, while pair-killed controls were normoglycemic. Anorexia prevented tumor-bearing animals from attenuating the hypoglycemia by drinking glucose-containing water while completely starved control animals survived more than 14 days with glucose-containing water as the only energy source. Adrenalectomy shortened survival in tumor-bearing animals, but survival of adrenalectomized tumor-bearing animals could be normalized by daily injections of pharmacologic doses of hydrocortisone (25 mg/25 g body wt/day) but not by physiologic replacement (20 micrograms/25 g body wt/day). Injections of pharmacologic doses of hydrocortisone did not influence on survival or body composition in tumor-bearing animals with intact adrenals. Glucagon was without effect on either survival, tumor growth or body composition. Based on the results in this study and in our previous reports we conclude that hypoglycemia is the cause of death in the majority of murine tumor models. This hypoglycemic theory is important, since any treatment modality in animal experiments that influences glucose metabolism in the host may indirectly change tumor growth and may thus be misinterpreted as a direct tumor effect.
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PMID:The cause of death in non-metastasizing sarcoma-bearing mice. A study with relevance for tumor treatment experiments in mice. 280 52

Our approach to develop platinum complexes with a selective effect on the hormone-dependent MC by exchanging the two NH3 groups of cisplatin by an 1,2-bis(4-hydroxy-phenyl)ethylenediamine derivative which possesses estrogenic activity, was successful. The most interesting compound of this new platinum complex series, meso-(1,2-bis(2,6-dichloro-4-hydroxyphenyl)ethylenediamine)dichloroplati num(II) (meso-1-PtCl2) and its water soluble sulfatoplatinum(II) derivative (meso-1-PtSO4) were significantly more active on the DMBA-MC and the receptor positive MXT-MC than cisplatin and the related ligand 1,2-bis(2,6-dichloro-4-hydroxyphenyl)ethylenediamine (meso-1). According to our proposed mechanism of action, meso-1-PtX (X = Cl2 or SO4) should be enriched in the nuclei of mammary tumor cells, which possess an intact ER system (i.e. an intact cytoplasma nucleus translocation process), thereby causing very strong tumor growth inhibition. Preliminary studies of meso-1-PtSO4 on the DMBA-MC confirm this assumption. In the tumor tissue we found higher Pt-levels than in uterine tissue, which also contains ERs. The Pt-levels of the tumor tissue are much higher than those of skeletal muscle and of blood. In therapeutic dosages meso-1-PtSO4 does not cause kidney damages in rats.
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PMID:Anticancer drugs: estrophilic cisplatin derivatives. 283 Sep 70

Deuterium-enriched water has an antiproliferative effect on transplantable mouse tumors without toxic side effects. Since the response to treatment of human carcinomas growing in nude mice is deemed to be a good indicator of the potential clinical behavior of these tumors, we studied the influence of this stable isotope of hydrogen on the growth of xenotransplanted human carcinomas of various histologic types, grades, and primary sites. Seven-week-old Balb/c-nu/nu mice were inoculated subcutaneously, either with oropharyngeal squamous cell carcinomas or with carcinomas of the large intestine. After tumor inoculation, the mice were given drinking water containing 30 atom% D2O. Heavy water effectively retarded the growth of the human carcinomas. At the end of the experiment, the weight of the tumors was reduced to values ranging from 22% to 65% of the control values. The reproducible antiproliferative effect was more conspicuous in poorly differentiated carcinomas than in moderately well-differentiated variants. Since animals in both groups, kept under identical conditions, drank the same amount of water and had similar body weights, the difference in tumor growth can be attributed to the moderate deuteration of the hosts.
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PMID:Heavy water delays growth of human carcinoma in nude mice. 283 79

Mice were given repeated injections, at 21 day intervals, of cyclophosphamide paired with a novel taste (saccharin) in the drinking water. Subsequent challenge with a syngeneic plasmacytoma tumor led to elevated tumor growth and mortality only in conditioned mice that were reexposed to saccharin. This effect was abolished by conditioned exposure to a histamine type II-receptor antagonist.
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PMID:Cimetidine reverses tumor growth enhancement of plasmacytoma tumors in mice demonstrating conditioned immunosuppression. 285 37

The purpose of this study was to investigate whether excitation of porphyrin could be related to nonlinear mechanisms of absorption of porphyrin itself or of the medium in which porphyrin is embedded. This possibility was proposed as an explanation for results of previous experiments where a Nd:YAG laser was used. An MS-2 sarcoma transplanted into the hind pad of BALB/c mice was used as the experimental tumor model. Mice were given HpD i.v. (25 mg/kg) 24 h before exposure to light delivered from an IR laser (1,060 nm). Since at dose-rates ranging between 600 and 1,200 mW/cm2 the thermal effect tended to mask the nonlinear effect, the temperature of the limb of mice was kept cold by running water. Irradiation performed under cooling conditions did not show any tumor growth inhibition. Experiments in vitro performed on HT-29 cells by a continuous wave (CW) or pulsed (Q-switch) Nd:YAG laser indicated no appreciable difference in DNA synthesis between irradiated and nonirradiated cells. Our results did not evidence nonlinear mechanisms of absorption by HpD with Nd:YAG laser both in CW and pulsed (nanosecond range) modes. Whether this effect should occur, in any case it is unlikely to be suitable to induce a photodynamic effect due to its low efficiency. Nd:YAG laser could induce a heating related effect, which can improve the therapeutic efficacy of PDT.
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PMID:A study on the possible involvement of nonlinear mechanism of light absorption by HpD with Nd:YAG laser. 294 43

We report that cyclic p.o. administration of alpha-difluoromethylornithine (DFMO), an inhibitor of polyamine biosynthesis, is an effective long-term (1-year) maintenance therapy for established implants of cultured human small cell lung carcinoma in athymic (nude) mice. Human small cell lung carcinoma cells, from a line which exhibited cell death in culture in the presence of DFMO, were inoculated into athymic mice and permitted to grow to palpable tumors (3-5-mm nodules with mean volume of 0.04 cm3). The animals were then randomized into untreated, continuous treatment and cyclic (3 weeks of 4 beginning 1 week after 8 weeks continuous) treatment groups. Treatment consisted of 3% DFMO in the drinking water (5.1 g/kg/day). The tumors in the untreated group grew to 27 cm3 by 8 weeks and the animals had a median survival of 7.6 weeks. Tumor growth was inhibited by 99% (0.3 cm3) in the continuous treatment group in comparison to untreated controls. Survival was prolonged with 93% survival at 10 weeks and a 101% increase in median survival to 15.3 weeks (P less than 0.05). The cyclic DFMO group had a 98.3% inhibition in tumor growth for longer than 1 year (0.56 cm3; P less than 0.05). Survival was also markedly prolonged compared to the untreated group with 100% survival up to 24 weeks and a median survival of 54.3 weeks (P less than 0.05). No significant toxicities were observed in the first 10 weeks of DFMO treatment even though antitumor effects were observed. With continuous DFMO treatment, the animals eventually became debilitated and developed marked weight loss and thrombocytopenia; by 20 weeks, mortality was 79%. With cyclic therapy, the animals resumed weight gain, recovered from thrombocytopenia and, at 20 weeks, had 0% mortality. By 55 weeks, mortality was 50% which, however, was not significantly different (P approximately 0.50) from mortality of a control group of nontumorous, athymic mice that had weekly body weight and skin fold measurements concurrently with the experimental, tumor-bearing animals. Thus, the observed mortality is ascribable to continuous encroachment on the normally sterile environment. These data suggest a role for DFMO in long-term therapy of sensitive human tumors such as small cell lung carcinoma, especially in patients with a low tumor burden. Furthermore, a cyclic regimen might be an important tool in maintaining clinical remissions induced by conventional combination chemotherapy.
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PMID:Long-term maintenance therapy of established human small cell variant lung carcinoma implants in athymic mice with a cyclic regimen of difluoromethylornithine. 300 8

A sensitive and specific blood test for cancer has long been sought. The water-suppressed proton nuclear magnetic resonance (NMR) spectrum of plasma is dominated by the resonances of plasma lipoprotein lipids. We measured the mean line widths of the methyl and methylene resonances, which were found to be correlated with the presence or absence of malignant tumors. Values for the average line width were lower in patients with cancer. We analyzed plasma from 331 people (normal controls, patients with malignant and benign tumors, patients without tumors, and pregnant patients); NMR analysis and measurement of line widths were blinded to diagnosis or patient group. The mean line width for 44 normal controls (+/- SD) was 39.5 +/- 1.6 Hz. For 81 patients with untreated cancer, demonstrated by biopsy, the line width was 29.9 +/- 2.5 Hz. Patients with malignant tumors were reliably distinguished from normal controls by this method (P less than 0.0001), and differed from patients with diseases that did not involve tumors (line width, 36.1 +/- 2.6 Hz; P less than 0.0001). Patients with benign tumors (e.g., those of the breast, ovary, uterus, and colon) had line widths of 36.7 +/- 2.0 Hz and were different from those with malignant tumors (P less than 0.0001). However, pregnant patients and those with benign prostatic hyperplasia had line widths consistent with the presence of malignant tumors. The narrowing of lipoprotein-lipid resonances with cancer is consistent with the response of a host to tumor growth. We conclude that these preliminary results demonstrate that water-suppressed proton NMR spectroscopy is a potentially valuable approach to the detection of cancer and the monitoring of therapy.
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PMID:Detection of malignant tumors. Water-suppressed proton nuclear magnetic resonance spectroscopy of plasma. 302 46

The effect of combined treatment with D,L-2-difluoromethylornithine (DFMO) and tamoxifen on the growth status, ornithine decarboxylase (ODC) activity and polyamine content of established 1-methyl-1-nitrosourea (MNU)-induced mammary tumors was investigated. DFMO treatment, a 0.125% solution provided as drinking water, inhibited the rate of tumor occurrence and reduced the number of mammary tumors induced by a high dose of MNU (50 mg/kg body weight) during the first 120 days post-carcinogen treatment. Tamoxifen was administered daily via s.c. injection (25 micrograms/100 g body weight) to tumor-bearing rats in both treatment groups, i.e. control and DFMO-treated, for a 30-day period beginning 120 days after carcinogen. Tamoxifen treatment induced tumor regression but the percentage of regressing, static or growing tumors was no different in the presence or absence of DFMO. Whereas the mammary tumors of DFMO-treated rats had reduced ODC activity and lower polyamine concentrations in comparison to the tumors of untreated animals, tamoxifen had no effect on these parameters independent of its effect on tumor growth status. DFMO did not increase the efficacy of tamoxifen in inducing tumor regression.
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PMID:Effect of tamoxifen and D,L-2-difluoromethylornithine on the growth, ornithine decarboxylase activity and polyamine content of mammary carcinomas induced by 1-methyl-1-nitrosourea. 308 21

The effects of step-up (42----44 degrees sequence) and step-down (44----42 degrees sequence) heating were studied on a transplantable mammary adenocarcinoma of C3H/He mouse. Tumor-bearing legs were immersed in a water bath and the response to hyperthermia was evaluated in terms of the delay in tumor growth. Tumor growth was delayed greatly with increase in the duration of treatment with 44 degrees hyperthermia, whereas with 42 degrees hyperthermia of up to 180 min, tumor growth was delayed only slightly. The effects of step-up heating were similar to those of 44 degrees hyperthermia alone and the response was enhanced by a factor of 0.9-1.1 with the 60-min treatment at 42 degrees followed by treatment at 44 degrees. Thermal resistance developed when the preheating time at 42 degrees was longer than 30 min. On the other hand, the tumor response was markedly enhanced by step-down heating by a factor of 1.8-2.4 with the treatment at 44 degrees followed by 60-min treatment at 42 degrees. Since the enhancement factor for skin damage found previously was similar to that for the tumor, therapeutic gain cannot be expected by the use of these combined heat treatments.
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PMID:Effects of step-up and step-down heating on a transplantable murine tumor. 309 20


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