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PubMed1980

Intraperitoneal hyperthermic treatment of implanted peritoneal cancer in rats.

The feasibility and efficacy of treating peritoneal cancer implants by applying heat to the peritoneal surfaces were studied in inbred Buffalo A rats given i.p. injections of Morris hepatoma 5123TC tumor cells. Heat was delivered to the peritoneum by contact with a heated physiological salt solution (Normosol-R) in the peritoneal cavity. A treatment temperature of 43.3 +/- 0.3 degrees was maintained for 30 min by an immersed stainless steel coil through which hot liquid circulated. Rats implanted with 0.5 to 1.0 x 10(8) tumor cells were treated at 1 to 4 hr (Group I), 4 to 5 days (Group II), and 22 to 24 days (Group III) after tumor implantation to simulate treatment for the clinical conditions of surgically spilled cancer cells, established microscopic cancer implants, and macroscopic cancer implants, respectively. A statistically significant improvement in survival was observed in Groups I and II compared with sham-treated control animals; 58% of the heat-treated animals were cured. Only a slight but statistically insignificant improvement was noted in Group III. These observations indicate that i.p. surface heat treatment of peritoneal implanted cancer is feasible and effective.

Animals↗
PubMed1977

Hormonal control of growth and progression in tumors of Nb rats and a theory of action.

A continuation of previous studies of hormone-dependent tumors in various organs in Nb rats concerns the effects of removal of the hormone stimulus from animals with growing tumors. Tumor regression usually followed this procedure, and in various models it was associated with an increased survival of the animal. A regressed tumor could be caused to grow at any time by estrogen treatment, and the resulting tumor remained hormone dependent, although some progression might occur. Continuous breeding rarely affected the growth or progression of transplanted adrenal or breast carcinomas. When spontaneous regrowth of tumors took place following removal of the estrogen stimulus all types of tumors (except leiomyomas of the uterus, showed progression usually to autonomy, and in the case of male rats bearing breast carcinomas it was inevitable. The substitution of pellets containing a reduced level of estrone to determine which prevented regression and allowed uninterrupted growth offered an assessment of the type or amount of hormone required for the growth of different tumors. By means of such a model of breast cancer in male rats, it was possible to demonstrate that a reduction in hormone levels sufficient to prevent advancing tumor growth, but adequate to reduce the extent of regression, also reduced the frequency or prevented the development of autonomous change. Although regression per se was not a prerequisite for autonomous change, the paradox was evident that progression towards autonomous growth was accelerated with procedures expected to check tumor growth and was minimal with procedures that accelerated it. Liver metastases of hormone-dependent adrenal carcinomas continued growth and could not be influenced by removal of estrogen, although the primary transplant regressed. When such metastases were transplanted, they were not found to have progressed to autonomy but retained a hormone-dependent status. Some tumors, when maintained in estrogen-conditioned hosts, apparently showed a reversion to a more hormone-dependent cell type rather than the expected progression towards autonomy. A theory is suggested to explain the experiments findings on the development and control of estrogen-responsive tumors.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Adoptive immunotherapy of cancer with immune and activated lymphocytes: experimental and clinical studies.

Recent studies of passive adoptive immunotherapy of experimental tumors indicate that histologically different neoplasms can be cured by this procedure in mice, rats and guinea pigs. In this paper two main approaches of adoptive immunotherapy with lymphocytes are considered. One which makes use of specific tumor-immune cells and is applicable to immunogenic tumors, and the other which uses activated (allostimulated and/or IL-2-activated) lymphocytes and is applicable to immunogenic and non-immunogenic neoplasms. Experimental models of both approaches and results provided by them are reviewed. These studies indicate that transfer of tumor-reactive lymphocytes with or without the combined administration of IL-2 into syngeneic tumor-bearing animals can lead to the eradication of a disseminated neoplasia when certain conditions are met. In particular, it was found that high tumor burdens, delay of treatment and low number of transferred lymphocytes can adversely affect the results. It has also been shown that the therapeutic effect of treatment with anti-cancer drugs or irradiation may be significantly improved by the addition of adoptive immunotherapy. The successful treatment of immunogenic tumors often requires the inhibition of suppressor lymphocytes by Cy or irradiation. Non-immunogenic tumors can be successfully treated only by providing activated lymphocytes and high doses of IL-2. Recent findings of few available human studies of adoptive immunotherapy are also reviewed, and the problems of toxicity and possible therapeutic effects of infusion of autologous, activated lymphocytes and IL-2 are discussed.

Animals↗
PubMed1996

Long-term effects of inhaled nicotine.

Tobacco smoking has been reported to be associated with increased risk of cardiovascular disease and cancer, particularly of the lungs. In spite of extensive research on the health effects of tobacco smoking, the substances in tobacco smoke exerting these negative health effects are not completely known. Nicotine is the substance giving the subjective pleasure of smoking as well as inducing addiction. For the first time we report the effect on the rat of long-term (two years) inhalation of nicotine. The rats breathed in a chamber with nicotine at a concentration giving twice the plasma concentration found in heavy smokers. Nicotine was given for 20 h a day, five days a week during a two-year period. We could not find any increase in mortality, in atherosclerosis or frequency of tumors in these rats compared with controls. Particularly, there was no microscopic or macroscopic lung tumors nor any increase in pulmonary neuroendocrine cells. Throughout the study, however, the body weight of the nicotine exposed rats was reduced as compared with controls. In conclusion, our study does not indicate any harmful effect of nicotine when given in its pure form by inhalation.

Administration, Inhalation↗
PubMed1993

Impact of stromal sensitivity on radiation response of tumors.

BACKGROUND: Irradiation of tumors causes the death of both parenchymal tumor cells as well as normal tissue stromal cells (e.g., endothelium, connective tissue). However, it has been difficult to distinguish the contributions to overall tumor response after irradiation from the two compartments. The development of the severe combined immunodeficient (SCID) mouse provides a model in which the contribution of stromal cell responses to ionizing radiation to overall tumor response can be defined, because its normal tissue cells are extremely radiosensitive. Therefore, the results of irradiation of tumors in radiation-sensitive (SCID) and radiation-resistant hosts can be compared, and the contribution of the normal tissue stroma clarified. PURPOSE: Our purpose was to investigate the effects of radiation-induced stromal cell damage on tumor cell death, using tumor growth delay (GD) and local control (complete and permanent regression of the irradiated tumor) as end points. METHODS: Tumor GD and local control experiments were performed in SCID, athymic, and C3H mice. Sixty SCID and 60 nude mice for each of three human tumor cell lines (HGL9, HSTS26, HCT15) and for each of five murine cell lines (FSC1, FSC2, FSM1, FSM2, E01) and 60 SCID and 60 C3H mice for the FSa2 spontaneous C3H sarcoma were studied. Neoplasms were produced by injection of 10(6) cells from in vitro tissue cultures into the flanks of donor mice; after tumors had grown, experimental neoplasms were produced by transplanting 2- to 3-mm fragments into recipient mice. Animals were randomly assigned to various groups when tumors reached average volumes of 120 mm3. Graded, single-dose x irradiations (15-115 Gy, dose rate about 7 Gy/min) were given under acutely hypoxic conditions. Tumors were scored one to two times per week until recurrence. RESULTS: The x-ray doses needed to achieve local control in 50% of the animals (tumor control doses, TCD50) ranged from 45.1 to 58.0 Gy for human tumors and from 36.3 to 114.0 Gy for murine tumors. On average, the TCD50 values in SCID mice were only about 3.5% lower than values in nude or C3H mice. The amount of GD defined at 66% of the TCD50 for the various groups was, however, 27% longer in the SCID mice (P = .004). CONCLUSIONS: While the three-fold higher radiation sensitivity of the normal tissue stromal cells in the SCID mice did not alter the percentage of tumors controlled by x irradiation in the SCID mouse hosts as compared with other hosts, there appear to be significant differences in GD. Radiation-induced stromal cell damage does not significantly contribute to tumor cell death; however, it can prolong the interval of tumor regression.

Animals↗
PubMed1981

Tumor-induced anorexia in the Wistar rat.

The transplantable Leydig cell tumor of Wistar rats, LTW(m), caused decreased food consumption and weight loss in the host within 2 weeks of implantation. The tumor was small, did not metastasize, and did not affect several parameters of biochemical function. When the tumors were removed, increases in food intake and body weight occurred within 72 hours and were sustained. Reimplantation of tumors caused anorexia to recur. Parabiotic pairs of rats with tumor in one partner also experienced weight loss. Those rats in parabiosis with tumor-bearing rats gained less weight than those in parabiosis with control rats. These observations suggest that the LTW(m) tumor causes anorexia and that this anorexia is mediated by a circulating substance.

Animals↗