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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors prepared the prolactin marker with iodine-125 and made iodine-125-human prolactin and iodine-125-sheep prolactin. To make the complex, iodine-125-human prolactin was incubated with prolactin receptors isolated from female rat liver cell membranes. This complex is reversible and can be replaced by cold human prolactin. Studies with mammary glands of various animals have indicated that the prolactin receptor seemed to be a peptide or a protein of macromolecules in chemical nature. Estrogen enhanced the binding ability of iodine-125-sheep prolactin to prolactin receptor of rat liver cell membranes. The mammary cells from hyposectomized animals lost the binding ability, and this ability was not recovered even by estrogen administration. In experimental animals, the growth of mammary cancer, induced by dimethyl benzanthracene, was enhanced by the administration of prolactin and reduced by the introduction of an antiprolactin serum. Ergocornine which would suppress the secretion of prolactin also reduced the cancer growth. The factors which would increase the secretion of prolactin increased the tumor growth. Mammary cancer cells have generally less binding ability to prolactin than the normal mammary cells. These cancer cells in animals seem not to be prolactin dependent and have an autonomic nature. The relationship between prolactin and human mammary cancer is not yet entirely clear. However, there is a possibility that prolactin may play a role in certain mammary cancer. Reports on prolactin receptor in human mammary cancer cells are sparse. Although the authors found estrogen receptor in some mammary cancer cases, they were not able to find a significant amount of prolactin binding ability in these cells.
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PMID:[Radioreceptor assay of prolactin]. 0 10

We have developed a model system which can be utilized for characterizing both the molecular basis of natural killer (NK):tumor interactions and the consequences of these interactions on tumor growth in vivo. This model system consists of several tumor lines which were derived from the murine lymphoma ASL1w under conditions which permitted the isolation of clonal lines that differ in their susceptibility to NK-mediated lysis. The NK-resistant clones used in this study (AW5J and AW5E) were susceptible to cytotoxic T-lymphocyte-mediated lysis and thus appear to be resistant to lytic processes utilized uniquely by NK cells. In competitive (cold target) inhibition assays, the AW5J clone did not inhibit NK recognition as well as the NK-sensitive clones. Thus AW5J may not be efficiently recognized by NK cells. The AW5E clone, on the other hand, competitively inhibited NK recognition as efficiently as the NK-sensitive clones; therefore, AW5E appears to evade a post-recognition event which is required for NK-mediated lysis. The susceptibility of these clones to killing by NK cells directly correlated with their lethality, suggesting that NK cells regulated the growth of these tumors in vivo. The level of host NK activity was also an important determinant of the level and site of tumor localization. Two-step immunofluorescence assays and flow cytometric analysis were used to quantitate the number of tumor cells in the bone marrow, spleen, and lymph nodes of mice with augmented or depleted NK activity. Increasing host NK activity decreased the number of tumor cells in each organ which could support the growth of the particular tumor tested. Furthermore, the extent of NK regulation was dependent, in part, upon the susceptibility of the particular tumor to NK-mediated lysis and the site of tumor growth. Thus, the data presented here demonstrate the utility of the ASL1w-derived clones as a model system which can be used to delineate the requirements and consequences of NK:tumor interactions.
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PMID:Development of a murine lymphoma model system for the characterization of natural killer:tumor cell interactions. 163 30

The mechanism of induction of antitumor activity by local administration of recombinant interleukin-2 (rIL-2) combined with cisplatin (CDDP) was investigated in order to establish a method of immunochemotherapy against head and neck cancer. Local administration of rIL-2 had significantly greater inhibitory effects on tumor growth in both Meth A and C26 tumor bearing mice than did systemic administration. The cytotoxic activity of tumor infiltrating lymphocytes (TILs) obtained from C26 tumor bearing mice was studied. Local injection of rIL-2 around the tumor site for 4 days induced augmentation of the cytotoxicity of TILs not only in NK sensitive tumors but also in NK resistant C26 tumors. This phenomenon was not observed in spleen cells. Both negative selection assay and cold target inhibition assay revealed that the effector cells were tumor nonspecific asialoGM1 positive activated NK cells. Additional experiments were performed to determine the effectiveness of combined immunochemotherapy using CDDP and rIL-2 in C26 tumor bearing mice. The intraperitoneal administration of CDDP following the local administration of rIL-2 was more effective in suppressing tumor growth and in promoting well-survival than the use of CDDP or rIL-2 alone. To investigate the mechanism of antitumor activity, the effects of CDDP on the tumor cells and immunological changes were observed in tumor bearing mice. The susceptibility of tumor cells to effector cells was enhanced after in vitro culture with CDDP. In vivo administration of CDDP augmented the cytotoxic activity of effector cells and responsiveness to IL-2 of TIL. These results suggest that local immunochemotherapy using locally administered rIL-2 combined with CDDP may be available as a therapy for head and neck cancers.
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PMID:[Experimental study of local immunochemotherapy of head and neck cancer]. 177 75

Methylcholanthrene-induced sarcomas (MCA-S) have different growth patterns in diabetic (D) and nondiabetic (ND) rats. Diabetes delays the early phase of tumor growth and prolongs survival. This study evaluated MCA-S growth and its relation to insulin receptors (IR) and glucose uptake. Fisher 344 rats 150-200 g were assigned to two groups: Diabetic tumor bearers (DTB, n = 26) and nondiabetic tumor bearers (NDTB, n = 18). Diabetes was induced with iv streptozocin (40 mg/kg); MCA-S was inoculated (1 X 10(6) cells) subcutaneously 10 days later. Animals were sacrificed during early growth (tumor volume less than or equal to 20 cc) or logarithmic growth (tumor volume greater than 20 cc). IR assay was performed (0-10(5) ng/ml cold insulin, 25 X 10(3) cpm/tube A14 125I-insulin, 90 min, 15 degrees C, pH 7.8) on a single cell preparation. Serum glucose milligrams per deciliter and insulin nanograms per milliliter were assayed. Glucose uptake (dpm/g tissue/hr) was assayed 2 hr after an ip injection of 0.5 microCi 3-O[14C]methylglucose. Diabetic, tumor-bearing animals had a significantly increased number of insulin receptors at the small [less than or equal to 20 cc, 28.7 (D) vs 8.3 (ND)] and large [greater than 20 cc, 82.8 (D) vs 27.8 (ND)] tumor volumes. Glucose uptake was increased in the tumor at both volumes in the non-diabetic animals compared to the diabetic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in insulin receptors on methylcholanthrene-induced sarcoma during growth. 219 Nov 69

More than 80% of BALB/c mice bearing BAMC-1 ascites tumor were completely cured after five consecutive (once every 2 days) i.p. injections of a 0.1 mg dose of OK-432, beginning on day 2 after tumor implantation. The antitumor effect of OK-432 was abolished in athymic nu/nu mice and in anti-thymocyte globulin-treated euthymic BALB/c mice, so although OK-432 treatment did increase the length of survival, all animals eventually died as a result of tumor growth. When peritoneal exudate cells (PEC), obtained on day 12 from OK-432-treated BAMC-1-bearing euthymic mice were evaluated for in vivo tumor neutralization activity, all mice receiving an i.p. injection of the admixture of the nonadherent PEC (1 X 10(7) cells) with BAMC-1 cells (1 X 10(5)) survived for more than 60 days. When the same nonadherent PEC (1 X 10(7) cells) were i.p. transferred adoptively 1 day after the inoculation of 1 X 10(5) BAMC-1 tumor cells, again all mice survived. When these in vivo active PEC were tested for cytotoxicity in vitro against fresh BAMC-1 tumor cells, natural killer (NK) sensitive syngeneic RL male 1, NK-sensitive allogeneic YAC-1 cells, NK-resistant syngeneic Meth-A cells, allogeneic tumor cells (EL4, B16, and P815) and xenogenic human cells, the PEC were found to be capable of lysing BAMC-1 tumor cells together with almost all of the other tumor cells, including NK-resistant cells. Nonadherent PEC contained at least two subpopulations of killer cells. One, directed to syngeneic BAMC-1 cells, was both Thy1.2 and asialo GM1 positive, and another, directed to allogeneic YAC-1 cells, was asialo GM1 positive but Thy1.2 negative. A cold target inhibition assay also suggested the presence of more than two subpopulations. These results indicate that T cells play a determined role in the immunotherapeutic effect of OK-432 on BALB/c mice bearing BAMC-1 tumor, although the participation of activated macrophages could not be excluded. The cells responsible for killing BAMC-1 and other tumor cells appearing in the PEC on day 12 were characterized as containing at least two kinds of lymphokine-activated killer cells.
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PMID:Pronounced antitumor effect of LAK-like cells induced in the peritoneal cavity of mice after intraperitoneal injection of OK-432, a killed streptococcal preparation. 242 68

If immunoregulation of cancer is to be effective, the tumor must express immunogenicity and the host immune mechanism must be capable of responding to that stimulus. Though neuroblastoma (NB) might be such a tumor, a systematic assessment of this complex host-tumor interaction is lacking. We report such an analysis using the murine NB system. C1300-NB is highly antigenic, locally growing, and nonmetastasizing, while its clonal counterpart, TBJ-NB, is minimally antigenic and demonstrates not only aggressive local growth but systemic metastases as well. We analyzed A/J mouse antitumor naturally occurring killer lymphocyte (NK cells), cytotoxic lymphocyte (CTL cells), and suppressor lymphocyte (SC cells) function in response to these tumor lines. NK and CTL activity was measured in 40 mice after 3 weeks of growth of either C1300-NB or TBJ-NB using a cold target inhibition test to either the YAC-1 or P815 mastocytoma cell line, respectively. SC activity was analyzed in an additional 24 mice treated with an SC destroying 15 mg/kg of cyclophosphamide (CYA) three days after tumor inoculation. After 4 weeks of tumor growth spleens were harvested, cell-mediated cytotoxicity was measured by chromium 51 release assay and tumor cell lysis was expressed as lytic unit 30 (LU-30), an arbitrary definition of the number of lymphocytes needed to lyse 30% of target cells. By increasing the concentration of the NK-sensitive YAC-1 cold target, there was a 56.8% inhibition of lymphocytotoxicity to C1300-NB, contrasting with this was the lack of inhibition (17.8%) by the non-NK sensitive P815 cell line.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systematic analysis of the immunoregulation of murine neuroblastoma. 252 62

This study was undertaken to determine whether in vitro treatment of Lewis lung carcinoma (3LL) cells with ultraviolet (UV) radiation could increase their immunogenicity. Tumor cells were irradiated with UV light from a germicidal lamp (254 nm; UV-C) at a dose of 720 J/sq m. After 2 weeks of culture, the surviving cell population was cloned by limiting dilution. Cell suspensions of each clone were injected intrafootpad in C57BL/6 mice at a dose of 2.5 X 10(5) cells per mouse. Eighty independent clones were tested. Fifty-one clones showed decreased tumorigenicity and failed to grow in 20 to 95% of immunocompetent mice, whereas they produced tumors in 100% of irradiated (550 R) and athymic nude mice. These clones were designated "tum-" (nontumorigenic) clones. In contrast, all 25 clones selected from the untreated parental 3LL induced progressively growing tumors in 100% of the mice. After two courses of UV treatment, the uncloned 3LL population was rejected in 45% of inoculated mice. Mice rejecting an inoculum of a tum- clone were completely resistant to subsequent challenge with higher doses of the same or unrelated tum- clones. This resistance was fully expressed even after irradiation of immune mice with 550 R. Mice immune to a tum- clone also were able to prevent the growth of various tum+ clones or untreated 3LL tumor cells. When tum- and tum+ clone cells were simultaneously inoculated intrafootpad in opposite legs, rejection of tum- clone resulted also in the prevention of the growth of tum+ clone. Spleen cells of immune mice caused rapid elimination of radiolabeled 3LL tumor cells from the place of their inoculation (intrafootpad) and prevented tumor growth. In an in vitro cytotoxic assay, spleen cells after in vivo and in vitro immunization with tum- clones demonstrated high cytotoxic activity against various tum+ clones and parental 3LL cells, as well as against tum- clones. In addition, parental 3LL tumor cells and tum- cells were similarly able to inhibit cytotoxic activity in the cold target inhibition assay. However, in contrast to tum- cells, 3LL cells were less efficient in in vitro restimulation of cytotoxic activity of immune spleen cells. Therefore, these data suggest that tum-, tum+, and parental 3LL cells share a common antigenic specificity, which is not immunogenic in 3LL cells. UV treatment presumably converted the antigenic determinants present in the 3LL cells into an immunogenic form.
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PMID:Induction of highly immunogenic variants of Lewis lung carcinoma tumor by ultraviolet irradiation. 258 Jun 24

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

The effect of chronic and intermittent cold exposure was studied in benzo(a)pyrene-induced fibrosarcoma of mice. Chronic exposure to 5 degrees C caused decrease in incidence, increase in latent period, and inhibition of tumor growth. Intermittent exposures to +5 degrees C and -10 degrees C induced significant enhancement of tumor growth which increased with the lowering of temperature. Concomitant with the tumor growth alterations, stress reactions assessed by plasma corticosterone levels, differed in these two regimes. The elevation of plasma corticosterone levels correlates with the tumor growth enhancement which is probably mediated by corticosterone-induced immuno-suppression. Inhibition of tumors appears to be a result of adaptation to chronic stress, or metabolic alterations in cold. Physiological alterations of the host, depending upon the nature and duration and severity of the "stress" exposure, determines in our opinion probably the course of neoplastic development.
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PMID:Differential responses of carcinogen-induced fibrosarcoma of mice to altered regimes of cold exposure. 373 18

Inactivated cellular preparations and cell wall materials of Candida albicans (CA) were tested for their capacity to suppress the growth of Friend Leukemia Cell (FLC)-induced tumours and the infection by Friend Leukemia Virus (FLV) in histocompatible mice. Factors affecting the inhibition of tumor growth by CA cellular preparations were: i) the schedule of agent administration; ii) the method of cell inactivation; iii) the FLC load. In particular, mice given 10(7) yeast cells, inactivated by cold alkali, on days -14 and +1 with respect to 10(4) FLC challenge on day 0 did not develop tumors. A crude cell wall fraction derived from cells extracted with hot alkali was still effective in reducing (but not suppressing) tumour growth whereas a purified, particulate glucan fraction (glucan "ghosts", essentially consisting of beta 1,3-1,6 glucan) was ineffective. No cellular preparation or cell wall fraction exerted anti-FLV effects (as shown by splenomegaly measurements) nor did any CA material induce interferon-like activity in the serum of animals injected with either FLC or FLV. Therefore, the observed antitumor activity by CA was not mediated by antiviral effects but possibly due to an "adjuvant-type", nonspecific, immunopotentiation of host antitumor response, as documented in other animal tumor models.
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PMID:Suppression of Friend leukemia cell-induced tumours by cellular preparations of Candida albicans. 635 74


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