Induction of Mitotic Synchrony by Intermittent Hyperthermia in Ehrlich Carcinoma in vivo

Nature ◽  
1973 ◽  
Vol 244 (5414) ◽  
pp. 299-300 ◽  
Author(s):  
MICHAEL D. SAPOZINK ◽  
ELEANOR E. DESCHNER ◽  
ERIC W. HAHN
Keyword(s):  
Ehrlich Carcinoma ◽  
Mitotic Synchrony

Репрограммированые in vitro на М3 фенотип макрофаги останавливают рост солидной карциномы in vivo

2018 ◽  
pp. 41-46
Author(s):  
А.А. Раецкая ◽  
С.В. Калиш ◽  
С.В. Лямина ◽  
Е.В. Малышева ◽  
О.П. Буданова ◽  
...  
Keyword(s):  
Solid Tumor ◽  
Antitumor Effect ◽  
Tumor Development ◽  
Significant Inhibition ◽  
The Body ◽  
Ehrlich Carcinoma ◽  
Solid Carcinoma ◽  
Ec Cells

Цель исследования. Доказательство гипотезы, что репрограммированные in vitro на М3 фенотип макрофаги при введении в организм будут существенно ограничивать развитие солидной карциномы in vivo . Методика. Рост солидной опухоли инициировали у мышей in vivo путем подкожной инъекции клеток карциномы Эрлиха (КЭ). Инъекцию макрофагов с нативным М0 фенотипом и с репрограммированным M3 фенотипом проводили в область формирования солидной КЭ. Репрограммирование проводили с помощью низких доз сыворотки, блокаторов факторов транскрипции STAT3/6 и SMAD3 и липополисахарида. Использовали две схемы введения макрофагов: раннее и позднее. При раннем введении макрофаги вводили на 1-е, 5-е, 10-е и 15-е сут. после инъекции клеток КЭ путем обкалывания макрофагами с четырех сторон область развития опухоли. При позднем введении, макрофаги вводили на 10-е, 15-е, 20-е и 25-е сут. Через 15 и 30 сут. после введения клеток КЭ солидную опухоль иссекали и измеряли ее объем. Эффект введения макрофагов оценивали качественно по визуальной и пальпаторной характеристикам солидной опухоли и количественно по изменению ее объема по сравнению с группой без введения макрофагов (контроль). Результаты. Установлено, что M3 макрофаги при раннем введении от начала развития опухоли оказывают выраженный антиопухолевый эффект in vivo , который был существенно более выражен, чем при позднем введении макрофагов. Заключение. Установлено, что введение репрограммированных макрофагов M3 ограничивает развитие солидной карциномы в экспериментах in vivo . Противоопухолевый эффект более выражен при раннем введении М3 макрофагов. Обнаруженные в работе факты делают перспективным разработку клинической версии биотехнологии ограничения роста опухоли, путем предварительного программирования антиопухолевого врожденного иммунного ответа «в пробирке». Aim. To verify a hypothesis that macrophages reprogrammed in vitro to the M3 phenotype and injected into the body substantially restrict the development of solid carcinoma in vivo . Methods. Growth of a solid tumor was initiated in mice in vivo with a subcutaneous injection of Ehrlich carcinoma (EC) cells. Macrophages with a native M0 phenotype or reprogrammed towards the M3 phenotype were injected into the region of developing solid EC. Reprogramming was performed using low doses of serum, STAT3/6 and SMAD3 transcription factor blockers, and lipopolysaccharide. Two schemes of macrophage administration were used: early and late. With the early administration, macrophages were injected on days 1, 5, 10, and 15 following the injection of EC cells at four sides of the tumor development area. With the late administration, macrophages were injected on days 10, 15, 20, and 25. At 15 and 30 days after the EC cell injection, the solid tumor was excised and its volume was measured. The effect of macrophage administration was assessed both qualitatively by visual and palpation characteristics of solid tumor and quantitatively by changes in the tumor volume compared with the group without the macrophage treatment. Results. M3 macrophages administered early after the onset of tumor development exerted a pronounced antitumor effect in vivo , which was significantly greater than the antitumor effect of the late administration of M3 macrophages. Conclusion. The observed significant inhibition of in vivo growth of solid carcinoma by M3 macrophages makes promising the development of a clinical version of the biotechnology for restriction of tumor growth by in vitro pre-programming of the antitumor, innate immune response.

Reprogrammed M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 extends lifespan of mice with experimental carcinoma

2017 ◽  
pp. 4-9
Author(s):  
С.В. Калиш ◽  
С.В. Лямина ◽  
А.А. Раецкая ◽  
И.Ю. Малышев
Keyword(s):  
Tumor Growth ◽  
Culture Medium ◽  
Ehrlich Carcinoma ◽  
Macrophage Phenotype ◽  
M1 Macrophages ◽  
M1 Macrophage ◽  
Ec Cells ◽  
Experimental Carcinoma

Цель исследования. Репрограммирование М1 фенотипа макрофагов с ингибированными факторами транскрипции М2 фенотипа STAT3, STAТ6 и SMAD и оценка их влияния на развитие карциномы Эрлиха (КЭ) in vitro и in vivo. Методика. Рост опухоли иницировали in vitro путем добавления клеток КЭ в среду культивирования RPMI-1640 и in vivo путем внутрибрюшинной инъекции клеток КЭ мышам. Результаты. Установлено, что M1макрофаги и in vitro, и in vivo оказывают выраженный противоопухолевый эффект, который превосходит антиопухолевые эффекты М1, M1, M1 макрофагов и цисплатина. Заключение. М1 макрофаги с ингибированными STAT3, STAT6 и/или SMAD3 эффективно ограничивают рост опухоли. Полученные данные обосновывают разработку новой технологии противоопухолевой клеточной терапии. Objective. Reprogramming of M1 macrophage phenotype with inhibited M2 phenotype transcription factors, such as STAT3, STAT6 and SMAD and assess their impact on the development of Ehrlich carcinoma (EC) in vitro and in vivo . Methods. Tumor growth in vitro was initiated by addition of EC cells in RPMI-1640 culture medium and in vivo by intraperitoneal of EC cell injection into mice. Results. It was found that M1 macrophages have a pronounced anti-tumor effect in vitro , and in vivo , which was greater than anti-tumor effects of M1, M1, M1 macrophages and cisplatin. Conclusion. M1 macrophages with inhibited STAT3, STAT6 and/or SMAD3 effectively restrict tumor growth. The findings justify the development of new anti-tumor cell therapy technology.

ANTITUMOR EFFECT OF COLLOIDAL SILVER BISILICATE IN EXPERIMENTAL IN VITRO AND IN VIVO STUDIES

2019 ◽  
Vol 65 (5) ◽  
pp. 760-765
Author(s):  
Margarita Tyndyk ◽  
Irina Popovich ◽  
A. Malek ◽  
R. Samsonov ◽  
N. Germanov ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Tumor Growth ◽  
Tumor Cells ◽  
Human Tumor ◽  
Significant Inhibition ◽  
In Vivo Studies ◽  
Ehrlich Carcinoma ◽  
In Vivo Experiments

The paper presents the results of the research on the antitumor activity of a new drug - atomic clusters of silver (ACS), the colloidal solution of nanostructured silver bisilicate Ag6Si2O7 with particles size of 1-2 nm in deionized water. In vitro studies to evaluate the effect of various ACS concentrations in human tumor cells cultures (breast cancer, colon carcinoma and prostate cancer) were conducted. The highest antitumor activity of ACS was observed in dilutions from 2.7 mg/l to 5.1 mg/l, resulting in the death of tumor cells in all studied cell cultures. In vivo experiments on transplanted Ehrlich carcinoma model in mice consuming 0.75 mg/kg ACS with drinking water revealed significant inhibition of tumor growth since the 14th day of experiment (maximally by 52% on the 28th day, p < 0.05) in comparison with control. Subcutaneous injections of 2.5 mg/kg ACS inhibited Ehrlich's tumor growth on the 7th and 10th days of the experiment (p < 0.05) as compared to control.

Expression of anionic sites on tumour cells at different stages of tissue invasion in vivo: a comparative study by X-ray microanalysis

1989 ◽  
Vol 94 (3) ◽  
pp. 561-566
Author(s):  
P.M. Evans ◽  
D.K. Suker ◽  
I. ap Gwynn
Keyword(s):  
Iron Hydroxide ◽  
Tumour Cells ◽  
Ehrlich Carcinoma ◽  
Similar Degree ◽  
Anionic Sites ◽  
Colloidal Iron ◽  
Cell Behaviour ◽  
X Ray ◽  
Invasion Stage

Quantification of colloidal iron hydroxide (CIH) labelling by X-ray microanalysis was used to investigate anionic sites at the surface of Ehrlich carcinoma cells from different locations in the mouse host. Individual tumour cells from peritoneal ascites suspensions (pre-invasion stage) varied up to threefold in their ability to bind CIH and a similar degree of intra-tumour heterogeneity was observed in different experimental animals. Pretreatment of the cells with neuraminidase confirmed that binding was at least partly due to surface sialic acid. Invasive cells isolated from mesenteric tumour nodules were also heterogeneous with regard to the availability of surface anionic sites, as were tumour cells adhering to the surface of the mesentery; however, in both these populations CIH binding was significantly greater on average than for free ascites tumour cells. The results suggest that surface anionic sites are determinants of the invasiveness of malignant cells in vivo, and that both the number and topography of these sites may be important in modulating tumour cell behaviour.

scholarly journals Fruticuline A, a chemically-defined diterpene, exerts antineoplastic effects in vitro and in vivo by multiple mechanisms

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Claudia Rita Corso ◽  
Maria Carolina Stipp ◽  
Débora Rasec Radulski ◽  
Marihá Mariott ◽  
Luisa Mota da Silva ◽  
...  
Keyword(s):  
Cyclin D1 ◽  
Molecular Mechanisms ◽  
Tumor Tissue ◽  
Human Cancer ◽  
Biological Properties ◽  
Ehrlich Carcinoma ◽  
Antitumor Effects ◽  
Mcf 7

Abstract Natural products have been recognized as important bioactive compounds on the basis of their wide biological properties. Here we investigated the antitumor effect and molecular mechanisms of the diterpene Fruticuline A (fruti) from Salvia lachnostachys, in human cancer cell lineages and Solid Ehrlich Carcinoma in mice. Fruti reduced MCF-7 and HepG2 proliferation by the reduction of Cyclin D1 levels and decreased NF-κB gene levels in both cell types. Furthermore, fruti also induced apoptosis in HepG2 cells, reduced Bcl-2 gene expression and induced necroptosis by increasing Ripk in MCF-7 cells. In mice, fruti prevented tumor development and reduced Cyclin D1, Bcl-2 and Rela gene levels, and reduced the p-NF-κB/NF-κB ratio in tumor tissue. Furthermore, fruti induced necrosis and apoptosis, increased N-acetyl-β-D-glucosaminidase and TNF-α levels and reduced IL-10 and Vegf levels in tumor tissue. Collectively, fruti exerts antitumor effects through the inhibition of the NF-κB pathway, reducing Cyclin D1 and Bcl-2 levels. In vitro the apoptosis and necroptosis pathways are involved in the cellular death, whereas in vivo, cells undergo necrosis by increased tumor inflammation and reduction of angiogenesis. Thus, fruticuline A acts in tumor cells by multiple mechanisms and represents a promising molecule for drug development in cancer treatment.

The metabolism of α-2′ -deoxythioguanosine in murine tumor cells

1968 ◽  
Vol 46 (7) ◽  
pp. 655-661 ◽  
Author(s):  
G. A. LePage
Keyword(s):  
Cell Growth ◽  
Tumor Cells ◽  
Human Blood ◽  
Blood Cells ◽  
Carcinoma Cells ◽  
Ehrlich Carcinoma ◽  
Human Blood Cells ◽  
Murine Tumor Cells ◽  
Rna And Dna

Preparations of α-2′-deoxythioguanosine (α-TGdR) completely free of β-2′-deoxythioguanosine (β-TGdR) were made and labeled with radiosulfur. A purified preparation of nucleoside phosphorylase obtained from human blood cells was found to be active on the β-anomer but completely inactive on the α-anomer. This property of the enzyme was used to characterize metabolites of α-TGdR. α-TGdR and β-TGdR were both found to be converted to the corresponding mono-, di-, and tri-phosphates and incorporated into the nucleic acids of Mecca lymphosarcoma cells in vivo. α-TGdR appeared predominantly in the terminal nucleoside positions of RNA and DNA. β-TGdR appeared predominantly in the nucleotide chain. Both Mecca lymphosarcoma and Ehrlich carcinoma cells formed significant quantities of analog nucleotides at all three levels of phosphorylation, probably exceeding the levels of guanine nucleotides in the cells for an appreciable time. The findings further support a correlation reported earlier between the incorporation of 6-thioguanine into DNA and the inhibition of cell growth.

L-rhamnose and L-fucose suppress cancer growth in mice

2011 ◽  
Vol 6 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Pavel Tomsik ◽  
Tomas Soukup ◽  
Eva Cermakova ◽  
Stanislav Micuda ◽  
Mohamed Niang ◽  
...  
Keyword(s):  
Tumour Growth ◽  
Intraperitoneal Administration ◽  
Optimal Dose ◽  
Suppressive Effect ◽  
Ehrlich Carcinoma ◽  
Tumour Bearing ◽  
Metastatic Setting ◽  
Days Of Therapy

AbstractIt is documented that deficient fucosylation may play an important role in the pathogenesis of cancer. Since the supplementation of L-fucose could restore fucosylation in both in vitro and in vivo conditions, our intent was to examine the effect of intraperitoneal administration of L-fucose and L-rhamnose (a similar deoxysaccharide) on tumour growth, mitotic activity and metastatic setting of a solid form of Ehrlich carcinoma as well as on the survival rate of tumour bearing mice. Both L-fucose and L-rhamnose exerted a significant suppressive effect on tumour growth (P<0.05). After 10 days of therapy, the greatest inhibition of tumour growth expressed as a percentage of controls was observed in L-rhamnose at a dose of 3 g/kg/day (by 62%) and L-fucose at a dose of 5 g/kg/day (by 47%). Moreover, the mitotic index decreased with increasing doses of L-fucose and L-rhamnose. Prolonged survival of tumour bearing mice was observed after 14 consecutive days of daily administering L-rhamnose. Its optimal dose was estimated to be 3.64 g/kg/day. L-Fucose, however, displayed only a slight effect on the survival of the mice. Our results suggest that L-fucose and especially L-rhamnose have anticancer potential. This study is the first to demonstrate the tumour-inhibitory effect of L-rhamnose.

scholarly journals Phytochemical profile, toxicological evaluation of Rhipsalis baccifera (Sol.) Stearn (Cactaceae) extract and their antitumor activity in Ehrlich carcinoma-bearing mice

2021 ◽  
Author(s):  
Jéssica Alves Cavalcantea ◽  
Luiz da Silva Maia Neto ◽  
Anna Lígia de Castro Figueiredo ◽  
Weslley Oliveira ◽  
José Roberto Pimentel Cabral de Seixas ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Therapeutic Potential ◽  
Lethal Dose ◽  
Artemia Salina ◽  
Subsequent Treatment ◽  
Ehrlich Carcinoma ◽  
Toxicological Evaluation ◽  
Phytochemical Profile

<i>Rhipsalis baccifera</i> (Sol.) Stearn is a typical cactus from tropical regions with wide geographic distribution, and its therapeutic potential is not yet fully understood, such as antitumoral property. Thus, this study evaluated the cytotoxic ethanolic extract of <i>R. baccifera</i> (EERB) and its antitumor activity against Erlich's tumor in mice. The EERB was obtained, and its phytochemical profile was filed by thin-layer chromatography. The toxicity was evaluated in vitro and in vivo using the microcrustacean<i> Artemia salina</i> Leach and mice. The lethal dose was determined after implantation of a tumor cell suspension, with subsequent treatment with EERB (200 mg/kg and 100 mg/kg) 48h after implantation. These values represent the tenth part of the DL<sub>50</sub> and CL<sub>50</sub>, respectively. The presence of phenols, tannins and triterpenes were demonstrated in the phytochemical results. Toxicity was dose-dependent, and the tumor inhibition was 84.1% and 75.8% at doses of 200 mg/kg and 100 mg/kg, respectively. We can highlight that the growth of Erlich's carcinoma suffered inhibitory effects against the EERB. EERB was found to have low acute toxicity and a high potential for use in antitumor therapy. Thus, new studies involving pre-clinical and clinical analyses of the extract are essential to determine the safe dose.

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