Journal articles: 'Experimental tumor'

1

Okajima, Eigoro, and Seiichiro Ozono. "EXPERIMENTAL BLADDER TUMOR." Japanese Journal of Urology 82, no. 5 (1991): 705–15. http://dx.doi.org/10.5980/jpnjurol1989.82.705.

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Grigore, Ana Camelia, Camelia Busila, Ioana Bianca Chesaru, Alina Calin, and Liliana Lacramioara Pavel. "Biological Features of Tumors Results of Experimental Studies." Revista de Chimie 68, no. 3 (April 15, 2017): 594–98. http://dx.doi.org/10.37358/rc.17.3.5508.

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Tumor anaplasia can be of varying degrees, being especially marked in fast-growing malignant tumors. Blastomatose tissue is characterized by morphological, chemical, physico-chemical and energetic anaplasia. Structural changes of the tissue specific to blastomatose growth often provide the opportunity to differentiate this tissue from a normal or any other growing tissue. Out of various factors that may influence the external environment of tumors, we should mention food, profession, living and working conditions. Tumors and especially malignant tumors are accompanied by changes in the entire body. These are not just a consequence of the blastomatose growth but also play a role in its subsequent development. Experimental tumors are one of the methods of studying the issue of blastomatose growth. The tumor transplantation method is widespread and extensively applied in laboratory practice. It uses standard strains of tumors (rats, mice, etc.). The simplicity of the tumor transplantation method, which consists of the inoculation under the skin of animals of tumor fragments using a trocar or of the injection of a tumor emulsion under aseptic conditions, enables researchers to maintain the purity of the strain for a long time. Various views have been formulated at different times on the origin of tumor growth in accordance with the level of knowledge on this issue.

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Sikora, K. "Brain Tumor Biology - Progress in Experimental Tumor Research." British Journal of Cancer 51, no. 3 (March 1985): 447. http://dx.doi.org/10.1038/bjc.1985.64.

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Ware, Jerry, Masahiko Zuka, Shaskank Jain, Susan Russell, Judith Dent, Jane Forsyth, Brigid Maruszak, and Brunhilde Felding-Habermann. "Platelet Glycoprotein Ibα Supports Primary Tumor Growth and Experimental Metastasis." Blood 108, no. 11 (November 16, 2006): 1463. http://dx.doi.org/10.1182/blood.v108.11.1463.1463.

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Abstract Successful tumor formation and metastatic spread depend on the ability of tumor cells to interact with their host microenvironment. Studies from our groups and others indicate that platelets contribute to tumor host interactions through adhesive and stimulatory functions that may promote tumor growth and dissemination. Here we show that platelet receptor GPIbα plays a critical role in the ability of platelets to support primary tumor development and hematogenous metastasis. We previously developed knockout mice lacking platelet GP Ibα (GPIbαNull, a model of the human Bernard-Soulier syndrome) and mice missing GPIbα, but expressing a fusion protein of cytoplasmic GP Ibα and the extracytoplasmic domain of the interleukin-4 receptor (Ibα/IL-4R). Expression of the Ibα/IL-4R ameliorates macrothrombocytopenia, a characteristic of the Bernard-Soulier syndrome. However, both models result in a severe hemorrhagic state owing to the absence of GPIbα. Congenic mouse strains of both GP Ibα models were generated by 10-generation backcrosses with wild-type (WT) C57BL/6J mice to study the tumorgenic and metastatic activity of syngeneic tumor cells. To analyze primary tumor growth, Lewis lung carcinoma cells (D121) were injected intradermally in the dorsal flank of the hind limb (105 cells/injection) and tumor development analyzed in its initial and advanced stages. Seventeen days after injection, tumors in GPIbαNull and Ibα/IL-4R mice were several-fold smaller than those in WT C57BL/6J mice. Histological examination of early and end-stage tumors revealed three major differences: a severe and immediate onset of tumor necrosis, a lack of new blood vessels large enough to connect to the circulation, and a significant reduction in tumor-associated macrophages. While the proliferation rate of tumor cells in non-necrotic areas of the tumors was unaffected by the lack of GPIbα, the percentage of necrosis in these tumors was 6-fold increased in GPIbαNull mice. Each necrotic area showed increased hemorrhage in the absence of GPIbα. The overall density of microvessels in early primary tumors appeared unchanged, but the number of larger vessels associated with tumors was reduced ~2-fold and the density of tumor-associated macrophages was reduced ~6-fold compared to tumors developing in WT mice. To analyze a contribution of platelet GPIbα to hematogenous tumor metastasis, another syngeneic tumor cell model was used and B16F10.1 melanoma cells were injected into the tail vein (105 cells/mouse) of GPIbαNull, Ibα/IL-4R, or WT mice, to determine the ability of tumor cells to colonize the lungs 14 days later. In the absence of functional GPIbα, the number of metastatic foci at the surface of the lungs was significantly reduced (15-fold, p = 0.0002). These results indicate that successful target organ colonization by tumor cells from the blood stream is severely affected by the lack of extracytoplasmic GPIbα in Ibα/IL-4R animals, and not necessarily by the reduced number of platelets in GPIbαNull animals. The results demonstrate a significant involvement of platelet GP Ibα in primary tumor growth by affecting tumor angiogenesis and the recruitment of tumor-associated macrophages while providing evidence GPIbα directly contributes to target organ colonization by circulating tumor cells. These studies identify platelet GP Ibα as a potential new target for anti cancer therapy.

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MuellerKlieser, W. "Tumor biology and experimental therapeutics." Critical Reviews in Oncology/Hematology 36, no. 2-3 (November 2000): 123–39. http://dx.doi.org/10.1016/s1040-8428(00)00082-2.

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6

Colmbo, M. P. "Gene therapy of experimental tumor." Melanoma Research 3, no. 1 (March 1993): 16. http://dx.doi.org/10.1097/00008390-199303000-00047.

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Hau, Dou-Mong, I.-Hsin Lin, Jaung-Geng Lin, Yung-Hsich Chang, and Ching-Ha Lin. "Therapeutic Effects of Moxibustion on Experimental Tumor." American Journal of Chinese Medicine 27, no. 02 (January 1999): 157–66. http://dx.doi.org/10.1142/s0192415x99000203.

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This work investigated the therapeutic effects of the improved form of moxibustion (MT) on experimental tumor. Sarcoma 180 cells (1 × 107) were transplanted into the subcutaneous tissue in the breast area of female ICR mice. Mice bearing a tumor were divided into one control and four experimental groups. The experimental groups were treated with MT for 1, 2, 3 and 4 times (abbreviated as MT1, MT2, MT3, MT4, respectively). This study showed that the experimental group treated with MT3 displayed the optimal therapeutic response. The longest mean survival time (87.8 days) within 120 days after treatment of MT3 significantly differed from the control group (60.2 days). In addition, uptake of 86Rb-radioactive tracer significantly decreased in tumors treated with MT3. The improved form of moxibustion used in this study is a reliable model of localized hyperthermia in tumor therapy.

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Wu, Q., B. Tyler, L. Sukay, L. Rhines, F. Dimeco, R. E. Clatterbuck, M. Guarnieri, and B. S. Carson. "Experimental Rodent Models of Brainstem Tumors." Veterinary Pathology 39, no. 3 (May 2002): 293–99. http://dx.doi.org/10.1354/vp.39-3-293.

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Despite recent advances in surgical technology, resection is not an option for many brainstem tumors. Experimental models have played essential roles in examining new approaches to therapy. The objective of the present study was to generate models by determining coordinates for safe inoculation into the brainstem of mice and rats, and to establish whether the implantation of heterotopic cells would create reproducible survival curves. Morbidity and survival studies were used to map stereotactic coordinates allowing successful inoculation of tumor cells. Survival studies were used to investigate the time course of tumor growth. Tumor location was examined by light microscopy and magnetic resonance imaging. Mice survived injections of 2 μL of saline at interaural, lateral, and depth coordinates of −2.5, 1.0, and 3.5 mm and −1.5, 1.0, and 3.5 mm. Rats survived injections at interaural, lateral, and depth coordinates of −2.0, 2.0, and 7.0 mm and −3.0, 0, and 7.0 mm. Median survival of mice challenged with 5 × 105 EMT6 and 104 B16 tumor cells was 11 and 10 days, respectively. Median survival for rats challenged with 104 9L and F98 cells was 14 and 13 days, respectively. The present study demonstrates a feasible approach to preparing models of brainstem tumors. Limitations of these models are discussed.

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9

Inamura, Takanori, and Keith L. Black. "Bradykinin Selectively Opens Blood-Tumor Barrier in Experimental Brain Tumors." Journal of Cerebral Blood Flow & Metabolism 14, no. 5 (September 1994): 862–70. http://dx.doi.org/10.1038/jcbfm.1994.108.

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Bradykinin, infused in low doses (10 μg/kg/min) through the carotid artery ipsilateral to RG2 glioma in rats, significantly increased the permeability in tumor capillaries to six different tracers of varying molecular weights compared with intracarotid infusion of saline alone. Permeability in normal brain capillaries was not significantly increased by intracarotid bradykinin infusion. Tracers used to examined permeability included radiolabeled α-aminoisobutyric acid (AIB; MW 103), sucrose (MW 342.3), inulin (MW 5000), and dextran (MW 70,000), horseradish peroxidase (HRP) and Evans blue (EB). Permeability was expressed as the unidirectional transfer constant Ki (μl/g/min). The permeabilities ( Ki) of tumors in the bradykinin group versus the control saline group for AIB, sucrose, inulin, and dextran were 25.91 ± 6.78 vs. 13.95 ± 4.29 (p < 0.01), 17.90 ± 2.65 vs. 10.75 ± 4.55 (p < 0.01), 23.92 ± 6.99 vs. 6.20 ± 4.37 (p < 0.01), and 17.84 ± 1.00 vs. 1.47 ± 1.24 (p < 0.001), respectively (mean ± SD). Permeability of RG2 gliomas to high molecular weight dextran (70,000) was 12-fold higher in the bradykinin group than in the saline infusion group. Intracarotid infusion of bradykinin did not significantly increase the blood volume in tumor or brain tissue despite its known vasodilative effect. The permeability of normal brain capillaries was unaffected by intracarotid bradykinin infusion. The increased permeability was reversed 20 min after stopping the intracarotid infusion. Electron microscopic and gross qualitative analysis was performed using HRP and EB. Intracarotid bradykinin infusion increased HRP and EB within tumor tissue but not normal tissue. We believe that intracarotid infusion of bradykinin will be a useful technique for selective delivery of antitumor compounds to brain tumors.

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10

Wong, Vernon G., and Ralph S. Viola. "Effect of rH Tumor Necrosis Factor on Experimental Intraocular Tumors." Cornea 10, no. 2 (March 1991): 131–35. http://dx.doi.org/10.1097/00003226-199103000-00008.

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11

Ostrovskaya, L. A., D. B. Korman, N. V. Bluhterova, M. M. Fomina, V. A. Rikova, A. K. Chigasova, E. I. Nekrasova, K. A. Abzaeva, O. O. Riabaya, and J. P. Burmiy. "AURUM POLYACRYLATE: THE EXPERIMENTAL STUDY OF THE ANTITUMOR ACTIVITY." Russian Journal of Biotherapy 19, no. 4 (December 9, 2020): 74–85. http://dx.doi.org/10.17650/1726-9784-2020-19-4-74-85.

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Introduction. The investigation of metal substituted organic compounds as potential antitumor drugs is one of the promising areas of research in experimental and clinical oncology.Objective. The pre-clinical study of the original antitumor drug aurum polyacrylate (aurumacryl) which belongs to such new for oncology group of compounds as polyacrylates of metals was the aim of this work.Materials and methods. Aurumacryl antitumor activity was determined as the tumor growth inhibitory effect against some of the murine solid tumors (Lewis lung carcinoma, Acatol adenocarcinoma and Ca-755 adenocarcinoma). Drug cytotoxic effect against some of the human tumor cells (Mel-Mo melanoma, A549 lung carcinoma, MCF-7 breast carcinoma, HCT116 colon adenocarcinoma) was evaluated with standard МТТ-test. The aurumacryl pharmacokinetics in tumor bearing mice (Lewis lung carcinoma) was studied. The inductively coupled plasma mass spectrometry method was used for the estimation of the aurum maintenance in the tested tissues (tumor, blood, kidneys, liver, lungs, spleen, brain).Results. The 80–90 % tumor growth inhibitory effect of aurumacryl against some solid tumors in mice had been revealed in vivo as well as the death of the 60–90 % human tumor cells of various origins in vitro. Beside this the strong decrease of the number of proliferating MCF-7 tumor cells had been shown. The distribution of aurumacryl in the body of the mice with the solid tumor had been revealed.Conclusion. On the base of the data obtained the further study of the aurumacryl as a potential antitumor agent seems rather promising.

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12

Leung, Ting-Kai, Pai-Jung Huang, Chi-Ming Lee, Chih-Hsiung Wu, Yi-Fan Chen, Li-Kuo Shen, and Wen-Tien Hsiao. "DYNAMIC MRI FOR TUMOR ENHANCEMENT: AN EXPERIMENTAL BREAST CANCER MODEL." Biomedical Engineering: Applications, Basis and Communications 25, no. 01 (February 2013): 1350011. http://dx.doi.org/10.4015/s1016237213500117.

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Dynamic contrast-enhanced magnetic resonance imaging (MRI) with post-processing is routinely used for the analysis of tumors. However, although breast MRI has gained broad clinical recognition, the relationship between imaging findings and tumor pathogenesis has yet to be fully elucidated. We grafted tumors on rats, to examine dynamic MRI images of the tumors, using post-processing subtraction with 3D maximum intensity projection (sMIP). We established a preliminary platform for analysis to compare hemodynamic-based images with histopathological findings and to further biomolecular research. This platform could facilitate future research on the mechanisms of breast tumor enhancement using MRI, improvements to MRI analysis and reduction of the false positive rate, and the development of novel drugs and contrast media.

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13

Gomes Neto, Antero, Antônio Felipe Leite Simão, Samuel de Paula Miranda, Lívia Talita Cajaseiras Mourão, Nilfácio Prado Bezerra, Paulo Roberto Carvalho de Almeida, and Ronaldo de Albuquerque Ribeiro. "Experimental rat lung tumor model with intrabronchial tumor cell implantation." Acta Cirurgica Brasileira 23, no. 1 (February 2008): 84–92. http://dx.doi.org/10.1590/s0102-86502008000100014.

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PURPOSE: The objective of this study was to develop a rat lung tumor model for anticancer drug testing. METHODS: Sixty-two female Wistar rats weighing 208 ± 20 g were anesthetized intraperitoneally with 2.5% tribromoethanol (1 ml/100 g live weight), tracheotomized and intubated with an ultrafine catheter for inoculation with Walker's tumor cells. In the first step of the experiment, a technique was established for intrabronchial implantation of 10(5) to 5×10(5) tumor cells, and the tumor take rate was determined. The second stage consisted of determining tumor volume, correlating findings from high-resolution computed tomography (HRCT) with findings from necropsia and determining time of survival. RESULTS: The tumor take rate was 94.7% for implants with 4×10(5) tumor cells, HRCT and necropsia findings matched closely (r=0.953; p<0.0001), the median time of survival was 11 days, and surgical mortality was 4.8%. CONCLUSION: The present rat lung tumor model was shown to be feasible: the take rate was high, surgical mortality was negligible and the procedure was simple to perform and easily reproduced. HRCT was found to be a highly accurate tool for tumor diagnosis, localization and measurement and may be recommended for monitoring tumor growth in this model.

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14

Moraes, Sandra Pedroso de, Aguinelo Cunha, José Alfredo dos Reis Neto, Humberto Barbosa, Cláudio Aurélio P. Roncolatto, and Renato Frediani Duarte. "Modelo experimental de tumor de Walker." Acta Cirurgica Brasileira 15, no. 4 (December 2000): 237–42. http://dx.doi.org/10.1590/s0102-86502000000400008.

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Com o objetivo de padronizar normas técnicas para obtenção de modelo animal com tumor de Walker 256 e de estabelecer o número de células tumorais necessárias para que esse tumor tenha grande porcentagem de pega e longevidade, possibilitando o desenvolvimento de pesquisas em várias áreas da saúde, foi realizado trabalho em duas etapas. Na primeira foram utilizados 120 ratos para treinamento e definição da técnica. Na segunda etapa foram utilizados 84 ratos, sendo estes separados em 7 grupos (G) de 12 animais cada. O tumor, na forma ascítica, foi inoculado no tecido celular subcutâneo do dorso dos ratos com os seguintes números de células: GI, 1 x 10(7); GII, 5 x 10(6); GIII, 2,5 x 10(6); GIV, 1 x 10(6); GV, 5 x 10(5); GVI, 3 x 10(5) e GVII, 2 x 10(5). Foram avaliadas a porcentagem de pega e a longevidade nos grupos. Os animais dos GI, GII, GIII e GIV obtiveram 100% de desenvolvimento tumoral, porém baixa longevidade. Os dos GV e GVI obtiveram desenvolvimento tumoral em frequência maior que 90% e longevidade satisfatória. Os do GVII não apresentaram desenvolvimento tumoral. Concluiu-se que todos os procedimentos devem ser exaustivamente treinados e que o número de células tumorais viáveis para inoculação, em tecido celular subcutâneo de ratos, deve estar na faixa entre 5 x 10(5) e 3 x 10(5).

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15

Nakada, Teruhiro. "Hyperbaric Oxygenation for Experimental Bladder Tumor." European Urology 14, no. 2 (1988): 145–49. http://dx.doi.org/10.1159/000472921.

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Akiya, Tohru, Teruhiro Nakada, Takashi Katayama, Kokichi Ota, Masaru Chikenji, Tokuyoshi Matsushita, and Haruo Saito. "Hyperbaric Oxygenation for Experimental Bladder Tumor." European Urology 14, no. 2 (1988): 150–55. http://dx.doi.org/10.1159/000472922.

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17

Buchsbaum, Donald J. "Experimental tumor targeting with radiolabeled ligands." Cancer 80, S12 (December 15, 1997): 2371–77. http://dx.doi.org/10.1002/(sici)1097-0142(19971215)80:12+<2371::aid-cncr6>3.0.co;2-e.

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18

Vinnitsky, V. B., and S. K. PROKOPOVICH. "Electrophysiological Phenomena in Experimental Tumor Growth." Annals of the New York Academy of Sciences 719, no. 1 The Aging Clo (May 1994): 257–70. http://dx.doi.org/10.1111/j.1749-6632.1994.tb56834.x.

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19

Confino, Hila, Ilan Hochman, Margalit Efrati, Michael Schmidt, Viktor Umansky, Itzhak Kelson, and Yona Keisari. "Tumor ablation by intratumoral Ra-224-loaded wires induces anti-tumor immunity against experimental metastatic tumors." Cancer Immunology, Immunotherapy 64, no. 2 (October 18, 2014): 191–99. http://dx.doi.org/10.1007/s00262-014-1626-8.

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20

Tolstorozhev, G. B., M. V. Belkov, I. V. Skornyakov, V. I. Pekhnyo, A. N. Kozachkova, H. V. Tsarik, I. P. Kutsenko, N. I. Sharykina, and V. A. Butra. "Infrared Spectra of Human Breast Tumor Tissue and Experimental Animal Tumors." Journal of Applied Spectroscopy 81, no. 6 (January 2015): 1012–18. http://dx.doi.org/10.1007/s10812-015-0043-x.

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21

Takamiya, Yoshiaki, M. Priscilla Short, Frederick L. Moolten, Christina Fleet, Toshihiro Mineta, Xandra O. Breakefield, and Robert L. Martuza. "An experimental model of retrovirus gene therapy for malignant brain tumors." Journal of Neurosurgery 79, no. 1 (July 1993): 104–10. http://dx.doi.org/10.3171/jns.1993.79.1.0104.

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✓ Recent research using rodent models of central nervous system gliomas indicates that a combination of gene transfer and drug treatment may be successful in killing tumor cells. In the present study, a mouse fibroblast-derived packaging cell line, psi 2, which releases a replication-defective retrovirus vector bearing the herpes simplex virus type 1 (HSV)-thymidine kinase (TK) gene, was grown with rat C6 tumor cells in the presence and absence of wild type Moloney murine leukemia virus (MoMLV). Consequently, tumor cells became sensitive to ganciclovir, which is selectively converted to a toxic nucleotide analog by HSV-TK. This killing effect was more effective in the presence than in the absence of wild type retrovirus both in culture and in subcutaneous tumors in nude mice. Tumors regressed in vivo and failed to regrow over a subsequent 10-day observation period after combined treatment with packaging cells, wild type MoMLV, and ganciclovir. This killing effect may be augmented by the ability of the helper retrovirus to package the vector in tumor cells and thus extend delivery of the HSV-TK gene to more tumor cells. This represents significant improvement in tumor therapy in this model system as compared with helper-free systems previously reported by the authors and others. Although additional improvements in the therapy can be envisioned, this approach may prove useful in combination with current modes of therapy for these insidious and lethal tumors.

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Sorianello, E., R. Schillaci, A. Chamson-Reig, V. Lux-Lantos, and C. Libertun. "Actions of Immunosuppressor Drugs on the Development of an Experimental Ovarian Tumor1." Experimental Biology and Medicine 227, no. 8 (September 2002): 658–64. http://dx.doi.org/10.1177/153537020222700816.

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Immunosuppression has been related to the incidence of tumor apparition, including endocrine tumors. The intrasplenic ovarian tumor (luteoma) is a typical benign endocrine tumor that develops under high gonadotropin stimulation and, from the immunological perspective, is located in a critical organ involved in immune response. To establish if immunosuppression could alter the development of this experimental tumor, the effects of cyclosporin A (CsA) and dexamethasone (Dex) were evaluated. After surgery, tumor-bearing and sham animals were kept without treatment for 4 weeks; thereafter, they were distributed into CsA (25 mg/kg), Dex (0.1 mg/kg), or vehicle (75:25 castor oll:ethanol) groups and were injected on alternate days for 50 days. Body weight was evaluated weekly. Animals were sacrificed after a jugular vein blood sample was obtained. Thymi were weighed. Tumors were measured and placed in formaline for histological studies. Serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), and estradiol were measured by radioimmunoassay. Hematological parameters were determined. CsA induced a significant decrease in survival rates both in tumor-bearing and sham animals (P < 0.01). Dex significantly impaired weight increase in both groups of animals. CsA induced a significant weight loss in sham animals, not observed in tumor-bearing animals. Dex induced thymus weight loss in both groups, whereas CsA induced thymus weight loss only in sham animals. Only Dex induced a decrease in lymphocyte number in both groups. CsA induced an increase in monocyte number only in sham animals. Treatments did not alter LH, FSH, or estradiol, whereas PRL was increased by CsA only in sham rats. Neither Dex nor CsA induced any significant variations in tumor volume, nor did they alter tumor histology. In addition, no visible metastases or alterations in other organs were observed. We conclude that, though immunological parameters were altered by the treatments, immunosuppressor drugs did not condition tumor development. In addition, tumors secrete one or more factor/s that counteract CsA effect.

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Gedye, Craig, Danylo Sirskyj, Nazleen Carol Lobo, Ella Hyatt, Andrew Evans, Antonio Finelli, Neil Eric Fleshner, et al. "Essential experimental steps and estimates of renal carcinoma initiating cells." Journal of Clinical Oncology 32, no. 15_suppl (May 20, 2014): 11127. http://dx.doi.org/10.1200/jco.2014.32.15_suppl.11127.

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11127 Background: Rare cancer stem cells (CSC), proposed to be solely responsible for tumor propagation and re-initiation, are functionally identified as tumor-initiating cells (TIC) from ex vivo tumors using xenotransplantation and clonogenic limiting dilution assays (LDA). TIC have not previously been described from ex vivohuman clear cell renal cell carcinoma (ccRCC). Methods: Primary human ccRCC samples (n=120) from patients undergoing nephrectomy were processed and implanted as subcapsular fragments or cell suspension injection LDAs with Matrigel in NOD/SCID/IL2Rγ-/- (NSG) mice, and observed for at least 6 months. In vitro clonogenic LDAs assays were performed from primary cell suspensions and ccRCC cell lines. LDAs were supplemented with human stromal cells and proteins, and the Y-26732 ROCK inhibitor. Multiparametric flow cytometry and immunofluorescence were used to investigate tumor heterogeneity and cell viability. Results: ccRCC TIC appeared rare from injected suspensions, but xenografts engrafted frequently from tiny fragments, and clonogenic frequencies were 103-104greater than TIC frequencies, suggesting that LDAs underestimated ccRCC tumor cell potential. We systematically identified multiple methodological steps that distort quantitation and identification of ccRCC TIC. For example cell viability was highly variable prior to processing, disaggregation itself destroyed up to 99% of tumor cells, standard assays substantially overestimated tumor cell viability in suspensions, and supplementation with human extracellular cells or proteins, or inhibition of anoikis by Y-26732 increased clonogenic and TIC frequencies in cell lines and primary ccRCC suspensions. Annexin-V staining revealed that tumor cells were more apoptotic then normal stromal cells, and that tumor cells positive for CD44 (a putative CSC marker) were more viable than CD44- tumor cells. Conclusions: We describe multiple, unappreciated and largely unavoidable observational errors in essential methods used to study TIC in ccRCC. ccRCC TIC may be more common than appreciated. Re-examination of the CSC hypothesis in other solid tumors is warranted in view of these previously unexplored methodological biases.

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Grzelak, Adrianna, Ingrid Polakova, Jana Smahelova, Julie Vackova, Lucie Pekarcikova, Ruth Tachezy, and Michal Smahel. "Experimental Combined Immunotherapy of Tumours with Major Histocompatibility Complex Class I Downregulation." International Journal of Molecular Sciences 19, no. 11 (November 21, 2018): 3693. http://dx.doi.org/10.3390/ijms19113693.

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Combined immunotherapy constitutes a novel, advanced strategy in cancer treatment. In this study, we investigated immunotherapy in the mouse TC-1/A9 model of human papillomavirus type 16 (HPV16)-associated tumors characterized by major histocompatibility complex class I (MHC-I) downregulation. We found that the induction of a significant anti-tumor response required a combination of DNA vaccination with the administration of an adjuvant, either the synthetic oligodeoxynucleotide ODN1826, carrying immunostimulatory CpG motifs, or α-galactosylceramide (α-GalCer). The most profound anti-tumor effect was achieved when these adjuvants were applied in a mix with a one-week delay relative to DNA immunization. Combined immunotherapy induced tumor infiltration with various subsets of immune cells contributing to tumor regression, of which cluster of differentiation (CD) 8+ T cells were the predominant subpopulation. In contrast, the numbers of tumor-associated macrophages (TAMs) were not markedly increased after immunotherapy but in vivo and in vitro results showed that they could be repolarized to an anti-tumor M1 phenotype. A blockade of T cell immunoglobulin and mucin-domain containing-3 (Tim-3) immune checkpoint had a negligible effect on anti-tumor immunity and TAMs repolarization. Our results demonstrate a benefit of combined immunotherapy comprising the activation of both adaptive and innate immunity in the treatment of tumors with reduced MHC-I expression.

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Lantos, P. "Progress in Experimental Tumour Research Series Vols 27 and 28: Brain Tumor Biology and Brain Tumor Therapy." Journal of Neurology, Neurosurgery & Psychiatry 48, no. 3 (March 1, 1985): 293–94. http://dx.doi.org/10.1136/jnnp.48.3.293-b.

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Baba, Takehiko, Chung-Ching Chio, and Keith L. Black. "The effect of 5-lipoxygenase inhibition on blood-brain barrier permeability in experimental brain tumors." Journal of Neurosurgery 77, no. 3 (September 1992): 403–6. http://dx.doi.org/10.3171/jns.1992.77.3.0403.

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✓ To determine if leukotrienes are important mediators of vascular permeability in brain tumors, the effect of 5-lipoxygenase inhibitors on blood-tumor barrier permeability in rats harboring HK Walker 256 brain tumors was examined using quantitative autoradiography with α-14C-aminoisobutyric acid. The 5-lipoxygenase enzyme converts arachidonic acid to leukotrienes. Three 5-lipoxygenase inhibitors were utilized: BW755C, nordihydroguaiaretic acid, and AA-861. All three 5-lipoxygenase inhibitors significantly decreased vascular permeability both within the tumors and in brain adjacent to tumor. This suggests that capillary permeability in and adjacent to tumors is influenced by endogenous leukotrienes and that leukotrienes play an important role in brain tumor edema.

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Berdel, Wolfgang E., Torsten Kessler, Christian Schwöppe, Ruediger Liersch, Torsten Persigehl, Christoph Bremer, Christoph Schliemann, and Rolf Mesters. "Targeting Tissue Factor to Tumor Vessels. Experimental Results and First-in-Man Experience." Blood 114, no. 22 (November 20, 2009): 469. http://dx.doi.org/10.1182/blood.v114.22.469.469.

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Abstract Abstract 469 Activation of blood coagulation in tumor vessels with subsequent tumor infarction is an experimental strategy in cancer therapy. We have fused different targeting peptides, including GRGDSP (RGD), GNGRAHA (NGR) and 5 cyclic derivates to the C-terminus of truncated tissue factor (tTF) to preferentially target tumor vessel endothelial cell integrins such as αvβ3 or aminopeptidase (CD13). tTF fusion proteins were expressed in E. coli, purified and refolded. Molecular integrity of the fusion proteins was evaluated by SDS-PAGE, immunoblotting and mass spectrometry. Subsequently, the tTF-fusion proteins were tested for biological activity with the following results: They retained the thrombogenic activity of tTF as measured by factor × activation in vitro. When tested with their respective target molecules either in a purified preparation or present on growing endothelial cells, there was specific binding. In vivo studies with human tumor xenograft models in nude mice showed either significant inhibition of tumor growth or regression of established tumors of different histologies (e.g. lung, breast, melanoma, sarcoma) by systemic application of the tTF-fusion proteins in contrast to controls including non-targeted tTF. Histology of the tumors treated with tTF fusion proteins revealed thrombotic occlusion of vasculature and blood pooling. Contrast-enhanced magnetic resonance imaging (MRI) of the tumors in vivo before and shortly after application of tTF-RGD and tTF-NGR showed a significant reduction of tumor perfusion. Degree of reduction correlated with in vivo tumor response. Toxicity studies showed acceptable therapeutic range and at therapeutic dosage there was no thrombo-embolic event in histology of normal organs, such as lung, heart, liver, and kidney. After upscaling production to amounts sufficient for clinical use, we have treated the first cancer patients with tTF-NGR. MRI studies even at the lowest dose (1 mg/kg i.v.) given showed reduction of tumor perfusion with no side effects. Targeted infarction of tumor vasculature with tTF fusion proteins may be promising as cancer therapy and should be further studied. Disclosures: Berdel: private: patent application on targeting tissue factor. Mesters:private: patent application on targeting tissue factor.

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Watanabe, Akira, Ryuichi Tanaka, Norio Takeda, and Kazuo Washiyama. "DNA synthesis, blood flow, and glucose utilization in experimental rat brain tumors." Journal of Neurosurgery 70, no. 1 (January 1989): 86–91. http://dx.doi.org/10.3171/jns.1989.70.1.0086.

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✓ The relationships between distribution of deoxyribonucleic acid (DNA)-synthesizing cells (S-phase cells) and blood flow and glucose utilization were investigated in rat brain tumors using an autoradiographic technique and immunoperoxidase staining for bromodeoxyuridine (BUdR). Two strains of rat brain tumor were used: strain A and B, both induced by the Rous sarcoma virus. Strain A was biologically more malignant than strain B. The blood flow was unevenly distributed in the tumor; compared with the contralateral cortex, the average blood flow in the tumor was about 50% in strain A and 60% in strain B. The distribution of blood flow did not correlate with the distribution of S-phase cells or with the distribution of vessels in the tumor in either strain A or B. The average glucose utilization in strain A was about 250% and in strain B about 170% of that of the contralateral cortex. The high glucose utilization area correlated well with the distribution of BUdR-positive nuclei in strain B. These findings suggest that the biological malignancy of a tumor correlates with glucose utilization rather than with blood flow, and that malignant brain tumors show a marked increase in glucose utilization for nucleic acid synthesis.

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Jain, Shashank, Susan Russell, and Jerry Ware. "Platelet Glycoprotein VI Contributes to Murine Experimental Metastasis." Blood 112, no. 11 (November 16, 2008): 2862. http://dx.doi.org/10.1182/blood.v112.11.2862.2862.

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Abstract A key receptor supporting the normal role of platelets in hemostasis and thrombosis is the collagen receptor, glycoprotein (GP)VI. GPVI is a member of the immunoglobulin super family and is uniquely expressed on the surface of platelets where it is assembled with the ITAM-bearing activation subunit, FcR-g. We have previously reported the generation of a murine model of GP VI deficiency that revealed profound defects in collagen-induced platelet aggregation and major defects in platelet activation following adhesion under flow to fibrillar collagen. More recently, we have generated congenic GPVI deficient animals through an extensive breeding scheme to the inbred C57BL/6J strain. The relevance of specific platelet receptors in experimental metastasis is emerging with work from our laboratory establishing a key role for the platelet glycoprotein Ib- IX complex. We have now performed similar studies using congenic GPVI deficient animals. In this experimental model, murine tumor cells are placed in the tail vein of mice and establishment of lung tumor burden or lung tumor foci is examined two weeks following injection. This model represents a syngeneic model where animals are fully immunocompetent and the injected tumor cells were originally derived from animals of the C57BL/6J strain. Experiments comparing B16F10.1 cells (murine melanoma) and D121 cells (murine Lewis lung carcinoma) have been performed revealing a consistent and statistically significant reduction in tumor foci as a consequence of GPVI absence. In the case of melanoma cell injections into wild type C57BL/6J mice, a mean of 270 foci (SEM 44.0, n=6) is reduced to a mean of 134 foci (SEM 11.6, n=7) in the absence of platelet GPVI (p = 0.013). Similar reductions were observed using Lewis lung carcinoma cells with wild type animals revealing a mean of 132 surface foci (SEM 13.4, n=15) and GPVI deficient animals having a mean of 69 foci (SEM 7.9, n=12; p = 0.0003). Using either cell line an approximate reduction of 50% in the number of visible tumor foci was observed. Additional studies have been performed to compare the size and growth rate of subcutaneously implanted tumor cells, i.e., primary tumor growth. Here, we observed no noticeable size difference in primary tumors harvested 17 days following subcutaneous injection of D121 cells comparing the presence or absence of platelet GPVI. These results demonstrate in the platelet GPVI facilitates experimental tumor metastasis but does not contribute in the growth of primary tumors. These studies underscore the well-established paradigm of platelet adhesion and activation in hemostasis and thrombosis being applicable to mechanisms participating in the spread of cancer. The importance of metastasis in the prognosis for recovery from cancer can not be under emphasized. Indeed, the spread of metastatic disease represents a fundamental change in significantly shortening the life span of the cancer patient. Thus, understanding the molecules that regulate metastasis identifies potential targets for therapeutic intervention that could significantly improve the patient’s prognosis.

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Lesniak, Maciej S., Prakash Sampath, Francesco DiMeco, Michael P. Viglione, Betty M. Tyler, Drew M. Pardoll, and Henry Brem. "Comparative analysis of paracrine immunotherapy in experimental brain tumors." Neurosurgical Focus 9, no. 6 (December 2000): 1–6. http://dx.doi.org/10.3171/foc.2000.9.6.5.

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Object Local delivery of cytokines has been shown to have a potent antitumor activity against a wide range of malignant brain tumors. In this study, the authors examined the efficacy of treating central nervous system (CNS) tumors by transfecting poorly immunogenic B16/F10 melanoma cells with interleukin (IL)-2, IL-4, or granulocyte-macrophage–colony stimulating factor (GM-CSF) gene, and using these cells to deliver the cytokine locally at the site of the CNS tumor. The object was to determine which cytokine would possess the greatest antitumor activity and to further elucidate its mechanism of action. Methods The transfected B16/F10 cells were irradiated to prevent replication and injected intracranially into C57BL/6 mice (10 mice per group) along with nonirradiated, nontransfected B16/F10 (wild-type) melanoma cells. Sixty percent of mice treated with IL-2 (p < 0.001 compared with control) and 10% treated with IL-4 (median survival = 31 days, p < 0.001 compared with control) were long term survivors (> 120 days). The median survival for animals treated with GM-CSF was 22 days with no long term survivors (p = 0.01 compared with control). Control animals that received only wild-type cells had a median survival of 18 days (range 15–20 days). Histopathological examination of brains from animals killed at different times showed minimal infiltration of tumor cells in the IL-2 group, moderate infiltration of tumor cells in the IL-4 group, and gross tumor invasion and tissue necrosis in the GM-CSF group. Animals treated with IL-2 showed a strong CD8 T cell–mediated response, whereas IL-4 evoked a prominent eosinophilic infiltrate in the area of the tumor. Conclusions High levels of locally expressed IL-2 rather than IL-4 or GM-CSF stimulate a strong immunological cytotoxic antitumor response that leads to significant prolongation of survival in mice challenged with B16/F10 intracranial melanoma tumor cells. Consequently, IL-2 may be a superior candidate for use in paracrine immunotherapy.

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31

Tateishi, Akira. "A Study of Experimental Hamster Lingual Tumor." Journal of the Kyushu Dental Society 40, no. 6 (1986): 1179–203. http://dx.doi.org/10.2504/kds.40.1179.

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32

KIDA, Yoshihisa, Tatsuya KOBAYASHI, Takayuki TANAKA, and Naoki KAGEYAMA. "Magnetic Induction Hyperthermia in Experimental Brain Tumor." Neurologia medico-chirurgica 27, no. 11 (1987): 1027–32. http://dx.doi.org/10.2176/nmc.27.1027.

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33

Green, W. B. "Book Review: Progress in Experimental Tumor Research." Veterinary Pathology 37, no. 2 (March 2000): 197. http://dx.doi.org/10.1354/vp.37-2-197.

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Sun, Hao, Timothy Eswothy, Kerlin P. Robert, Jiaoyan Li, L. G. Zhang, and James D. Lee. "Experimental and Analytical Studies of Tumor Growth." Molecular & Cellular Biomechanics 16, S2 (2019): 75. http://dx.doi.org/10.32604/mcb.2019.07090.

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35

Norton, Larry. "Tumor dormancy: separating observations from experimental science." Nature Clinical Practice Oncology 4, no. 12 (December 2007): 671. http://dx.doi.org/10.1038/ncponc1001.

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36

Sun, Hao, Timothy Eswothy, Kerlin P. Robert, Jiaoyan Li, L. G. Zhang, and James D. Lee. "Experimental and theoretical studies of tumor growth." Journal of Micromechanics and Molecular Physics 04, no. 03 (September 2019): 1950004. http://dx.doi.org/10.1142/s2424913019500048.

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Most biological phenomena commonly involve growth and expansion mechanics. In this work, we propose an innovative model of cancerous growth which posits that an expandable tumor can be described as a poroelastic medium consisting of solid and fluid components. To verify the feasibility of the model, we utilized an established epithelial human breast cancer cell line (MDA-MB-231) to generate an in vitro tumorsphere system to observe tumor growth patterns in both constrained and unconstrained growth environments. The tumorspheres in both growth environments were grown with and without the FDA-approved anti-breast cancer anthracycline, Doxorubicin (Dox), in order to observe the influence small molecule drugs have on tumor-growth mechanics. In our biologically informed mechanical description of tumor growth dynamics, we derive the governing equations of the tumor’s growth and incorporate them with large deformation to improve the accuracy and efficiency of our simulation. Meanwhile, the dynamic finite element equations (DFE) for coupled displacement field and pressure field are formulated. Moreover, the porosity and growth tensor are generalized to be functions of displacement and pressure fields. We also introduce a specific porosity and growth tensor. In both cases, the formalism of continuum mechanics and DFE are accompanied by accurate numerical simulations.

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37

Al-Mondhiry, Hamid, Joseph Drago, and Mary J. Bartholomew. "The Fibrinolytic System in Experimental Prostate Tumor." Thrombosis and Haemostasis 56, no. 02 (1986): 133–36. http://dx.doi.org/10.1055/s-0038-1661626.

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SummaryHypofibrinogenemia and disseminated intravascular coagulation are common events in patients with metastatic prostate carcinoma. This study tests the hypothesis that prostate tumor growth and metastasis is associated with sustained activation of fibrinolysis secondary to increased release of plasminogen activator. We implanted an androgen-insensitive prostate tumor into an inbred strain of rats and serially measured plasminogen, plasminogen activator, plasmin and fibrinogen. Control groups included animals without tumor and a group implanted with transitional cell bladder carcinoma, a locally infiltrating tumor not usually associated with hemostatic complications. Our results showed a significant and steady rise in plasma plasminogen activator, plasmin and fibrinogen levels in animals implanted with prostate cancer. This, however, is not specific for prostate tumor. Similar, perhaps more profound changes were noted in animals implanted with the transitional cell carcinoma.

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38

Kurz, Haymo, Dietrich Lauer, Maria Papoutsi, Bodo Christ, and Jörg Wilting. "Pericytes in experimental MDA-MB231 tumor angiogenesis." Histochemistry and Cell Biology 117, no. 6 (April 6, 2002): 527–34. http://dx.doi.org/10.1007/s00418-002-0388-0.

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39

van der Kogel, Albert J. "Rodent tumor models in experimental cancer therapy." Radiotherapy and Oncology 12, no. 3 (July 1988): 248. http://dx.doi.org/10.1016/0167-8140(88)90271-x.

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40

Padberg, G. "Experimental neurooncology, brain tumor and pain therapy." Journal of the Neurological Sciences 85, no. 3 (July 1988): 347. http://dx.doi.org/10.1016/0022-510x(88)90193-1.

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41

Antonsson, Per, Johan Hansson, Terje Kalland, Peter A. Lando, Lennart Ohlsson, Elinor Schad, Anders Svensson, and Mikael Dohlsten. "Genetically engineered superantigens in experimental tumor therapy." Springer Seminars in Immunopathology 17, no. 4 (December 1996): 397–410. http://dx.doi.org/10.1007/bf01795137.

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42

Drexler, Dániel András, Tamás Ferenci, András Füredi, Gergely Szakács, and Levente Kovács. "Experimental data-driven tumor modeling for chemotherapy." IFAC-PapersOnLine 53, no. 2 (2020): 16245–50. http://dx.doi.org/10.1016/j.ifacol.2020.12.619.

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Peyman, Gholam A., Bahram Khoobehi, Andrew Moshfeghi, Murat Sonmez, Darius Moshfeghi, Sanan Shaibani, and A. Alghadyan. "Blood Velocity in an Experimental Iris Tumor." Ophthalmic Surgery, Lasers and Imaging Retina 29, no. 6 (June 1998): 506–9. http://dx.doi.org/10.3928/1542-8877-19980601-13.

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BEHAMMER, WERNER, MICHAEL KLUGE, JOSEF RÜSCHOFF, and DANIELA N. MÄNNEL. "Tumor Necrosis Factor Effects on Ascites Formation in an Experimental Tumor Model." Journal of Interferon & Cytokine Research 16, no. 5 (May 1996): 403–8. http://dx.doi.org/10.1089/jir.1996.16.403.

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45

Thomas, D. G. T. "Brain Tumor Biology (Progress in Experimental Tumor Research, Vol. 27 and 28)." Trends in Neurosciences 8 (January 1985): 370. http://dx.doi.org/10.1016/0166-2236(85)90128-6.

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46

Stone, Simone Cardozo, Renata Ariza Marques Rossetti, Aleida Maria Lima, and Ana Paula Lepique. "HPV associated tumor cells control tumor microenvironment and leukocytosis in experimental models." Immunity, Inflammation and Disease 2, no. 2 (May 18, 2014): 63–75. http://dx.doi.org/10.1002/iid3.21.

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47

Sedlacek, H. H., K. H. Bengelsdorff, G. Hagmayer, and F. R. Seiler. "Tumor therapy of neoplastic diseases with tumor cells and neuraminidase: Experimental studies on chessboard vaccination in transplantation tumors." International Journal of Immunopharmacology 9, no. 7 (January 1987): 841–50. http://dx.doi.org/10.1016/0192-0561(87)90081-6.

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Sun, Da-zhi, Da-wei Ju, Jin He, Ye Lu, Feng Wu, Chang Li, and Pin-kang Wei. "Tumor interstitial fluid and postoperative recurrence of tumors: An experimental study for verifying hypothesis of “tumor-phlegm microenvironment”." Chinese Journal of Integrative Medicine 16, no. 5 (September 25, 2010): 435–41. http://dx.doi.org/10.1007/s11655-010-0537-6.

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49

Lang, S. A., C. Moser, E. M. Jung, K. Pfister, E. K. Geissler, and H. J. Schlitt. "Effects of ASA404, a vascular disrupting agent, on tumor growth of gastric cancer in an experimental model." Journal of Clinical Oncology 29, no. 4_suppl (February 1, 2011): 48. http://dx.doi.org/10.1200/jco.2011.29.4_suppl.48.

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48 Background: A functional vascular system is essential for growth of solid malignancies including gastric cancer. For establishment and maintenance of such a vascular system endothelial cells (ECs) and pericytes (e.g. vascular smooth muscle cells, VSMC) are required. We hypothesized that targeting tumor vasculature with the vascular disrupting agent (VDA) ASA404 (Novartis Oncology) reduces tumor growth in a model of gastric cancer. Methods: Gastric cancer (GC) cell lines, ECs and VSMCs were used for experiments. Effects of ASA404 on growth of GC, EC and VSMC were assessed by MTT assays. Impact of ASA404 (20 mg/kg on day 1, 5, 9) in combination with paclitaxel (10 mg/kg on day 1 and 7) on tumor growth was assessed in a subcutaneous tumor model. Treatment was started when tumors reached a size of approximately 200 mm3. Tumors were measured and harvested on day 23 for IHC analyses. Effect of ASA404 on blood perfusion of tumors during therapy was monitored by contrast-enhanced ultrasound (CEUS). Results: In vitro ASA404 impaired growth of ECs and VSMCs upon stimulation with condition media from gastric cancer cells. No direct effect on tumor cells was observed. In vivo, treatment with ASA404 led to marked decrease of tumor perfusion and an increase of necrosis as determined by CEUS. Furthermore, combination of ASA404 with paclitaxel showed significant reduction of tumor growth compared to controls (p < 0.05). In addition, tumor vascularisation and tumor cell proliferation were significantly reduced as determined by CD31-positive vessel area and BrdU-positive cells (p < 0.05). Conclusions: Combination of the VDA ASA404 with paclitaxel impairs tumor growth and perfusion of gastric cancer in an experimental model. Hence, targeting tumor vasculature with ASA404 appears to be a promising strategy for therapy of gastric cancer. No significant financial relationships to disclose.

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Orosz, P., B. Echtenacher, W. Falk, J. Rüschoff, D. Weber, and D. N. Männel. "Enhancement of experimental metastasis by tumor necrosis factor." Journal of Experimental Medicine 177, no. 5 (May 1, 1993): 1391–98. http://dx.doi.org/10.1084/jem.177.5.1391.

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The influence of endogenous and exogenous tumor necrosis factor (TNF) on metastasis was investigated in an experimental fibrosarcoma metastasis model. A single intraperitoneal injection of recombinant human (rh) TNF or recombinant mouse (rm) TNF into mice 5 h before intravenous inoculation of methylcholanthrene-induced fibrosarcoma cells (CFS1) induced a significant enhancement of the number of metastases in the lung. Dose responses of rmTNF and rhTNF demonstrated a stronger metastasis-augmenting effect by rmTNF compared with rhTNF. This effect was time dependent, as administration of rmTNF 5 h before or 1 h but not 24 h after tumor cell inoculation caused an increase of tumor cell colony formation on the lung surface, suggesting an influence of TNF on the vascular adhesion and diapedesis of tumor cells. Since tumor-bearing mice showed an enhanced ability to produce TNF after endotoxin injection compared to control mice, tumor-bearing mice were treated with anti-mTNF antibodies. Neutralization of endogenous tumor-induced TNF led to a significant decrease of the number of pulmonary metastases. Histological analysis of micrometastases in the lung on day 5 by silver staining of proteins associated with nucleolar organizer regions revealed more metastatic foci and augmented proliferative activity of the tumor cells after rmTNF pretreatment of mice. However, no direct effect of rmTNF on the proliferation rate of tumor cells was seen in vitro. These findings suggest that low doses of endogenous TNF or administered TNF during cytokine therapy might enhance the metastatic potential of circulating tumor cells.

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Journal articles on the topic 'Experimental tumor'

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