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Relevant bibliographies by topics / Mouse carcinoma cells

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Academic literature on the topic 'Mouse carcinoma cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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Journal articles on the topic "Mouse carcinoma cells"

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Li, Rongshan, Jorge L. Yao, Patricia A. Bourne, P. Anthony di Sant'Agnese, and Jiaoti Huang. "Frequent Expression of Human Carcinoma-Associated Antigen, a Mucin-Type Glycoprotein, in Cells of Prostatic Carcinoma." Archives of Pathology & Laboratory Medicine 128, no. 12 (December 1, 2004): 1412–17. http://dx.doi.org/10.5858/2004-128-1412-feohca.

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Abstract Context.—Human carcinoma-associated antigen (HCA) is a mucin glycoprotein recognized by antibodies raised against epiglycanin, the latter having been originally purified from mouse mammary carcinoma cells. Human carcinoma-associated antigen expression is increased in sera of patients with various carcinomas, including prostatic carcinoma. However, to our knowledge, expression of HCA in benign and neoplastic prostatic tissue has not been studied. Objective.—To compare the expression of HCA in cells of primary and metastatic prostatic carcinomas with its expression in non–carcinoma-associated cells. Design.—We studied 40 cases of primary and 36 cases of metastatic prostatic carcinomas by immunohistochemical staining with anti-HCA monoclonal antibodies G1 and HAE3. The blocks from primary carcinomas also contained normal prostatic tissue (40 cases), benign prostatic hyperplasia (16 cases), and high-grade prostatic intraepithelial neoplasia (32 cases). Results.—The 2 antibodies stained carcinomas more frequently than normal prostatic tissue, hyperplasia, and prostatic intraepithelial neoplasia (P < .001). The differences in the staining of low-grade versus high-grade tumors was not statistically significant with either antibody. The staining was present in the cytoplasm and on the luminal membrane surface of the tumor cells and in the luminal secretions. In metastatic prostatic carcinomas, G1 and HAE3 staining was positive in 44% and 67% of the cases, respectively. Conclusions.—Our results showed that mucin protein HCA is overexpressed in cells of prostatic carcinoma, which may have value in diagnosis and therapy. Its role in carcinogenesis also merits further study.

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Sleigh, Merilyn J. "Differentiation and proliferation in mouse embryonal carcinoma cells." BioEssays 14, no. 11 (November 1992): 769–75. http://dx.doi.org/10.1002/bies.950141109.

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Paterno, G. D., C. N. Adra, and M. W. McBurney. "X chromosome reactivation in mouse embryonal carcinoma cells." Molecular and Cellular Biology 5, no. 10 (October 1985): 2705–12. http://dx.doi.org/10.1128/mcb.5.10.2705.

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The embryonal carcinoma cell line, C86S1, carries two X chromosomes, one of which replicates late during S phase of the cell cycle and appears to be genetically inactive. C86S1A1 is a mutant which lacks activity of the X-encoded enzyme, hypoxanthine phosphoribosyltransferase (HPRT). Treatment of C86S1A1 cells with DNA-demethylating agents, such as 5-azacytidine (5AC), resulted in (i) the transient expression in almost all cells of elevated levels of HPRT and three other enzymes encoded by X-linked genes and (ii) the stable expression of HPRT in up to 5 to 20% of surviving cells. Most cells which stably expressed HPRT had two X chromosomes which replicated in early S phase. C86S1A1 cells which had lost the inactive X chromosome did not respond to 5AC. These results suggest that DNA demethylation results in the reactivation of genes on the inactive X chromosome and perhaps in the reactivation of the entire X chromosome. No such reactivation occurred in C86S1A1 cells when the cells were differentiated before exposure to 5AC. Thus, the process of X chromosome inactivation may be a sequential one involving, as a first step, methylation of certain DNA sequences and, as a second step, some other mechanism(s) of transcriptional repression.

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Paterno, G. D., C. N. Adra, and M. W. McBurney. "X chromosome reactivation in mouse embryonal carcinoma cells." Molecular and Cellular Biology 5, no. 10 (October 1985): 2705–12. http://dx.doi.org/10.1128/mcb.5.10.2705-2712.1985.

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The embryonal carcinoma cell line, C86S1, carries two X chromosomes, one of which replicates late during S phase of the cell cycle and appears to be genetically inactive. C86S1A1 is a mutant which lacks activity of the X-encoded enzyme, hypoxanthine phosphoribosyltransferase (HPRT). Treatment of C86S1A1 cells with DNA-demethylating agents, such as 5-azacytidine (5AC), resulted in (i) the transient expression in almost all cells of elevated levels of HPRT and three other enzymes encoded by X-linked genes and (ii) the stable expression of HPRT in up to 5 to 20% of surviving cells. Most cells which stably expressed HPRT had two X chromosomes which replicated in early S phase. C86S1A1 cells which had lost the inactive X chromosome did not respond to 5AC. These results suggest that DNA demethylation results in the reactivation of genes on the inactive X chromosome and perhaps in the reactivation of the entire X chromosome. No such reactivation occurred in C86S1A1 cells when the cells were differentiated before exposure to 5AC. Thus, the process of X chromosome inactivation may be a sequential one involving, as a first step, methylation of certain DNA sequences and, as a second step, some other mechanism(s) of transcriptional repression.

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LUO, Huaxing, Yingxue HAO, Bo TANG, Dongzhu ZENG, Yan SHI, and Peiwu YU. "Mouse forestomach carcinoma cells immunosuppress macrophages through TGF-?1." Turkish Journal of Gastroenterology 23, no. 6 (December 1, 2012): 658–65. http://dx.doi.org/10.4318/tjg.2012.0563.

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Batth, Balvinder K., Rachana Tripathi, and Usha K. Srinivas. "Curcumin-induced differentiation of mouse embryonal carcinoma PCC4 cells." Differentiation 68, no. 2-3 (October 2001): 133–40. http://dx.doi.org/10.1046/j.1432-0436.2001.680207.x.

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Pierce, G. Barry, Juan Arechaga, Alan Jones, Andrea Lewellyn, and Robert S. Wells. "The fate of embryonal-carcinoma cells in mouse blastocysts." Differentiation 33, no. 3 (February 1987): 247–53. http://dx.doi.org/10.1111/j.1432-0436.1987.tb01564.x.

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Lockett, Trevor J., and Merilyn J. Sleigh. "Oncogene expression in differentiating F9 mouse embryonal carcinoma cells." Experimental Cell Research 173, no. 2 (December 1987): 370–78. http://dx.doi.org/10.1016/0014-4827(87)90277-1.

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Simonneau, Michel, Bernard Eddé, Jean-François Nicolas, and Hedwig Jakob. "Single channel currents in mouse embryonal multipotential carcinoma cells." Cell Differentiation 17, no. 1 (July 1985): 21–28. http://dx.doi.org/10.1016/0045-6039(85)90534-2.

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Hassan, Bardes B., Lucas A. Altstadt, Wessel P. Dirksen, Said M. Elshafae, and Thomas J. Rosol. "Canine Thyroid Cancer: Molecular Characterization and Cell Line Growth in Nude Mice." Veterinary Pathology 57, no. 2 (February 21, 2020): 227–40. http://dx.doi.org/10.1177/0300985819901120.

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Thyroid cancer is the most common endocrine malignancy in dogs. Dogs and humans are similar in the spontaneous development of thyroid cancer and metastasis to lungs; however, thyroid cancer has a higher incidence of metastasis in dogs. This study developed a preclinical nude mouse model of canine thyroid cancer using a canine thyroid adenocarcinoma cell line (CTAC) and measured the expression of important invasion and metastasis genes in spontaneous canine thyroid carcinomas and CTAC cells. CTAC cells were examined by electron microscopy. Short tandem repeat analysis was performed for both the original neoplasm and CTAC cells. CTAC cells were transduced with luciferase and injected subcutaneously and into the tail vein. Tumors and metastases were monitored using bioluminescent imaging and confirmed with gross necropsy and histopathology. Invasion and metastasis genes were characterized in 8 follicular thyroid carcinomas (FTCs), 4 C-cell thyroid carcinomas, 3 normal thyroids, and CTAC cells. CTAC cells grew well as xenografts in the subcutis, and they resembled the primary neoplasm. Metastasis to the kidney and lung occurred infrequently following subcutaneous and tail vein injection of CTAC cells. STR analysis confirmed that CTAC cells were derived from the original neoplasm and were of canine origin. Finally, 24 genes were differentially expressed in spontaneous canine thyroid carcinomas, CTAC, and normal thyroids. This study demonstrated the usefulness of a nude mouse model of experimental canine thyroid carcinoma and identified potential molecular targets of canine follicular and C-cell thyroid carcinoma.

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Dissertations / Theses on the topic "Mouse carcinoma cells"

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Tassios, Panayotis. "Control of transcription in embryonal carcinoma cells." Thesis, University College London (University of London), 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283568.

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Paterno, Gary David. "X chromosome inactivation in mouse embryonal carcinoma cells." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4629.

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Bell, S. M. "The cellular immune response to murine embryonal carcinoma cells." Thesis, University of Oxford, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.354817.

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Sheardown, Steven Andrew. "The developmental genetics of mouse embryonal stem cells and embryonal carcinoma cells." Thesis, University of Edinburgh, 1989. http://hdl.handle.net/1842/24310.

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Rehbini, Ohoud Mohammedsabri M. "The role of high mobility nucleosomal binding protein (Hmgn2) in undifferentiated mouse epiblast carcinoma stem cells." Thesis, University of Glasgow, 2016. http://theses.gla.ac.uk/7190/.

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High mobility group nucleosome binding (HMGN) proteins belong to the superfamily of high mobility group (HMG) proteins. HMGN1 and HMGN2 are ubiquitously expressed in all vertebrates, and are most highly expressed in embryonic tissue. Moreover, HMGN1 and HMGN2 were found to be highly expressed in neural stem/progenitor cells in the mouse brain. Here, mouse embryonal carcinoma cells (P19 EC) were used as a model system to study the role of HMGN proteins in pluripotent stem cells. Previously, experiments using short interfering RNA (siRNA) technology to knockdown HMGN1 and HMGN2 have suggested that HMGN proteins are important for the expression of key pluripotent genes, Oct4, Sox2 and Nanog, in P19 EC cells (Mohan, 2012). The aim of this thesis was to develop a lentiviral system for the long term knockdown of Hmgn2, in order to investigate more fully the role of this protein in stem cell pluripotency and differentiation. Constitutive and inducible lentiviral shRNAmir systems were tested and optimized, and a constitutive system was chosen for further work. HMGN2 knockdown in undifferentiated P19 EC cells resulted in the down-regulation of Oct4 protein levels. ChIP assays showed that HMGN2 binding over the Oct4 gene was absent in HMGN2 knockdown cells. Furthermore, binding of HMGN1 at this locus was increased in the absence of HMGN2. Consistent with the reduction in Oct4 expression, levels of the active histone modification, H3K4me3, were also decreased at the Oct4 gene. These results support a role for HMGN2 in the regulation of Oct4 expression in P19 cells, and imply that HMGN2 may be important for maintaining stem cell pluripotency.

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Thompson, Alexandra Inés. "Investigation of the role of hepatic stellate cells in acute liver failure and hepatocarcinogenesis." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28936.

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Introduction: Hepatic stellate cells (HSC) and myofibroblasts may be relevant stromal drivers of human hepatocellular carcinoma (HCC). It was hypothesised that targeted inhibition of αv integrin-mediated TGF-β activation, by HSC or hepatocytes, may result in reduced peri-tumoural and intra-tumoural extracellular matrix formation, and reduced hepatic carcinogenesis. The role of HSC in acute liver injury is less well characterised. It was anticipated that integrin signalling on HSC and hepatocytes might also be relevant in the acute setting. The emerging technique of intravital microscopy (IVM) allows detailed, real-time investigation of the cellular processes involved in hepatocyte injury, cell death and repair. It was hypothesised that this could be coupled with mouse models of HCC and acute liver injury, to perform sequential imaging under anaesthesia. Aims: (i) To determine the effect of targeted inhibition of αv integrins on HSC and hepatocytes, during hepatocarcinogenesis, in a mouse model of HCC. (ii) To investigate the effect of targeted inhibition of αv and other integrins on HSC, hepatocytes, and liver sinusoidal endothelial cells (LSEC), during acute liver injury, in the mouse model of paracetamol-induced liver injury. (iii) To develop IVM of the liver, via an abdominal imaging window, with optimisation of surgical and imaging techniques, to allow sequential imaging of the same animal. Methods: The diethylnitrosamine (DEN)-induced mouse model of hepatocarcinogenesis was used, and PDGFRβ-Cre;αvfl/fl and Alb-Cre;αvfl/fl mice were employed to deplete αv integrins on HSC and hepatocytes respectively. Tumours were harvested at 40 weeks post-DEN. Tumour size and number was evaluated in all animals. PDGFRβ-Cre;αvfl/fl and Alb-Cre;αvfl/fl mice were used in the paracetamol model, to investigate the role of αv integrins in acute liver injury. PDGFRβ-Cre;β8fl/fl and Alb-Cre;β 8fl/fl animals were also tested in this model. The role of integrins in liver sinusoidal endothelial cells (LSEC) during paracetamol-induced liver injury was evaluated using Cdh5-Cre mice. IVM of the liver was performed by surgical implantation of an abdominal imaging window, consisting of a titanium ring and coverslip, secured in place with a purse string suture. Fluorescent reporter mice were used to identify hepatic and vascular architecture, and other label-free microscope technologies were utilised to image collagen, lipid distribution, necrotic areas and blood flow within tissues. Results: In large cohorts of PDGFRβ-Cre;αvfl/fl, Alb-Cre;αvfl/fl, and control animals, there was no difference in mean tumour size or number, at 40 weeks. Targeted inhibition of α v integrins and β 8 integrin on hepatocytes, HSC or LSEC was not protective in paracetamol-induced liver injury. IVM of the liver can be performed on animals with HCC and throughout paracetamol-induced liver injury, to obtain high quality, real-time images of multiple cell lineages and the hepatic microenvironment. Conclusions: The role of TGF-β in HCC pathogenesis is complex and context-dependent. Targeted loss of αv integrin did not result in reduction in tumour burden in this non-cirrhotic model of HCC. IVM of the liver is a powerful tool to quantify inflammatory infiltrates and assessment of vascular remodelling throughout the course of acute liver injury and regeneration, providing insights into the biological processes determining recovery.

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Aghsani, Parisa. "Effects of a plant extract from Ruptiliocarpon caracolito on the growth and differentiation of P19 mouse embryonal carcinoma cells." Thesis, University of Ottawa (Canada), 2004. http://hdl.handle.net/10393/26560.

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Present data indicate that the Ruptiliocarpon caracolito extract exerted significant anti-proliferative activity against P19 EC cells, in the absence of toxicity and significant alterations in the differentiation status of the cells. The focus of this study was to determine whether the proliferation of P19 EC cells would decrease in response to Ruptiliocarpon caracolito extract and whether the anti-proliferative activity, if observed, would be accompanied by alterations in the cell differentiation status. According to the data obtained in the present study, the plant extract exerted a significant anti-proliferative activity against the P19 EC cell line. This activity was exhibited in a dose-related fashion. Amongst the doses tested (5--70mug/ml), concentrations ranging from 30--70mug/ml showed a significant anti-proliferative activity (P < 0.001). The highest growth reduction activity of the extract was noticed at a concentration of 50mug/ml of culture medium. Viability studies indicated that the decrease in cell proliferation was not secondary to the toxicity of the extract. (Abstract shortened by UMI.)

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Mejetta, Stefania 1984. "1)Jarid2 regulates mouse epidermal stem cell activation and differentiation ; 2)Tumor heterogeneity and metastasis-initiation in human squamous cell carcinoma." Doctoral thesis, Universitat Pompeu Fabra, 2013. http://hdl.handle.net/10803/283482.

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Jarid2 is required for the genomic recruitment of the polycomb repressive complex-2 (PRC2) in embryonic stem cells. However, its specific role during late development and adult tissues remains largely uncharacterized. In this first part of my thesis, we show that deletion of Jarid2 in mouse epidermis reduces the proliferation and potentiates the differentiation of postnatal epidermal progenitors, without affecting epidermal development. In neonatal epidermis, Jarid2 deficiency reduces H3K27 trimethylation, a chromatin repressive mark, in epidermal differentiation genes previously shown to be targets of the PRC2. However, in adult epidermis Jarid2 depletion does not affect interfollicular epidermal differentiation but results in delayed hair follicle (HF) cycling as a consequence of decreased proliferation of HF stem cells and their progeny. We conclude that Jarid2 is required for the scheduled proliferation of epidermal stem and progenitor cells necessary to maintain epidermal homeostasis. Several human and mouse solid tumors, including squamous cell carcinomas (SCC), contain a population of Cancer Stem Cells (CSCs). CSCs are characterized by their unique ability to initiate and propagate the tumor; however, very little is known about their capacity to disseminate to distant organs and give rise to metastasis. CSCs display a great functional and molecular heterogeneity, and it has been proposed that different CSC subclones might exist to either maintain the primary tumor or to metastasize in distant sites. However, the identity of these heterogeneous populations of CSCs, as well as their molecular and functional characteristics for most type of tumors remains to be elucidated. Using a novel xenograft system that we have developed to study human head and neck squamous cell carcinoma, we have identified a labelretaining (LRC) population inside the cancer stem cell pool defined by the high expression of CD44 and high activity of Aldh1. Unexpectedly, tumor LRC harbor poor initiating potential, and are more sensitive to chemotherapy than their proliferating counterparts. Intriguingly, tumor LRCs are defined by a unique transcriptome signature previously linked with bone and lung identity, two major sites of SCC metastasis, suggesting they might be involved in the colonization of distant tissues by SCC tumors. We have also identified surface molecules, including CD36 and CD37, that are uniquely expressed by tumor LRCs, that can be used as surrogate markers to isolate and characterize them from primary human SCCs. Based on this signature, we could demonstrate that the presence or absence of this population in the primary tumor of a large cohort of patients with cutaneous SCC is highly predictive of the metastatic occurrence. In addition, several markers exclusively expressed by tumor LRCs can be targeted with drugs currently in clinical trials for the treatment of other diseases. We are testing whether some of these therapeutical strategies are effective to preventing or reducing the metastatic potential of SCC tumors.
Jarid2 es necesario para la localización genómica del complejo represor polycomb repressive complex-2 (PRC2) en células stem embrionarias. Sin embargo, la función de Jarid2 en las últimas fases del desarrollo embrionario y su papel en la función de los tejidos adultos no ha sido aún caracterizada en profundidad. En esta primera parte de mi tesis doctoral, mostramos que la deleción de Jarid2 en la piel de ratón no afecta al desarrollo de la epidermis, pero reduce la proliferación y potencia la diferenciación de las células progenitoras epidermales en neonatos. La piel de los ratones neonatos Jarid2-KO muestra niveles reducidos de la marca represora de la cromatina, H3K27me3, en genes necesarios para la diferenciación de las células progenitoras. En cambio, en piel adulta la depleción de Jarid2 no afecta la diferenciación de la epidermis, pero sí que resulta en una reducción del número de células stem activas de los folículos pilosos, lo que desemboca en el retraso del crecimiento de los folículos. Por lo tanto, nuestros resultados demuestran que Jarid2 es necesario para la activación y diferenciación de diferentes células stem del compartimento queratinocítico de la piel necesarios para mantener la homeostasis epidermal. Diversos tipos de tumores sólidos humanos y de ratón, incluyendo carcinomas de células escamosas (SCCs del inglés: Squamous Cell Carcinomas), contienen una población de células madre cancerosas (CSCs del inglés Cancer Stem Cells). Las CSCs se caracterizan porque pueden iniciar y propagar el tumor; sin embargo, se conoce muy poco sobre su capacidad de alcanzar órganos lejos del tumor primario y de formar metastasis. Las CSCs pueden ser muy heterogéneas tanto a nivel funcional como molecular, y se ha propuesto que podrían existir diferentes subclones sea para mantener el tumor primario, sea para formar metástasis. No obstante, no se conoce por ahora ni la identidad de estas poblaciones heterogéneas de CSCs, ni sus características a nivel funcional o molecular. Usando un nuevo sistema de xenoinjerto que hemos desarrollado en nuestro laboratorio para estudiar SCC de cabeza y cuello, hemos identificado una población que es capaz de retener el marcaje con el tiempo (LRC de inglés: Label-retaining Cells), dentro de la población total de CSSs, definidas como células dentro del tumor que muestran alta expression de CD44 y alta actividad de Aldh1. En contra de lo que esperábamos, las LRC del tumor tienen dificultad para iniciar tumores por sí solas y son más sensibles a tratamientos de quimioterapia cuando las comparamos con otras células más proliferativas. Por otra parte, las LRC del tumor se pueden definir con un transcriptoma único que ha sido relacionado anteriormente con hueso y pulmón, que son dos de los órganos donde los SCC forman metástasis preferentemente. Esto sugiere que podrían estar involucradas en la colonización de órganos alejados del SCC primario. Hemos identificado también moléculas de superficie, incluyendo CD36 y CD37, que se expresan exclusivamente en las LRC de tumor y que se pueden usar como marcadores para aislar y caracterizar las LRC de SCCs primarios humanos. Basándonos en estos marcadores, hemos podido demostrar que la presencia o no de esta población en el tumor primario predice la formación de metástasis en pacientes con SCC cutáneos. Además, diversos marcadores que hemos identificado como únicos en LRC de tumor, son diana de fármacos ya usados en la actualidad en ensayos clínicos para tratamiento de otras enfermedades. En la actualidad estamos probando si alguno de estos tratamientos puede ser efectivo para prevenir o reducir el potencial de formar metástasis en SCC.

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Zeng, Yi [Verfasser], and Stefan [Akademischer Betreuer] Endres. "Gene expression profiles of T cells after adoptive transfer in a mouse model of pancreatic carcinoma / Yi Zeng ; Betreuer: Stefan Endres." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1126407313/34.

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Hall, Charles. "Ex vivo reprogramming of tumor-reactive immune cells from FVBN202 mice bearing lung metastatic mammary carcinoma: an immunotherapeutic opportunity revealed against recurrence." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3176.

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Metastatic breast cancer treatment has seen few advances in recent years, yet treatment resistance continues to rise, causing disease recurrence. A pilot study was performed to determine the efficacy of ex vivo expansion and reprogramming of tumor-reactive immune cells from experimental metastatic tumor-sensitized mice. Also, phenotypic changes in tumors due to metastasis or tumor microenvironment influences were characterized. Metastatic neu+ mouse mammary carcinoma (mMMC) and its distant relapsing neu-antigen-negative variant (mANV) were investigated in FVBN202 mice. Tumor-reactive central memory CD8+ T cells and activated NK/NKT cells were successfully reprogrammed and expanded during 6-day expansion from mMMC- and/or mANV-sensitized mice, resulting in tumor-specific cytotoxicity. mMMC exhibited a flexible neu-expression pattern and acquired stem-like, tumorigenic phenotype following metastasis while mANV remained stable except decreased tumorigenicity. Myeloid-derived suppressor cell (MDSC) levels were not increased. Adoptive cellular therapy (ACT) with reprogrammed tumor-reactive immune cells may prove effective prophylaxis against metastatic or recurrent breast cancer.

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Book chapters on the topic "Mouse carcinoma cells"

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Nakashima, Toshiro, and Masamichi Kojiro. "Tissue Culture of Hepatocellular Carcinoma Cells and Hetero-Transplantation to the Nude Mouse." In Hepatocellular Carcinoma, 227–43. Tokyo: Springer Japan, 1987. http://dx.doi.org/10.1007/978-4-431-68334-6_15.

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Mezger, Valérie, Vincent Legagneux, Charles Babinet, Michel Morange, and Oliver Bensaude. "Heat Shock Protein Synthesis in Preimplantation Mouse Embryos and Embryonal Carcinoma Cells." In Results and Problems in Cell Differentiation, 153–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-540-46712-0_11.

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Glaves, D., L. Weiss, and F. Vidal-Vanaclocha. "Site-associated differences in endogenous lectin expression by mouse colon carcinoma cells." In Lectins and Cancer, 137–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76739-5_10.

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Zhao, Botao, Bing Huang, Wei Li, and Youxin Jin. "MicroRNA Expression Profiling During Neural Differentiation of Mouse Embryonic Carcinoma P19 Cells." In MicroRNA Protocols, 105–16. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-083-0_9.

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Hohjoh, Hirohiko. "MicroRNA Expression During Neuronal Differentiation of Human Teratocarcinoma NTera2D1 and Mouse Embryonic Carcinoma P19 Cells." In MicroRNA Protocols, 257–69. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-62703-083-0_20.

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Isemura, Mamoru, Masaki Sazuka, Hirokazu Imazawa, Tsutomu Nakayama, Tadataka Noro, Yoshiyuki Nakamura, and Yukihiko Hara. "Inhibitory Effects of Green Tea Infusion on In Vitro Invasion and In Vivo Metastasis of Mouse Lung Carcinoma Cells." In Food Factors for Cancer Prevention, 134–37. Tokyo: Springer Japan, 1997. http://dx.doi.org/10.1007/978-4-431-67017-9_26.

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Hasegawa, Ryohei, Yoshifumi Miyakawa, and Hidetaka Sato. "Squamous Cell Carcinoma, Skin, Mouse." In Integument and Mammary Glands, 31–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-83749-4_5.

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Frith, Charles H. "Transitional Cell Carcinoma, Urinary Tract, Mouse." In Urinary System, 331–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-96956-0_41.

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Frith, Charles H. "Transitional Cell Carcinoma, Urinary Tract, Mouse." In Urinary System, 393–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-80335-2_38.

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Heath, James E. "Adenoma and Carcinoma, Thyroid Follicular Cell, Mouse." In Endocrine System, 254–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-60996-1_28.

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Conference papers on the topic "Mouse carcinoma cells"

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Li, Yan, Harshul Pandit, Xuanyi Li, Suping Li, Jingwen Zhang, Guozhen Cui, and Robert C. Martin. "Abstract 4069: Abolish cancer progenitor cells in a mouse model of diabetes associated hepatocellular carcinoma." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4069.

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Ostroumov, D., J. Wingerath, N. Woller, E. Gürlevik, MP Manns, T. Longerich, S. Kubicka, F. Kühnel, and TC Wirth. "Analysis of T cell exhaustion in tumor-specific CD8 T cells utilizing an orthotopic hepatocellular carcinoma mouse model." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677223.

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Li, Dan, Nan Li, Yifan Zhang, Haiying Fu, Zhijian Duan, Alissa Hummer, Hongjia Yang, et al. "Abstract 2311: Analysis of glypican 3-targeted chimeric antigen receptor T cells in hepatocellular carcinoma cell and mouse models." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2311.

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Li, Dan, Nan Li, Yifan Zhang, Haiying Fu, Zhijian Duan, Alissa Hummer, Hongjia Yang, et al. "Abstract 2311: Analysis of glypican 3-targeted chimeric antigen receptor T cells in hepatocellular carcinoma cell and mouse models." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2311.

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Liu, Ping, Xiaomin Ren, and Lisa X. Xu. "Alternate Cooling and Heating Thermal Physical Treatment: An Effective Strategy Against MDSCs in 4T1 Mouse Mammary Carcinoma." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80229.

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An alternate thermal physical treatment was developed to destroy tumor tissue using liquid nitrogen cooling and RF heating treatment in our pervious study. Our pervious reports had shown that anti-tumor immunity was induced by the alternate treatment. Myeloid derived suppressor cells (MDSCs) are a subset of heterogeneous, bone marrow derived hematopoietic cells that accumulate in the spleen, bone marrow, blood and tumor sites of tumor-bearing mice and cancer patients. MDSCs are one of the key suppressor cells that regulate anti-tumor immune responses in tumor-bearing hosts. MDSCs have been shown to inhibit the function of various types of cells mediating anti-tumor immunity, such as T cells, B cells, NK cells and dendritic cells. MDSCs are recruited specifically to the tumors and contribute indirectly to angiogenesis, growth and metastasis. MDSCs also exert resistance to cancer therapies, such as anti-VEGF strategies and cancer immunotherapy. Given the role of MDSCs in tumor invasion and metastasis and anti-tumor immune responses, therapeutics targeting MDSCs might offer a new strategy for cancer treatment. In this study, the therapeutic effect and MDSCs changes after the alternate cooling and heating treatment was studied using the 4T1 murine mammary carcinoma, a common animal model of human metastatic breast cancer. Due to its highly invasive and poorly immunogenic characters, the 4T1 tumor could cause death even after the primary tumor was surgically removed. The treatment was carried out when micro-metastases were well established. Comparisons were made with the results from the surgery and hyperthermia groups, respectively. The results showed that MDSCs in blood increased rapidly with time after tumor inoculation, and in 66 days, all the mice died in the control group. The statistical results indicated a significant increase in circulating MDSC numbers at different tumor growth stages. In the surgical resection group, MDSCs in blood did not decrease, but increased rapidly to a level much higher that of the control group in 39 day after tumor inoculation. In the hyperthermia group, MDSCs in blood increased rapidly with time after tumor inoculation, and in 39 day, MDSCs was up to 3 times higher than that of the control group. Mice died in 45 day after initial tumor inoculation. But in the alternate treatment group, the number of MDSCs decreased rapidly and recovered to the normal healthy level in 11 days after the treatment. No metastatic tumor could be observed in these mice, and they were in good physiological conditions as observed in the following 3 month. In conclusion, the alternate treatment was found extremely effective against MDSCs in the very aggressive and highly metastatic mouse mammary carcinoma. The good prognosis was expected in relation to the significant decrease in MDSCs and thus the relief of the immune suppression, induced by the alternate cooling and heating treatment. It could be further developed as a novel therapeutic method against metastatic tumor. On the other hand, combining the alternate treatment with other strategies, such as anti-VEGF and cancer immunotherapy, the best therapeutic effect would be achieved through synergy.

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Kasuga, Akiyoshi, Takashi Semba, Hiromasa Takaishi, Takanori Kanai, Hideyuki Saya, and Yoshimi Arima. "Abstract 4083: Intrahepatic cholangiocarcinoma and gallbladder carcinoma mouse model based on transplantation of syngeneic tumor-initiating cells." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-4083.

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Salmanzadeh, Alireza, Harsha Kittur, Michael B. Sano, Mark A. Stremler, P. Christopher Roberts, Eva M. Schmelz, and Rafael V. Davalos. "Investigating Dielectrophoretic Signature of Mouse Ovarian Surface Epithelial Cells, Macrophages and Fibroblasts." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80872.

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Epithelial ovarian carcinomas are the fourth leading cause of death in women in the United States among all cancers and the leading cause of death from gynecological malignancies1. The main reason for this high rate of mortality is the inability to properly detect these carcinomas early. Investigations for diagnosing ovarian cancer in early stages have been hindered by two major obstacles: lack of adequate cell models to study different cancer stages and lack of a reliable technique to isolate these cancer cells from peritoneal fluid. In trying to solve the first challenge, Dr. Schmelz and collaborators presented a transformed mouse ovarian surface epithelial (MOSE) cell model by isolating different transitional stages of ovarian cancer as cells progressed from a premalignant nontumorigenic phenotype to a highly aggressive malignant phenotype2, 3. In this model four stages of transformed cells, namely early (MOSE-E), early-intermediate (MOSE-E/I), intermediate (MOSE-I) and late (MOSE-L) cells, were distinguishable3. In the current study, we attempt to solve the second challenge of isolating cancer cells from macrophages and fibroblasts, which are found in the peritoneal fluid. Based on differences in cells’ intrinsic electrical properties, a new cell manipulation technique, contactless dielectrophoresis (cDEP), was implemented.

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Nagaoka, Tadahiro, Kazuhide Watanabe, Monica Gonzales, Nadia Castro, Maria-Cristina Rangel, Kelly Rollman, Jeffrey S. Rubin, David S. Salomon, and Caterina Bianco. "Abstract 1053: Modulation of Wnt/β-catenin signaling pathway by Cripto-1 in mouse embryonal carcinoma F9 cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1053.

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Zacharski, L., V. Memoli, and S. Rousseau. "THROMBIN-SPECIFIC SITESOF FIBRINOGEN IN SMALL CELL CARCINOMA OF THE LUNG." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643670.

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Thrombin-generated cleavage sites of human fibrinogen have been identified within the connective tissue stroma adjacent to viable tumor cells in fresh frozen sections of small cell carcinomaof the lung (SCCL) by means of immunohistochemical techniques using mouse monoclonal antibodies (designated alpha and beta) to the N-terminal peptides of the fibrinogen alpha and beta chains(provided by G. Matsueda and E. Haber).Specific connective tissue staining with antibody alpha was diffuse while staining with antibody beta was linear and focal. These results indicate thatthrombin is generated in situ in this tumor type. Previous demonstration of an initiator of coagulation together with coagulation factor intermediates associated with viable SCCL tumor cellsin situ(Cancer Res. 43:3963, 1983; Blood 66 (Suppl.1):329, 1985) is consistent with the hypothesis that the tumorcells themselves are responsible for the local thrombin generation. Because favorable effects of anticoagulant therapy with warfarin in SCCL have been demonstrated previouslyin two randomized clinical trials (J.A.M.A. 145:831, 1981; Proc. Am.Soc. Clin. Oncol. 4:191,1985), we postulate that local tumor cell-induced thrombin formation may contributeto self-regulated progression of SCCL through formation of a supportive, fibrin-rich connective tissue stroma (N. Engl. J. Med. 315:1650, 1986) and/or stimulation of cell proliferation (e.g. E.M.B.0. J. 4: 2927,1985; Proc. Natl. Acad. Sci. U.S.A. 83:976, 1986). These results suggest novel treatment strategies for this particular tumor type and justify efforts to identify other tumortypes in which similarmechanisms exist.

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Pandit, Harshul, Yan Li, Guozhen Cui, Suping Li, Salina Li, and Robert C. Martin. "Abstract 1909: Non-alcoholic steatohepatitis promotes EpCAM positive cancer stem cells mediated tumorigenesis in immunocompetent mouse model of hepatocellular carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1909.

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