Relevant bibliographies by topics / Tumoral cell

Academic literature on the topic 'Tumoral cell'

Author: Grafiati
Published: 10 March 2023
Last updated: 24 August 2024

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Journal articles on the topic "Tumoral cell"

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Martins, A. M. C. R. P. da F. "METABOLISMO DA GLUTAMINA NA CÉLULA TUMORAL." Arquivos do Instituto Biológico 70, no. 2 (April 2003): 231–37. http://dx.doi.org/10.1590/1808-1657v70p2312003.

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RESUMO Neoplasias são doenças com alterações no DNA, provocadas por diversos eventos.Sua origem é monoclonal e com desenvolvimento e instabilidade gênica, novos clones surgem. Os atributos neoplásicos (cariótipo, invasibilidade, suscetibilidade a anti-neoplásicos, ritmo de crescimento, suscetibilidade hormonal, capacidade metastática) são heterogêneos, exigindo fluxo energético alto, macromoléculas e nitrogênio. Assim, as vias metabólicas nessas células garantem-lhes precursores para a síntese de lipídeos estruturais e reguladores, DNA e RNA. Célula tumoral usa qualquer substrato como fonte energética: glicose, lipídeos, corpos cetônicos e aminoácidos, competindo com o hospedeiro pela glicose. Glutamina e alanina são dois transportadores de nitrogênio e esqueleto carbônico entre os diferentes tecidos.O íon amônio é extremamente tóxico às células devendo ser carreadas por aminoácido.Portanto, a glutamina torna-se a principal fonte de nitrogênio das células tumorais, acarretando profundas mudanças no metabolismo do hospedeiro pelas crescentes necessidades de glutamina pelas células. Glicólise e glutaminólise não são essenciais a neoplasias, são antes oportunidades estratégicas favoráveis á sobrevivência e proliferação em circunstâncias de carência de nutrientes e oxigênio. Nas células tumorais ocorre a expressão de glutaminase P-dependente mitocondrial e de malato-NAD(P)-dependente descaboxilase mitocondrial,enzimas que oxidam piruvato e acetil CoA. Conversão de glutamina à lactato, é chamada glutaminólise e tem a função de produzir energia, glutamato,citrato e aspartato.A concentração da glutamina é inversamente proporcional ao crescimento da neoplasia, com aumento da glutaminase e diminuição, prescindível nos tumores, da glutamina sintetase. O estudo das vias metabólicas das células tumorais oferece subsídios ao combate às neoplasias. Como os tumores também sintetizam menos aminoácidos que as células normais e (necessitam receber suplementos em aminoácidos do fluido extracelular e carbono,) tornam-se vulneráveis aos bloqueadores de transporte de aminoácidos sendo esta uma base de terapia contra o câncer.
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Quinelato, Ayra Daneluzzi, Murilo Bonatelli, Patrik Da Silva Vital, Eduardo Caetano Albino da Silva, Paula Roberta Pastrez, Adhemar Longatto-Filho, and Céline Pinheiro. "O Efeito Warburg em carcinoma de pulmão de pequenas células: caracterização da expressão de proteínas relacionadas ao metabolismo glicolítico em amostras preservadas em meio líquido." Manuscripta Médica 5 (December 28, 2022): 3–16. http://dx.doi.org/10.59255/mmed.2022.73.

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Introdução: O câncer de pulmão de pequenas células (CPPC) afeta, em média,200.000 pessoas no mundo, anualmente, correspondendo a 15-20% de todos os cânceres de pulmão. Em geral, tumores sólidos reprogramam seu metabolismo aumentando a dependência na glicólise, mesmo em condições aeróbias (efeito Warburg), sendo uma das características fundamentais do câncer. Objetivo: Avaliar a expressão de proteínas relacionadas ao metabolismo glicolítico em amostras de CPPC preservadas em meio líquido. Material e Métodos: Foram incluídos 45 pacientes diagnosticados com CPPC, submetidos a lavagem brônquica em ambos os pulmões, cujas amostras (normal e tumoral) foram armazenadas em meio líquido (BD SurePathÒ). A expressão das proteínas MCT1, MCT4, GLUT1 e CA9 foi avaliada por imunocitoquímica (ICQ) em cell blocks, seguida de avaliação por patologista e, por fim, análise estatística. Resultados: Foi observada uma perda importante de amostras durante a construção dos cell blocks, na ICQ e por falta de representatividade celular. Das remanescentes, 1 amostra tumoral (12,5%) foi positiva para MCT1, 2 amostras normais (9,1%) e 2 tumorais (14,3%) foram positivas para MCT4, 1 amostra normal (4,2%) e 3 amostras tumorais (21,4%) foram positivas para GLUT1 (p=0,043) e 1 amostra tumoral (7,1%) foi positiva para CA9. Devido ao reduzido número de casos positivos, não foi possível verificar possíveis associações com os dados clínicos e patológicos dos pacientes. Conclusão: A expressão de MCT1, MCT4 e CA9 foi observada em poucas amostras, não sendo observada diferença entre amostras normais e tumorais. Para GLUT1, observou-se um aumento significativo da expressão citoplasmática nas amostras tumorais, comparando às normais.
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He, Z., Z. Meng, P. Liang, L. Xing, X. Zheng, and G. Wang. "P13.15 Pre-clinical trial of T601 oncolytic virus for high grade glima via intra-tumoral injection." Neuro-Oncology 23, Supplement_2 (September 1, 2021): ii35—ii36. http://dx.doi.org/10.1093/neuonc/noab180.122.

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Abstract BACKGROUND An effective therapeutic method still hasn’t been devised for lethal high grade glioma. Thus, a method with high anti-tumoral efficiency, tumoral targeting, and acceptable side effect needs to be designed. Oncolytic virotherapy which can specifically lyse tumor cells via mass replication and deleting nucleotide metabolism related gene, like TK, required in viral replication and overexpressed in tumor cells, provides hope for patients. However, the virus only contained TK deletion is unable to show sufficient specificity of anti-tumoral response in tumor cells. Here, the adapted strain of vaccinia virus with high tumoral specificity due to TK and RR deletion and FUC1 insertion, named T601, is chosen in this project. In clinical application, intra-tumoral injection showed improved anti-tumoral efficiency and acceptable side effect. However, intra-tumoral viral injection in orthotropic glioma model is rare. In this project, various biosafety and antitumoral efficiency parameter would be tested for confirming the biosafety and reliability of intra-tumoral T601 viral injection for future clinical trials. MATERIAL AND METHODS For measuring the IC50 of T601, 10 different amounts of virus was tested in vitro via calculating cell viability with CCK-8(cell counting kit-8). For measuring the further antitumoral response of FCU1, different concentration of the 5-FC was added into the medium with IC50 viral amount. To ensure the biosafety of T601, MTD (maximum tolerance dose) was measured. Based on the MTD result, for evaluating the anti-tumoral efficiency, 106 pfu,105 pfu,104 pfu of virus was intra-tumoral injected in orthotopic GBM bearing mice. Tumor size was measured once a week through in vivo bioimaging system. RESULTS 0.022 MOI, the IC50 of T601, showed high cytotoxicity of T601. Moreover, the significantly decreased cell viability under the combined treatment of 5-FC and 0.22MOI T601 showed intact anti-tumoral function. In MTD assay, except for 107 group, no significant weight loss was found. However, in 107 pfu group, mean body weight decreased around 10% and animal fatality happened on day 9. According to the MTD result, certain amount of virus was intra-tumorally injected. In all treatment group, the tumor size was significantly shrined. At the same time, the survival rate of mice under viral treatment was significantly extended. CONCLUSION In summary, T601 exhibited efficient anti-tumoral function and acceptable side effect. T601 treatment prolonged the survival period of GBM mice with acceptable neurotoxicity, demonstrating that T601 contains necessary criterial for intra-tumoral injection. Ultimately, this project provided basic reference information of dose for future clinical trial.
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Shah, Sumedh, Garima Yagnik, Alan Nguyen, Harsh Wadhwa, Jordan Spatz, Michael Safaee, Justin Cheng, and Manish Aghi. "TMIC-57. PRO-TUMORAL EFFECTS OF INTRA-TUMORAL NEUTROPHILS IN THE GLIOBLASTOMA MICROENVIRONMENT." Neuro-Oncology 21, Supplement_6 (November 2019): vi260. http://dx.doi.org/10.1093/neuonc/noz175.1091.

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Abstract While macrophage enrichment and lymphocyte depletion have been described in glioblastoma, intratumoral neutrophils and their effect on glioblastoma have been under-characterized. While tumor-associated neutrophils (TANs) were initially regarded as passive bystanders due to their short-lived nature, investigation of TANs in other cancer types revealed pro-tumoral roles. Therefore, we sought to characterize TANs in the glioblastoma microenvironment using transcriptomic analysis and define their oncologic effects. Flow cytometric analysis of patient samples for neutrophils (CD11b+/CD15+/CD66b+) revealed higher percentages of TANs in glioblastoma compared to low-grade gliomas (1.76% [n=13] vs. 0.33% [n=6], p=0.03). Using the Transwell migration assay with glioblastoma tumor conditioned-media (CM), we found that recruitment of circulating neutrophils to tumor sites is mediated by leukotriene-B4 chemoattraction and that this interaction can be blocked with the addition of LtB4 receptor antagonist, LY293111. TANs were morphologically activated, unlike circulating neutrophils from GBM patients (P< 0.05) and, while not intravascular, were close to blood vessels. We performed single-cell RNA sequencing of isolated TANs and found a distinct transcriptomic profile relative to circulating neutrophils from these patients, particularly upregulated osteopontin. Osteopontin concentration was significantly higher in TAN CM than in patient-matched peripheral blood neutrophil CM (3.2ng/mL [n=3] vs. 0.02ng/mL [n=3], p< 0.05). Because osteopontin is linked to GBM stem cell-like phenotype maintenance and TANs localized to the perivascular niche where GBM stem cells reside, we investigated TAN-GBM stem cell interactions and osteopontin as a potential mediator. We found TAN CM increased proliferation and stem cell markers (Nanog, Oct4, Sox2) of stem cell-containing GBM neurospheres (p< 0.01). These effects were blocked by osteopontin-neutralizing antibodies (p< 0.01). Our work defines neutrophil-mediated pro-tumoral effects and their mechanisms and identifies a novel approach to target GBM stem cells—by disrupting the immune cell mediators that create their supportive microenvironment in the perivascular niche.
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Derakhshani, Afshin, Zeinab Rostami, Hossein Safarpour, Mahdi Abdoli Shadbad, Niloufar Sadat Nourbakhsh, Antonella Argentiero, Sina Taefehshokr, et al. "From Oncogenic Signaling Pathways to Single-Cell Sequencing of Immune Cells: Changing the Landscape of Cancer Immunotherapy." Molecules 26, no. 8 (April 14, 2021): 2278. http://dx.doi.org/10.3390/molecules26082278.

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Over the past decade, there have been remarkable advances in understanding the signaling pathways involved in cancer development. It is well-established that cancer is caused by the dysregulation of cellular pathways involved in proliferation, cell cycle, apoptosis, cell metabolism, migration, cell polarity, and differentiation. Besides, growing evidence indicates that extracellular matrix signaling, cell surface proteoglycans, and angiogenesis can contribute to cancer development. Given the genetic instability and vast intra-tumoral heterogeneity revealed by the single-cell sequencing of tumoral cells, the current approaches cannot eliminate the mutating cancer cells. Besides, the polyclonal expansion of tumor-infiltrated lymphocytes in response to tumoral neoantigens cannot elicit anti-tumoral immune responses due to the immunosuppressive tumor microenvironment. Nevertheless, the data from the single-cell sequencing of immune cells can provide valuable insights regarding the expression of inhibitory immune checkpoints/related signaling factors in immune cells, which can be used to select immune checkpoint inhibitors and adjust their dosage. Indeed, the integration of the data obtained from the single-cell sequencing of immune cells with immune checkpoint inhibitors can increase the response rate of immune checkpoint inhibitors, decrease the immune-related adverse events, and facilitate tumoral cell elimination. This study aims to review key pathways involved in tumor development and shed light on single-cell sequencing. It also intends to address the shortcomings of immune checkpoint inhibitors, i.e., their varied response rates among cancer patients and increased risk of autoimmunity development, via applying the data from the single-cell sequencing of immune cells.
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Chih, Y., K. Sahm, A. Sadik, T. Bunse, N. Trautwein, S. Pusch, S. Stevanovic, et al. "KS01.3.A Tumoral MHC class II expression in gliomas drives T cell exhaustion." Neuro-Oncology 23, Supplement_2 (September 1, 2021): ii3. http://dx.doi.org/10.1093/neuonc/noab180.007.

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Abstract BACKGROUND Neoepitopes are presented on major histocompatibility class II (MHCII) molecules. In glioma, for instance, the recurrent driver mutation IDH1R132H was shown to bear an MHCII-restricted epitope in preclinical and clinical vaccine studies. The general relevance of MHCII expression in glioma for antitumor immunity, however, remains unknown. Here we evaluate stromal and tumoral MHCII expression, functionality, and its association with survival in gliomas. MATERIAL AND METHODS Immunostaining of human glioma tissues was used to identify tumoral, endothelial, and microglial MHCII expression and to enumerate T cell infiltrates. To gain insights into tumoral MHCII expression, bulk transcriptomic data from TCGA and single-cell transcriptomic data from publicly available datasets were analyzed. MHC ligandome analyses of an MHCII+ glioma cell line and human glioma tissues were used to determine the functionality of MHCII in vitro and ex vivo. Functional in vitro co-culture assays with an HLA-DR-matched tetanus toxoid (TT) epitope-overexpressing glioma cell line and in vitro-expanded TT-reactive T cells from healthy donors were used to examine direct target recognition by T helper cells. CRISPR-Cas9-mediated knockout of MHCII in preclinical hypermutant glioblastoma cell line GL261 was employed to further validate the consequences of tumoral MHCII expression and to probe potential clinical intervention with existing therapies. RESULTS MHCII is expressed in the majority of gliomas and associated with increased infiltration of T cells. In 10% of the analyzed glioma tissues and a subset of single cells, tumoral MHCII expression is detected. Clinical and transcriptomic data reveal that tumoral MHCII is associated with poor prognosis, cytokine responses, immune inhibition and T cell differentiation. Ligandome analyses evidence presentation of peptides by MHCII molecules on glioma cells. In in vitro assays, TT-reactive T helper cells specifically produce IFNg when co-cultured with MHCII+ glioma cells upon the presence of co-stimulation. In agreement with the clinical data, preclinical murine models demonstrate that tumoral MHCII expression leads to reduced survival. Co-culture assay shows that tumoral MHCII results in upregulation of PD-1 on T helper cells antigen-specifically. Concordantly, immune checkpoint blockade (ICB) therapy slows the disease progression of mice carrying MHCII+ tumors. CONCLUSION MHCII is expressed in gliomas by a subset of tumor cells. Although tumoral MHCII is functional, it is associated with poor survival in both clinical data and preclinical models. T cell exhaustion induced by tumoral MHCII expression can, in part, be overcome by ICB in vivo. Further experiments are required to decipher tumor cell intrinsic and microenvironmental consequences of tumoral MHCII expression.
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Montes, Marta, and Maite Huarte. "8G modifications rewire tumoral microRNAs." Nature Cell Biology 25, no. 9 (September 2023): 1243–44. http://dx.doi.org/10.1038/s41556-023-01179-9.

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Masetti, Michela, Federica Portale, Roberta Carriero, Bianca Partini, Nicolò Morina, Andrea Ponzetta, Piergiuseppe Colombo, et al. "High-dimensional single cell-based immune profiling of the tumor immune microenvironment in prostate cancer." Journal of Clinical Oncology 38, no. 6_suppl (February 20, 2020): 376. http://dx.doi.org/10.1200/jco.2020.38.6_suppl.376.

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376 Background: Genetic lesions that drive prostate cancer (PCa) development are able to modify the immune response and tumor infiltrating immune subsets, resulting in tumor progression. We investigated the profile of the immune microenvironment in PCa by high dimensional single cell analysis. Methods: We conducted an immune profiling study based on integrated RNA single cell sequencing and multiparametric flow cytometry in order to dissect the immune landscape of PCa. CD45+ immune cells infiltrating tumoral and adjacent non tumoral tissues were isolated from patients with PCa who underwent software assisted fusion biopsy, based on MRI, and/or radical prostatectomy, and analyzed by single cell sequencing. The primary endpoint was to evaluate the effectiveness of single cell RNA sequencing on CD45+ cell sorted from tumoral and adjacent non-tumoral tissues. Secondary endpoint was the identification of tumor-driven immune changes in prostatic lesions. Results: The cohort consisted of 3 patients who underwent radical prostatectomy (RP) and 45 patients with positive prostate biopsy; the negative control was checked by pathological assessment. In patients who underwent RP the gene expression analysis identified a modulation in the abundance of several immune subsets infiltrating the tumoral tissue, when compared with the non tumoral, evident for Tumor associated macrophages (TAMs), Natural Killer cells (NK) and T regulatory cells. We then implemented a 22 parameters flow cytometry panel that we tested on fresh prostatic tissue and peripheral blood from positive PCa biopsies. We identified a subset of tumor infiltrating macrophages showing an altered gene expression profile when compared with macrophages infiltrating the non-tumoral tissue. Importantly we derived a genetic signature from this subset of tumoral TAMs that resulted to be associated with cancer progression. Conclusions: Our findings support the effectiveness of single cell RNA sequencing in the dissection of the immune landscape in PCa and identified immune changes in patients when comparing neoplastic tissue with non tumoral areas. Such data may be useful for understanding the role of immune system in PCa carcinogenesis.
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Lombardo, Dominique, Carole Siret, and Sadia Beloribi-Djefaflia. "Exosomal lipids impact on tumoral cell behavior." Cell Cycle 14, no. 4 (February 16, 2015): 461–62. http://dx.doi.org/10.1080/15384101.2015.1006538.

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Rennó, Magdalena N., Gleyce M. Barbosa, Patricia Zancan, Venicio F. Veiga, Celuta S. Alviano, Mauro Sola-Penna, Fábio S. Menezes, and Carla Holandino. "Crude ethanol extract from babassu (Orbignya speciosa): cytotoxicity on tumoral and non-tumoral cell lines." Anais da Academia Brasileira de Ciências 80, no. 3 (September 2008): 467–76. http://dx.doi.org/10.1590/s0001-37652008000300008.

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Plant-derived substances have been considered as important sources of drugs, including antineoplasic agents. Babassu mesocarp is popularly used in Brazil as a food additive, and in popular medicine against several conditions, such as inflammations, menstrual pains and leukaemia. From babassu Orbignya speciosa (Mart.) Barb. Rodr. [Arecaceae (Palmae)] epicarp/mesocarp, an ethanol extract was prepared and named OSEME, which was tested on the viability,morphology and metabolism of several cell lines, such as the leukaemic cell lines, HL-60, K562 and the latter multidrug resistant counterpart K562-Lucena 1, the human breast cancer cell line MCF-7, the mouse fibroblast cell line 3T3-L1 and fresh human lymphocytes. OSEME promoted a dose-dependent decrease on the viability of all cells. This effect was much more pronounced on the tumoral cell lines than on non-tumoral cells, a phenomenon revealed by the dose of OSEME which promotes half of maximal effect (ID50). The decrease on viability was followed by shrinkage of cells, alteration on their morphology, and a markedly nuclear condensation. Curiously, stimulation of 6-phosphofructokinase activity (6.6-times) was observed on HL-60 cells, treated with OSEME, when compared to control treated with ethanol (vehicle). These results support evidences to suggest OSEME as a promising source of novel antineoplasic agents.
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Dissertations / Theses on the topic "Tumoral cell"

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Ramos, Grasieli de Oliveira. "O microambiente tumoral como fator modificador no processo de invasão e progressão tumoral no carcinoma espinocelular de origem bucal." reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/147112.

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INTRODUÇÃO: O carcinoma espinocelular de origem bucal (CEC) apresenta uma alta taxa de mortalidade devido à invasividade das células tumorais. A migração celular, principal evento da invasão e metástase, pode ser regulada tanto por fatores intrínsecos, como adesão e contratilidade celular, quanto extrínsecos, como composição, densidade e remodelagem da matriz extracelular (MEC). OBJETIVO: Avaliar o papel de elementos intrínsecos e extrínsecos sobre o processo invasivo do carcinoma espinocelular de origem bucal. MÉTODOS: Foi realizada imuno-histoquímica para as proteínas: Miosina II (isoformas A, B e C), metaloproteinases de matriz (1, 2, 9 e 14); imunofluorescência as proteínas: e-caderina, n-caderina, FAK, paxilina, vinculina e fibronectina em amostras de CEC oral. Foi realizado ensaio de migração nas seguintes condições: 1 – matriz 2D com o substrato de fibronectina, ou laminina ou matrigel; 2 – matriz 3D com colágeno na presença ou não de fibronectina ou laminina; 3 – matriz 3D com diferentes concentrações de colágeno (0,6; 1,2 e 1,8 mg/ml) + fibronectina na presença ou não de um inibidor de MMP. Foi realizado análise de adesão celular utilizando-se o microscópio TIRF e o microscópio confocal, tanto em matrizes 2D quanto 3D. Foram realizados esferoides celulares para avaliar a contratilidade celular, através do plaqueamento das células em gel de agarose e a utilização de drogas que inibem ou que induzem a contratilidade, bem como a partir de células transfectadas com versões fosfomiméticas para a cadeia leve de miosina. Foi realizado ainda western blotting para proteínas: e-caderina, FAK, vinculina, paxilina, N-caderina, integrinas e as isoformas de miosina II, bem como foi avaliado os níveis de ativação das proteínas da família RhoGTPase, as quais estão envolvidas no controle da migração celular. RESULTADOS: A expressão das MMPs analisadas e das isoformas de miosinas foi maior nas zonas de invasão tumoral, sendo que o CEC oral também apresenta uma maior expressão de proteínas associadas à adesão com a MEC. A migração celular foi afetada pela densidade e a composição da MEC, bem como pela atividade das MMPs. Adicionalmente, a modulação das proteínas de adesão célula-matriz altera a velocidade de migração, a direcionalidade dessa migração e também a forma de migração, mudando de uma migração coletiva para uma migração individual. O aumento na contratilidade células resulta numa dispersão celular enquanto que a diminuição da contratilidade resulta numa melhor adesão célula – célula. CONCLUSÕES: O comportamento das células tumorais pode ser modulado através de fatores extrínsecos como, por exemplo, a alteração no microambiente tumoral, seja ela por mudança no substrato ou na densidade da matriz, e também dos fatores intrínsecos como a alteração nos níveis de miosina.
INTRODUCTION: Oral squamous cell carcinoma (OSCC) presents high mortality index due to the invasive phenotype of tumor cells. Cell migration is the main event in cell invasion and metastasis and it can be regulated by intrinsic factor, such as adhesion and cell contractility, and extrinsic factors, such as density and extracellular matrix (EMC) remodeling. OBJECTIVE: Analyze the role of intrinsic and extrinsic factor during the invasive process of oral squamous cell carcinoma. METHODS: We performed immunostaining in OSCC samples for the following proteins: myosin II (isoforms A, B and C), matrix metalloproteinase (1, 2, 9 and 14) e-cadherin, n-cadherin, FAK, paxillin, vinculin and fibronectin. We also performed migration assays with OSCC cell line in the following conditions 1 – 2D matrix with fibronectin or laminin or matrigel; 2 – 3D matrix with collagen in the presence or not of fibronectin or laminin; 3 – 3D matrix with different collagen concentration (0,6; 1,2 e 1,8 mg/ml) with fibronectin in the presence or not of the MMP inhibitor. In order to analyze cell adhesion, it was performed Total Internal Reflectance Fluorescence and Confocal microscopy, in 2D and 3D matrix. To analyze cell contractility, cells were plated in agarose gel in order to produce spheroids, which were treated with drugs that inhibit or induce cell contractility or cells were previously transfected with Myosin Light Chain phosphomimetics mutants. It was also performed western blotting to: e-cadherin, n-cadherin, FAK, paxillin, vinculin and myosin II isoforms, as well as it was analyze the levels in RhoGTPase family, which are involved in cell migration control. RESULTS: The expression to MMPs and myosin II isoforms were higher at invasion zone of the tumor, and the OSCC presented higher expression of proteins associated to adhesion to ECM. Cell migration was affected by the EMC composition and density and by MMP activity. Also, the modulation of cell-matrix adhesion proteins altered migration speed, cell directionality as well as influenced the switch between collective and single cell migration. The increase in cell contractility resulted in cell dispersion while the decrease in cell contractility resulted in a better cell-cell adhesion. CONCLUSIONS: The behavior of cell tumor can be modulate by extrinsic factors, for example, the change in tumor microenvironment, by the change in the EMC substrate or density and by intrinsic factors such as the alteration in myosin levels.
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Granados, Colomina Carla. "Unraveling the biological role of latexin in cell fate specification." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/385107.

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Latexin es un gen de respuesta a ácido retinoico (RA) cuya función celular se conoce escasamente. Latexin se encuentra silenciada por un mecanismo de hipermetilación en numerosas líneas tumorales, sugiriendo que ésta podría estar ejerciendo una función como supresor tumoral. Con el objetivo de elucidar su potencial implicación en cáncer, empleamos líneas derivadas de neuroblastoma ya que representan modelos adecuados para estudiar tanto procesos de apoptosis como de diferenciación. En este estudio revelamos que la escasa expresión de latexin parece una característica común de las líneas de neuroblastoma y que dicha expresión puede ser modulada mediante el tratamiento con RA. La sobreexpresión estable de latexin no altera los procesos proliferación celular ni de muerte celular en la línea SH-SY5Y. Sin embargo, su sobreexpresión sí que tiene un efecto significativo promoviendo la aparición de células del tipo S (del linaje Schwanniano) cuando son tratadas con RA. Además, su expresión también facilita la emergencia del fenotipo S cuando las células se exponen al agente 5-bromo-2’-deoxyuridine (BrdU). De hecho, la inhibición del axis PI3K/Akt impide la activación de senescencia Estas evidencias sugieren que latexin podría ser un determinante en la decisión del destino celular entre apoptosis y senescencia en células de neuroblastoma, probablemente modulando dicha cascada de señalización. Estos resultados nos alentaron a tratar de desvelar el panorama de expresión génico que promovueve latexin con el objetivo de identificar piezas claves en los efectos previamente mencionados que promueve latexin. Interesantemente, latexin promueve la expresión de un gran número de genes, principalmente involucrados en procesos de adhesión celular, desarrollo y morfogénesis. Curiosamente, la mayoría de genes promovidos por latexin, ya sea en presencia o ausencia de RA, pertenecen a la matriz extracelular (ECM), sugiriendo una potencial asociación entre la ECM y los efectos favorecidos por latexin en células SH-SY5Y. Cuando extendimos nuestros resultados a otros modelos celulares, observamos que latexin también fomenta el proceso de senescencia en respuesta al estímulo adecuado en la línea de neuroblastoma SK-N-LP y en la línea derivada de Glioblastoma Multiforme (GBM) LN-18. Sorprendentemente, una bajada en la expresión de latexin en las células U87-MG resulta en diferenciación tipo astrocitario cuando las células son tratadas con el agente genotóxico doxorubicina. Cabe remarcar que las células U87-MG con una expresión disminuida de latexin tienen perturbada la activación del proceso de senescencia. De una manera general, estos descubrimientos revelan una nueva función de latexin en la regulación de la especificación celular hacia la adquisición de un fenotipo senescente en diferentes modelos celulares.
Latexin is a recently discovered and poorly known retinoic acid (RA)-responsive gene whose cellular function is scarcely known. Latexin expression appears downregulated through promoter hypermethylation in several types of cancer, suggesting it can function as a tumor suppressor. With the aim to elucidate its potential role in cancer, we employed neuroblastoma-derived cells since they represent canonical and well-established models of apoptosis and differentiation. We first reveal that the lack of latexin expression appears as a common hallmark in neuroblastoma-derived cells although it can be modulated by RA treatment. The stable overexpression of latexin does not significantly alter cell proliferation or cell death responses in SH-SY5Y cells. However, the overexpression of latexin remarkably favors the emergence of S-type cells (Schwannian lineage) upon RA treatment. Consistently, latexin overexpression also facilitates the appearance of the S-type phenotype upon exposure to 5-bromo-2’-deoxyuridine (BrdU). Moreover, latexin-overexpressing cells display enhanced Akt activation upon RA or BrdU stimuli, or even in basal growth conditions. This activation allows latexin-overexpressing cells to survive for long periods under unfavorable extracellular conditions and to undergo cellular senescence. Indeed, the inhibition of the PI3K/Akt axis impedes the activation of cellular senescence. These evidences suggest that latexin could be a critical determinant of cell fate choices between apoptosis or senescence in neuroblastoma cells likely by modulating this cascade. These results encouraged us to unveil the landscape of gene expression promoted by latexin to identify key targets involved in the aforementioned latexin-mediated effects. Interestingly, latexin upregulated a large number of genes, most of them involved in cell adhesion, cell development and morphogenesis processes. Surprisingly, the vast majority of genes upregulated by latexin either in the presence or in the absence of RA belong to the extracellular matrix (ECM), therefore suggesting the potential involvement of the ECM in latexin-promoted effects in SH-SY5Y cells. When extending our results to other cellular models, we observe that latexin also promotes cellular senescence upon the adequate stimuli in the neuroblastoma cell line SK-N-LP and in the Glioblastoma Multiforme (GBM)-derived cell line LN-18. Intriguingly, latexin knock down in U87-MG cells results in astrocytic-like differentiation upon treatment with the genotoxic drug doxorubicin. Remarkably, U87-MG cells with decreased levels of latexin expression remarkably impair the activation of cellular senescence. Altogether, these findings disclose a novel functional role of latexin in regulating cell specification towards the acquisition of a senescent phenotype in different cellular models.
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3

Long-Mira, Élodie. "Identification de biomarqueurs tissulaires et sanguins impliqués dans la progression, la réponse et la résistance aux thérapies ciblées des mélanomes cutanés." Thesis, Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4129.

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Contexte : Le mélanome est un cancer agressif chez l’homme, développé aux dépens des mélanocytes. L’identification de la mutation BRAF conditionne la prescription d’une thérapie ciblée. L’objectif de ce travail a été de mettre au point dans les tissus tumoraux et dans le sang (cellules tumorales circulantes, ADN libre tumoral plasmatique) des approches technologiques de biologie moléculaire et d’immunohistochimie (IHC) pour identifier des biomarqueurs prédictifs d’une réponse ou de résistance thérapeutique. Nous montrons que l’IHC BRAF (clone VE1, Roche, Ventana) pourrait remplacer l’analyse en biologie moléculaire dans certaines indications, notamment sur un matériel tumoral de petite taille. Parallèlement, nous montrons que la présence de cellules mélanocytaires circulantes [détectées par cytomorphologie (Technique ISET)] chez des patients atteints de mélanome métastatique est un facteur prédictif indépendant de mauvais pronostic de la survie globale. Enfin, nous montrons que le système Biocartis Idylla™ (processus automatisé couplant l’extraction, le séquençage et l’analyse de l’ADN) est sensible et spécifique pour la détection plasmatique des mutations BRAF et NRAS et que cette technique pourrait être indiquée dans le suivi de la maladie résiduelle (apparition de résistance) après traitement des patients atteints de mélanomes métastatiques. Conclusion : L’identification des biomarqueurs tissulaires et sanguins (BRAF, NRAS et CTC) permettent : 1- Une optimisation des délais diagnostiques de la mutation BRAF/NRAS – 2) L’identification de facteurs de mauvais pronostic – 3) De détecter une récidive précoce et de suivre la maladie résiduelle après traitement
Background: Knowledge of the BRAFV600E status is mandatory in metastatic melanoma patients (MMP). Molecular biology is currently the gold standard method for status assessment. The aim of this work was to assess and compare several methods of molecular biology and immunohistochemistry (IHC) in tissue and blood (cell-free circulating tumor DNA, circulating tumor cell (CTC)) to identify predictive biomarkers of response or resistance to targeted treatment. Results: We showed that BRAFV600 IHC could be a substitute for molecular biology in the initial assessment of the BRAFV600E status in MPP. We also found that the presence of circulating tumor cell detetcted by a cytomorphological approach ISET (Isolation by Size of Epithelial Tumor Cell – Rarecells Diagnostics, Paris, France) in MMP is an independent predictor of shorter survival. Then, in a monocentric study conducted at the University of Nice Hospital, we evaluated a novel and fully automated CE-IVD PCR-based system (IdyllaTM, Biocartis, Mechelen, Belgium) for plasmatic BRAF and NRAS mutation detection. We showed that this technology is highly sensitive and specific and provide promising potential to assess tumor progression, identify targets for therapy, and evaluate clinical response to treatment. In conclusion, identification of tissue and blood biomarkers with these technologies allow a quick turnaround-time to BRAF/NRAS diagnosis and improve monitoring of treatment response and development of resistance in metastatic melanoma patients
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4

Long-Mira, Élodie. "Identification de biomarqueurs tissulaires et sanguins impliqués dans la progression, la réponse et la résistance aux thérapies ciblées des mélanomes cutanés." Electronic Thesis or Diss., Université Côte d'Azur (ComUE), 2016. http://www.theses.fr/2016AZUR4129.

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Contexte : Le mélanome est un cancer agressif chez l’homme, développé aux dépens des mélanocytes. L’identification de la mutation BRAF conditionne la prescription d’une thérapie ciblée. L’objectif de ce travail a été de mettre au point dans les tissus tumoraux et dans le sang (cellules tumorales circulantes, ADN libre tumoral plasmatique) des approches technologiques de biologie moléculaire et d’immunohistochimie (IHC) pour identifier des biomarqueurs prédictifs d’une réponse ou de résistance thérapeutique. Nous montrons que l’IHC BRAF (clone VE1, Roche, Ventana) pourrait remplacer l’analyse en biologie moléculaire dans certaines indications, notamment sur un matériel tumoral de petite taille. Parallèlement, nous montrons que la présence de cellules mélanocytaires circulantes [détectées par cytomorphologie (Technique ISET)] chez des patients atteints de mélanome métastatique est un facteur prédictif indépendant de mauvais pronostic de la survie globale. Enfin, nous montrons que le système Biocartis Idylla™ (processus automatisé couplant l’extraction, le séquençage et l’analyse de l’ADN) est sensible et spécifique pour la détection plasmatique des mutations BRAF et NRAS et que cette technique pourrait être indiquée dans le suivi de la maladie résiduelle (apparition de résistance) après traitement des patients atteints de mélanomes métastatiques. Conclusion : L’identification des biomarqueurs tissulaires et sanguins (BRAF, NRAS et CTC) permettent : 1- Une optimisation des délais diagnostiques de la mutation BRAF/NRAS – 2) L’identification de facteurs de mauvais pronostic – 3) De détecter une récidive précoce et de suivre la maladie résiduelle après traitement
Background: Knowledge of the BRAFV600E status is mandatory in metastatic melanoma patients (MMP). Molecular biology is currently the gold standard method for status assessment. The aim of this work was to assess and compare several methods of molecular biology and immunohistochemistry (IHC) in tissue and blood (cell-free circulating tumor DNA, circulating tumor cell (CTC)) to identify predictive biomarkers of response or resistance to targeted treatment. Results: We showed that BRAFV600 IHC could be a substitute for molecular biology in the initial assessment of the BRAFV600E status in MPP. We also found that the presence of circulating tumor cell detetcted by a cytomorphological approach ISET (Isolation by Size of Epithelial Tumor Cell – Rarecells Diagnostics, Paris, France) in MMP is an independent predictor of shorter survival. Then, in a monocentric study conducted at the University of Nice Hospital, we evaluated a novel and fully automated CE-IVD PCR-based system (IdyllaTM, Biocartis, Mechelen, Belgium) for plasmatic BRAF and NRAS mutation detection. We showed that this technology is highly sensitive and specific and provide promising potential to assess tumor progression, identify targets for therapy, and evaluate clinical response to treatment. In conclusion, identification of tissue and blood biomarkers with these technologies allow a quick turnaround-time to BRAF/NRAS diagnosis and improve monitoring of treatment response and development of resistance in metastatic melanoma patients
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5

LE, HOANG BA PATRICK. "Interet diagnostic du squamous cell carcinoma en pathologie pleuropulmonaire." Nice, 1988. http://www.theses.fr/1988NICE6550.

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6

SORDAGE, MONIQUE. "Interet d'un marqueur tumoral, le squamous cell carcinoma, en pathologie anale." Nice, 1989. http://www.theses.fr/1989NICE6558.

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7

Calderón, Celmira [UNESP]. "Imunomarcação de COX-2, PGE-2, VEGF e CASPASE-3 em mastocitomas cutâneos caninos." Universidade Estadual Paulista (UNESP), 2008. http://hdl.handle.net/11449/104672.

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Universidade Estadual Paulista (UNESP)
O mastocitoma canino (MCT) é uma neoplasia maligna de grande importância na clínica oncológica devido ao seu comportamento biológico agressivo e alta freqüência. A COX-2 e a PGE2 têm sido associadas à promoção e progressão tumoral e seus principais mecanismos envolvem estímulos da angiogênese tumoral e a inibição da morte celular programada. O VEGF é um potente indutor da angiogênese e a caspase-3 tem um importante papel na via efetora da apoptose. Compreender o mecanismo pela qual a COX-2 pode estimular a progressão tumoral no mastocitoma, permite ampliar o conhecimento do comportamento biológico desta neoplasia e direcionar tratamentos mais eficazes. O presente trabalho fez um estudo retrospectivo em 24 casos de mastocitoma canino (MCT). As neoplasias foram classificadas de acordo com Patnaik et al. (1984) e a expressão da COX-2, PGE2, VEGF e caspase-3 foram avaliadas usando a técnica de imunoistoquímica. A expressão da COX-2 foi correlacionada à expressão do VEGF, PGE2 e caspase-3 nos diferentes graus histopatológicos. A imunomarcação da caspase-3 foi menor nos tumores indiferenciados comparados com os bem diferenciados. Comparando os dados da expressão da COX-2 com os demais marcadores foi observado a correlação positiva entre COX-2 e PGE2, COX-2 e VEGF nas graduações II e III. A correlação entre COX-2 e caspase-3 foi somente detectada no grau III.
The canine mast cell tumor (MCT) is a malignant neoplasia with great importance on the clinical practice due to its aggressive behavior and high frequency. The COX-2 and the PGE2 have been associated to the tumor initiation, promotion and progression, and its main mechanisms involve the stimuli of tumor angiogenesis and the inhibition of apoptosis. The VEGF is a powerful inductor of angiogenesis and the caspase-3 is responsible for most part of the apoptotic effects. The understanding of the mechanism by which the COX-2 stimulates the tumor progression in the mast tumor cells provides an extension through the biological behavior of this neoplasia and leads to a better and effective treatment. The present work was a retrospective study in 24 cases of MCT. The neoplasias were classified according to Patnaik et al. (1984) and the expression of COX-2, PGE2, VEGF and caspase-3 were evaluated using the immunohistochemistry technique. The expression of COX-2 was correlated to the expression of VEGF, PGE2 and caspase-3 in the different histopathologic grades. Caspase-3 immunolabeling was lower in the undifferentiated tumors compared to the more differentiated ones. Comparing the COX-2 expression data to the other markers it was observed a positive correlation between COX-2 and PGE2, COX-2 and VEGF in grade II and III. Correlation between COX-2 and caspase-3 was detected only on grade III. Keywords: COX-2, PGE2, VEGF, caspase-3, mast cell tumor.
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8

PIALAT, RINGENBACH CHRISTINE. "Scc (squamous cell carcinoma) antigene : un nouveau marqueur tumoral, et cancer bronchique." Montpellier 1, 1989. http://www.theses.fr/1989MON11131.

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9

Barbosa, Andrà Luiz dos Reis. "ModificaÃÃo da resposta inflamatÃria sistÃmica em ratos inoculados com carcinossarcoma 256 de Walker: papel da degranulaÃÃo mastocitÃria." Universidade Federal do CearÃ, 2007. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=2891.

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CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
No presente estudo avaliou-se os efeitos da inoculaÃÃo do carcinosarcoma 256 de Walker, bem como o curso de seu desenvolvimento, sobre a reaÃÃo inflamatÃria sistÃmica. Ratos Wistar machos, pesando entre 180 a 220g, foram inoculados, por via intramuscular, com 106 cÃlulas tumorais na coxa direita. Os experimentos foram realizados apÃs o 4Â, 7Â e 10Â dias (4D, 7D e 10D) da inoculaÃÃo do carcinossarcoma 256 de Walker. O grupo controle nÃo foi inoculado as cÃlulas tumorais. Os ratos foram divididos em grupos experimentais com n = 6, nos quais foram avaliados os seguintes parÃmetros: edema de pata por carragenina (Cg; 300μg/pata direita) ou dextrana (Dxt; 500μg/pata direita), atividade da enzima mieloperoxidase (MPO), migraÃÃo de neutrÃfilos para cavidade peritoneal induzidas por carragenina (Cg; 300μg/pata direita), permeabilidade vascular cutÃnea induzidas por bradicinina (2μg/sÃtio), histamina (30μg/sÃtio), serotonina (1μg/sÃtio), substÃncia P (250ng/sÃtio), capsaicina (50μg/sÃtio) ou composto 48/80 (1μg/sÃtio) e degranulaÃÃo mastocitÃria induzida por composto 48/80. A intensidade do edema foi avaliada na pata contralateral ao tumor 1, 2, 3 e 4 hs (Cg) e 30â ,1 2, 3, ,4 hs (Dxt) por pletismometria. A migraÃÃo de neutrÃfilos foi induzida pela administraÃÃo de Cg (300μg/pata) na pata contralateral ao tumor ou na cavidade peritoneal. ApÃs 4 horas, os ratos foram sacrificados e as peles das patas foram retiradas para medir indiretamente a infiltraÃÃo de neutrÃfilos, pela tÃcnica da dosagem da atividade da MPO, e a migraÃÃo de neutrÃfilos para cavidade peritoneal foi avaliada atravÃs da contagem total e diferencial de leucÃcitos. Em relaÃÃo a permeabilidade vascular cutÃnea, imediatamente apÃs as injeÃÃes intradÃrmicas dos estÃmulos (bradicinina, histamina, serotonina, substÃncia P, capsaicina ou composto 48/80), foi administrado azul de Evans (0,1mL/100g do animal), na veia do plexo peniano. ApÃs 30 min, os ratos foram sacrificados e a pele do dorso retirada, para avaliar o extravasamento do azul de Evans por espectrometria. A degranulaÃÃo de mastÃcitos do mesentÃrio foi avaliada apÃs coloraÃÃo com azul de toluidina, sendo contados os mastÃcitos degranulados num total de 100 cÃlulas. Os animais com tumor apresentaram uma inibiÃÃo significativa do edema de pata, com efeito mÃximo observado nos 7 Â e 10 Â dias, tanto com a Cg, quanto com Dxt, quando comparados com o controle sem tumor. Em nenhum dos dias estudados, foram observadas diferenÃas na atividade da MPO na pata e nem na avaliaÃÃo da migraÃÃo de neutrÃfilos para a cavidade pÃritoneal induzidas por Cg. ApÃs 4 e 7 dias da inoculaÃÃo do tumor, o animais apresentaram uma significativa diminuiÃÃo na permeabilidade vascular cutÃnea induzida por bradicinina, serotonina, e composto 48/80. No entanto, o aumento da permeabilidade vascular induzida por histamina, substÃncia P e capsaicina nÃo foi alterada nesses dois dias. No 10 Â dia, observou-se uma diminuiÃÃo da permeabilidade vascular induzida por todos os estÃmulos quando comparado com o grupo sem tumor. A degranulaÃÃo mastÃcitÃria foi inibida em animais com tumor nos 4Â, 7Â e 10Â dias em comparaÃÃo com o grupo controle. Tais dados sugerem que o microambiente do tumor de Walker diminui o curso da resposta inflamatÃria atravÃs da inibiÃÃo da degranulaÃÃo dos mastocitos
Our objective was to evaluate the effect of the 256 Walker carcinossarcoma inoculation, as well as the time course of tumoral development, upon the acute inflammatory response in rats. Wistar rats, 180-220g, received intramuscular 106 tumor cells injections. At the end of 4, 7 or 10 days, wistar rats were separated into 4 groups, with 6 animals per group. The control group, were not inoculated with tumoral cells. Several parameters were evaluated: paw edema induced by carrageenan (Cg; 300μg/hind) or dextran (Dxt, 500μg/hind paw), myeloperoxidase activity (MPO), neutrophil migration to peritoneal cavity induced by carrageenan, cutaneous vascular permeability induced by bradykinin (2μg/site), serotonin (1μg/site), histamine (30μg/site), substance P (250ng/site), capsaicin (50μg/site) or 48/80 compound (1 μg/site) and mast cell degranulation induced by 48/80 compound. Paw edema was evaluated in the contra lateral hind paw of the tumor and measured at 0, 1, 2, 3 and 4h for Cg, and 0, 30â, 1, 2, 3 and 4h.for Dxt by plethysmometry. Neutrophil migration was induced by Cg injection in the contralateral hind paw or in the peritoneal cavity. After 4h, rats were sacrificed and the skin of the hind paw was harvested to measure neutrophil infiltration by MPO assay. Neutrophil migration induced by Cg was also evaluated in the peritoneal cavity, with the total e differential leucocytes counted. In order to measure cutaneous vascular permeability, immediately after intradermic stimulus injections (bradykinin, histamine, serotonin, substance P, capsaicin or 48/80 compound) Evans Blue dye was administrated (0,1mL/100g of per animal) by endovenous route. After 30 min rats were sacrificed and the skin was harvested to evaluate Evans Blue extravasations by spectrofotometry. Mast cells degranulation was evaluated in the in mesentery incubated with 48/80 compound and colored with toluidine blue. Our results shows that, in animals inoculated with the carcinossarcoma, there was a significant inhibition in the Cg and Dxt- induced paw edema, with maximal effect at the 7th and 10th days. There were no differences in MPO activity and neither in the peritoneal neutrophil infiltration induced by Cg in rats inoculated with the carcinossarcoma when compares to normal animals. After 4 and 7 days of the tumor inoculation, we observed a significant inhibition of the vascular permeability induced only by bradikinin, serotonin and 48/80 compound.. In the 10th day after the carcinossarcoma inoculation, there was a significant inhibition of the vascular permeability induced by all inflammatory stimulus tested, when we compared animals not inoculated. Mast cell degranulation was decreased in the 4th, 7th and 10th days after carcinossarcoma inoculation. These results suggested that the tumor microenvironment decreased the acute inflammatory response probably due to a inhibition of the mast cell degranulation.
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10

Grégoire, Murielle. "Polynucléaires neutrophiles, cellules stromales, lymphocytes B : interaction tripartite dans la niche des lymphomes B." Thesis, Rennes 1, 2014. http://www.theses.fr/2014REN1S156/document.

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Les polynucléaires neutrophiles ont longtemps été considérés comme des cellules n’intervenant que dans la réponse immune innée. Cependant, au cours de ces dernières années, de nombreuses publications suggèrent que ces cellules, retrouvées au sein du microenvironnement de nombreux cancers, pourraient également jouer un rôle dans la tumorigénèse et la progression tumorale. Ces études mettent en évidence leur fréquence comme marqueur pronostique dans différents cancers solides, mais peu de travaux se sont intéressés à la caractérisation fonctionnelle de ces cellules dans la progression tumorale. Dans de nombreux cancers dont les lymphomes B issus du centre germinatif, les cellules tumorales, qui sont incapables de proliférer et de survivre seules, sont dépendantes de leur microenvironnement de soutien. Dans cette étude, nous avons évalué la fonctionnalité des polynucléaires neutrophiles dans la croissance des lymphomes B. Ainsi, nous avons démontré pour la première fois que les polynucléaires neutrophiles soutiennent directement la croissance et la survie des cellules tumorales de lymphomes B. De plus, un dialogue bidirectionnel existe entre les polynucléaires neutrophiles et les cellules stromales. D’une part, les cellules stromales soutiennent la survie des polynucléaires neutrophiles, qui en retour induisent les caractéristiques d’un stroma lymphoïde. L’induction de ce phénotype permet aux cellules stromales d’acquérir de meilleures capacités de soutien envers les cellules tumorales. Cette étude confirme donc que les polynucléaires neutrophiles sont une composante importante du microenvironnement tumoral, et pourraient devenir une nouvelle cible thérapeutique pour le traitement des lymphomes B issus du centre germinatif
For long time, neutrophils have only been considered as cells involved in the innate immune response. More recently, in descriptive publications, neutrophils were found in the microenvironment of many solid cancers, hypothesizing that they could also play a role in tumorigenesis and cancer progression. These studies highlighted the prognostic value of their frequency, but few of them focused on the functional characterization of these cells in tumor growth. In many cancers, including germinal centre-derived B-cell lymphomas, tumor cells are dependent on their microenvironment to proliferate and survive. In this study, we focused on the role of neutrophils in the progression of B-cell lymphomas, and for the first time we demonstrated that neutrophils directly support the growth and survival of tumor Bcells. In addition, we highlighted the existence of bidirectional cooperation between neutrophils and stromal cells. In one hand stromal cells support the survival of neutrophils. On the other hand, neutrophils induce a lymphoid stroma phenotype which is well known to enhance their supportive effect on tumor cells. This study demonstrates that neutrophils are a significant component of the tumor microenvironment and may be considered as a potential therapeutic target for the treatment of B-cell lymphomas
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Books on the topic "Tumoral cell"

1

1938-, Hay Robert, Park Jae-Gahb, and Gazdar Adi F, eds. Atlas of human tumor cell lines. San Diego: Academic Press, 1994.

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Derek, Raghavan, ed. Germ cell tumors. Hamilton, [Ont.]: BC Decker, 2003.

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Raghavan, Derek. Germ cell tumors. Hamilton [Ont.]: BC Decker, 2003.

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Aarbakke, Jarle, Peter K. Chiang, and H. Phillip Koeffler, eds. Tumor Cell Differentiation. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4594-0.

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Mazurek, Sybille, and Maria Shoshan, eds. Tumor Cell Metabolism. Vienna: Springer Vienna, 2015. http://dx.doi.org/10.1007/978-3-7091-1824-5.

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Frazier, A. Lindsay, and James F. Amatruda, eds. Pediatric Germ Cell Tumors. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-38971-9.

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Bagrodia, Aditya, and James F. Amatruda, eds. Testicular Germ Cell Tumors. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-0860-9.

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Sawamura, Yutaka, Hiroki Shirato, and Nicolas de Tribolet, eds. Intracranial Germ Cell Tumors. Vienna: Springer Vienna, 1998. http://dx.doi.org/10.1007/978-3-7091-6821-9.

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Yutaka, Sawamura, Shirato Hiroki, and Tribolet Nicolas de, eds. Intracranial germ cell tumors. Wien: Springer, 1998.

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Fan, Z. Hugh. Circulating tumor cells: Isolation and analysis. Hoboken, New Jersey: John Wiley & Sons, Inc., 2016.

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Book chapters on the topic "Tumoral cell"

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Brix, Nikko, and Kirsten Lauber. "Immune Checkpoint Inhibition and Radiotherapy in Head and Neck Squamous Cell Carcinoma: Synergisms and Resistance Mechanisms." In Critical Issues in Head and Neck Oncology, 11–21. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-23175-9_2.

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AbstractImmune checkpoint inhibition has emerged as an integral part of the standard-of-care for head and neck squamous cell carcinoma (HNSCC) in recurrent and/or metastatic stages. Clinical responses are impressive but remain limited to a minority of patients. Primary resistance of never-responders is considered to derive from host- and tumor-specific characteristics, the latter comprising tumor immune checkpoint activity, immune contexture, tumor mutational burden, neo-antigen load, and others. Secondary resistance of initially responding patients in addition, appears to be driven predominantly by irreversible T-cell exhaustion and therapy-induced selection of tumor cell clones with mutations in critical genes involved in the response to immune checkpoint inhibition. With particular focus on primary resistance against immune checkpoint inhibition, scientific interest of preclinical and clinical researchers currently aims at the development and evaluation of combined modality treatment approaches. Radiotherapy is a highly promising partner in this regard and represents a crucial treatment modality for patients with locally advanced HNSCC. Historically established as cytotoxic anti-cancer treatment, a growing body of evidence has shown additional locoregional and systemic immunomodulatory effects of radiotherapy. These are largely attributed to reprogramming of the tumor microenvironment driven by dying and senescent irradiated tumor and normal tissue cells and the concomitant cascade of danger signals, chemokines, and cytokines which stimulate immune cell recruitment and activation. Moreover, the irradiated state of tumor cells bears interesting analogy to the anti-viral state, since fragments of nuclear and mitochondrial DNA that are released into the cytosol can stimulate cytosolic nucleic acid sensors to produce intra-tumoral type I interferons which are essential to (re-)activate the cancer immunity cycle and (re-)invigorate systemic anti-tumor T-cell responses. Apart from these tumor adjuvanticity enhancing effects, several reports have also described increased tumor antigenicity upon radiotherapy originating from radiation-induced exposure of neo-antigens. Collectively, radiotherapy thus may serve as a means of personalized in situ vaccination which can synergize with immune checkpoint inhibition and may help to undermine primary resistance. First clinical experiences have shown that scheduling and dosing of such combined modality treatment regimens are challenging. Moreover, recent preclinical evidence suggests that particularly the role of radiation-induced cytokines and interferons appears to be complex in such combined modality settings due to their ambiguous effects on tumor and immune cells in the tumor microenvironment. The signaling cascades that orchestrate immune cell (re-)activation and cell fate decisions in irradiated tumor cells, including tumor cell survival, proliferation, and/or metastasis formation, are intimately interconnected and require further in-depth investigation.
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Nistal, Manuel, Pilar González-Peramato, and Álvaro Serrano. "Differential Diagnosis of Sertoli Cell Nodules." In Clues in the Diagnosis of Non-tumoral Testicular Pathology, 67–74. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49364-0_9.

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Villegas, Maria Rocio, Victoria Lopez, Verónica Rodríguez-García, Alejandro Baeza, and María Vallet-Regí. "Janus-Type Mesoporous for Sequential Tumoral Cell and Targeting." In Methods in Molecular Biology, 341–61. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1262-0_22.

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Nageswaran, Gayathri, Suzanne Byrne, Selvaraju Veeriah, and Benny Chain. "The Intra-Tumoral T Cell Receptor Repertoire: Steps Towards a Useful Clinical Biomarker." In Methods in Molecular Biology, 135–58. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2712-9_6.

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Escribano, Julio, M. José M. Díaz-Guerra, Hans H. Riese, Alberto Alvarez, Remedios Proenza, Damián Garcia-Olmo, Dolores C. Garcia-Olmo, Jesús Ontañón, and José Antonio Fernández. "A Glycoconjugate Isolated from the Saffron Plant (Crocus sativus L.) is Cytolytic Against Tumoral Cells and Activates Macrophages In Vitro." In Cell and Developmental Biology of Arabinogalactan-Proteins, 289–90. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4207-0_36.

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Ruiz-Llorente, Lidia, María Jesús Ruiz-Rodríguez, Claudia Savini, Teresa González-Muñoz, Erica Riveiro-Falkenbach, José L. Rodríguez-Peralto, Héctor Peinado, and Carmelo Bernabeu. "Correlation Between Endoglin and Malignant Phenotype in Human Melanoma Cells: Analysis of hsa-mir-214 and hsa-mir-370 in Cells and Their Extracellular Vesicles." In Advances in Experimental Medicine and Biology, 253–72. Cham: Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-26163-3_14.

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AbstractEndoglin (CD105) is an auxiliary receptor of transforming growth factor (TGF)-β family members that is expressed in human melanomas. It is heterogeneously expressed by primary and metastatic melanoma cells, and endoglin targeting as a therapeutic strategy for melanoma tumors is currently been explored. However, its involvement in tumor development and malignancy is not fully understood. Here, we find that endoglin expression correlates with malignancy of primary melanomas and cultured melanoma cell lines. Next, we have analyzed the effect of ectopic endoglin expression on two miRNAs (hsa-mir-214 and hsa-mir-370), both involved in melanoma tumor progression and endoglin regulation. We show that compared with control cells, overexpression of endoglin in the WM-164 melanoma cell line induces; (i) a significant increase of hsa-mir-214 levels in small extracellular vesicles (EVs) as well as an increased trend in cells; and (ii) significantly lower levels of hsa-mir-370 in the EVs fractions, whereas no significant differences were found in cells. As hsa-mir-214 and hsa-mir-370 are not just involved in melanoma tumor progression, but they can also target endoglin-expressing endothelial cells in the tumor vasculature, these results suggest a complex and differential regulatory mechanism involving the intracellular and extracellular signaling of hsa-mir-214 and hsa-mir-370 in melanoma development and progression.
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Hainfeld, J. F., and H. M. Smilowitz. "Gold Nanoparticles and Infrared Heating: Use of wIRA Irradiation." In Water-filtered Infrared A (wIRA) Irradiation, 117–27. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92880-3_9.

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AbstractwIRA-transparent small gold nanoparticles (AuNPs) were shown to be shifted to wIRA absorbing when targeted to receptors on tumor cells and aggregated in the tumor cell by enzyme degradation and pH effects. In this way, AuNPs loaded into mouse-grown subcutaneous tumors after both direct intratumoral and intravenous injections cured tumors after either wIRA treatment ablation or wIRA treatment combined with X-ray irradiation. Some GNP constructs, e.g., nanoshells and nanorods, have already progressed to veterinary and human clinical trials. If AuNP/NIR therapy is proven to be useful to treat an appropriately superficial human tumor, the use of the wIRA radiator might make such therapy accessible to large numbers of patients in low- and middle-income countries that lack access to very high-tech expensive therapies.
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Nadel, Helen, Barry Shulkin, Zvi Bar-Sever, and Francesco Giammarile. "Pediatric Malignancies." In A Practical Guide for Pediatric Nuclear Medicine, 199–231. Berlin, Heidelberg: Springer Berlin Heidelberg, 2023. http://dx.doi.org/10.1007/978-3-662-67631-8_12.

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AbstractThe most common childhood malignancy is leukemia (30%), followed by brain tumors (20%), lymphomas, both Hodgkin’s (HL) and non-Hodgkin’s lymphoma (NHL) (14%), neuroblastoma (7%), soft tissue sarcoma (7%), Wilms’ tumor (6%), bone tumors (5%), germ cell tumors (3%), melanoma (3%), and hepatic tumors (1%). Their incidence varies according to patient age. Less common pediatric malignancies include head and neck cancer, Langerhans cell histiocytosis (LCH), germ cell tumors, neurofibromatosis type 1 with suspected malignant transformation, adrenocortical carcinoma, gastrointestinal stromal tumor (GIST), hepatoblastoma, hepatocellular carcinoma, carcinoid, insulinoma, and pheochromocytoma (Steliarova-Foucher et al., Lancet Oncol 18(6):719–731, 2017; Institute, NC. https://nccrexplorer.ccdi.cancer.gov/). Neuroblastoma is the second most common solid tumor in young children. It is a NET derived from the primitive neural crest. Although currently MIBG is embedded and required by international therapy protocols for patients with neuroblastoma and has a large body of evidence proving its validity and usefulness, PET tracers such as FDOPA, FDG, and 68Ga-peptides are increasingly used in imaging of neuroblastoma (Pai Panandiker et al., Clin Nucl Med 40(9):737–739, 2015). Additional pediatric NETs include ganglioneuroma, bronchial carcinoid (most common primary malignant pulmonary tumor in children), abdominal carcinoid (rare), pheochromocytoma, and PPGL. Approximately 75% of juvenile nasopharyngeal carcinomas also express surface membrane SSTRs. FDG-PET/CT is the scintigraphic study of choice for the assessment of lymphoma and sarcoma.
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Müller, Sabina, Liza Filali, Marie-Pierre Puissegur, and Salvatore Valitutti. "Measuring CTL Lytic Granule Secretion and Target Cell Membrane Repair by Fluorescent Lipophilic Dye Uptake at the Lytic Synapse." In The Immune Synapse, 463–76. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3135-5_30.

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AbstractCD8+ cytotoxic T lymphocytes (CTL) play a key role in anti-tumor immune response. They are therefore at the heart of current immunotherapy protocols against cancer. Despite current strategies to potentiate CTL responses, cancer cells can resist CTL attack, thus limiting the efficacy of immunotherapies. To optimize immunotherapy, it is urgent to develop rapid assays allowing to assess CTL-cancer cell confrontation at the lytic synapse.In this chapter, we describe a flow cytometry-based method to simultaneously assess the extent of CTL activation and of tumor cell reparative membrane turnover in CTL/target cell conjugates. Such a method can be performed using a limited number of cells. It can therefore be employed in clinical settings when only a few patient-derived cells might be available.
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Kalil, Ricardo K. "Langerhans Cell Histiocytosis." In Tumors and Tumor-Like Lesions of Bone, 805–13. London: Springer London, 2015. http://dx.doi.org/10.1007/978-1-4471-6578-1_58.

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Conference papers on the topic "Tumoral cell"

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Mugnano, Martina, Zhe Wang, Vincenza Cerbone, Giulia Scalia, Annalaura Montella, Mario Capasso, Silvia Mari, et al. "Amnis Image Stream-Analysis of Tumor Cells." In Digital Holography and Three-Dimensional Imaging, W4A.22. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/dh.2024.w4a.22.

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Imaging flow cytometry is a cutting-edge technology for analyzing cell features. Here we show the advantage of using this system to study cell nucleus of tumor cells, using ovarian cancer A2780 cell line as model. Amnis Image stream it has been used as a standard comparison tool respect to quantitative phase imaging to study cell features.
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Andreu, David, Beatriz G. de la Torre, and Gandhi Rádis-Baptista. "NrTP, a cell penetrating peptide exquisitely targeting the nucleolus of tumoral cells." In XIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2009. http://dx.doi.org/10.1135/css200911001.

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Ugele, I., K. Singer, L. Symeou, M. Wehrstein, M. Kapsreiter, C. Bohr, and M. Kreutz. "Intra-tumoral immune cell composition is not heterogeneous in HNSCC." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686085.

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Kammer, M. N., S. Zhao, H. Mori, Y. Zou, S. Deppen, M. E. Lenburg, E. Grogan, A. Borowsky, and F. Maldonado. "Tumoral Genetic Mutations Correlated With Mast Cell Infiltration in Early-stage Lung Adenocarcinoma." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6606.

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Diamant, Gil, Hadar Simchony, Tamar Shiloach, Anat Globerson-levin, Zelig Eshhar, Rachel Grossman, Zvi Ram, and Ilan Volovitz. "Abstract 621: Evaluating the compatibility of tumor treating electric fields with key anti-tumoral T cell functions." 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.am2018-621.

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Silverman, Deborah A., Emily Ashkin, Benjamin Whitfield, Simone Punt, Soraya Zorro Manrique, Yunfei Wang, Anil Korkut, et al. "Abstract 2372: Tumoral p53 mutations differentially mediate poor T-cell infiltration and autologous T-cell killing in preclinical 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.sabcs18-2372.

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Silverman, Deborah A., Emily Ashkin, Benjamin Whitfield, Simone Punt, Soraya Zorro Manrique, Yunfei Wang, Anil Korkut, et al. "Abstract 2372: Tumoral p53 mutations differentially mediate poor T-cell infiltration and autologous T-cell killing in preclinical 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.am2019-2372.

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Leblanc, Raphael, Sue-Chin Lee, Dereck Norman, Johnny Ribeiro, Gabor Tigyi, and Olivier Peyruchaud. "Abstract 5209: Non-tumoral autotaxin stored into platelet α-granules promotes breast cancer cell metastasis." 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.am2015-5209.

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Antonio, Eduardo C., Marcelo A. Bragatte, and Gustavo F. Vieira. "Abstract 3381: Investigating the structural aspects that confer differential immunogenicity in tumoral T cell epitopes." 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.am2019-3381.

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Antonio, Eduardo C., Marcelo A. Bragatte, and Gustavo F. Vieira. "Abstract 3381: Investigating the structural aspects that confer differential immunogenicity in tumoral T cell epitopes." 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.sabcs18-3381.

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Reports on the topic "Tumoral cell"

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Brooks, James D. Single Cell Characterization of Prostate Cancer-Circulating Tumor Cells. Fort Belvoir, VA: Defense Technical Information Center, September 2013. http://dx.doi.org/10.21236/ada596639.

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Brooks, James B. Single Cell Characterization of Prostate Cancer Circulating Tumor Cells. Fort Belvoir, VA: Defense Technical Information Center, August 2011. http://dx.doi.org/10.21236/ada550987.

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Condeelis, John. Isolation of Motile Tumor Cells From Live Breast Tumors. Fort Belvoir, VA: Defense Technical Information Center, June 2001. http://dx.doi.org/10.21236/ada395259.

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Condeelis, John. Isolation of Motile Tumor Cells from Live Breast Tumors. Fort Belvoir, VA: Defense Technical Information Center, June 2002. http://dx.doi.org/10.21236/ada412991.

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Tran, Emily, Jasmine J. Park, Nandini N. Kulkarni, and Vinay S. Gundlapalli. Left Facial Primary Leiomyosarcoma Misdiagnosed as Atypical Fibroxanthoma and Immunochemical Markers Relevant to Diagnosis: A Case Report. Science Repository, February 2024. http://dx.doi.org/10.31487/j.ajscr.2023.04.03.

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Soft tissue sarcomas are relatively rare neoplasms of mesenchymal origin that generally make up less than 2% of all adult malignant neoplasms. Atypical fibroxanthoma is a benign soft tissue tumor often confused with malignant variants of similar tumors such as leiomyosarcoma due to similar staining markers and cell morphology. We report a case of a 70-year-old caucasian male who initially presented with a 2 cm exophytic left facial lesion that was misdiagnosed as atypical fibroxanthoma upon biopsy. The patient underwent a wide local excision of the growing 11 cm mass and immediate reconstruction with a cervicofacial flap and full thickness skin graft. Pathological analysis of the specimen revealed the final diagnosis as confirmed primary leiomyosarcoma. Both the patient’s biopsy report and the surgical pathology report revealed similar negative findings (desmin, cytokeratin AE1/AE3, p63, SOX10) as well as similar positive findings (smooth muscle actin and CD68). Critical distinctions that led to a change in diagnosis from atypical fibroxanthoma to leiomyosarcoma emerged during the final pathological analysis, which revealed more widespread positive staining for smooth muscle actin and muscle-specific actin throughout the surgical specimen along with detailed cell and nucleus morphology of atypical spindle cells in the dermis and subcutis. This valuable information was not available during the initial biopsy when the lesion was smaller. It is possible that earlier diagnosis of primary leiomyosarcoma could have resulted in advanced pre-operative treatment and excision of the facial lesion, preventing involvement of surrounding areas such as the patient’s left eye, ear, and facial nerve.
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Baldwin, Albert S. Promotion of Tumor-Initiating Cells in Primary and Recurrent Breast Tumors. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada613713.

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Baldwin, Albert S. Promotion of Tumor-Initiating Cells in Primary and Recurrent Breast Tumors. Fort Belvoir, VA: Defense Technical Information Center, July 2013. http://dx.doi.org/10.21236/ada596410.

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Furbert-Harris, Paulette. Growth Inhibition of Breast Tumor Cells by Hypodense and Normodense Eosinophilic Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada394003.

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Furbert-Harris, Paulette M. Growth Inhibition of Breast Tumor Cells by Hypodense and Normodense Eosinophilic Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada383068.

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Pacheco-Ojeda, Luis, Carolina Sáenz-Gómez, Stalin Cañizares-Quisiguiña, Tatiana Borja-Herrera, Juan Carlos Vallejo-Garzón, and Sergio Poveda. Function Sparing Conservative Approach of a Low-Grade Chondrosarcoma of the Larynx: Case Report and Literature Review. Science Repository, March 2024. http://dx.doi.org/10.31487/j.scr.2024.01.04.

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Background: Laryngeal cancer is relatively uncommon in Ecuador. Usually epithelial in origin, the most frequent histological type is squamous cell carcinoma. The most common mesenchymal tumor is chondrosarcoma. Most laryngeal chondrosarcomas are treated with total laryngectomy, but a conservative function sparing resection is recommended in low-grade limited tumors. Case Report: In a 68-year-old female nonsmoker patient, a small tumor was found in the posterior left aspect of the cricoid cartilage in a computed tomography (CT) performed immediately after an unexpected difficulty to pass the endotracheal tube for a thoracoscopic biopsy of 4 cm tumor of the left lung, in another hospital. The patient underwent, then, an initial tracheostomy, a total thyroidectomy for a goiter and a biopsy of the tumor of the cricoid cartilage whose pathological study was inconclusive. One month later, a low-grade neuroendocrine pulmonary tumor was completed resected. Two years later, a CT scan showed the cricoid lesion with the same characteristics. At endoscopic video laryngoscopy, two subglottic masses that narrowed the airway in approximately 60% of the normal caliber, were observed located at the posterior and left walls. An intraluminal resection was performed through a transcricoid anterior approach. The pathological diagnosis was a low-grade chondrosarcoma. Tracheal decannulation was performed one month later. At an endoscopic video laryngoscopy performed six months post-operatively, the tracheal caliber and mucosa were normal. The patient remained with normal voice and breathing. Conclusion: We report the second case of chondrosarcoma of the larynx in our country, treated by a conservative approach.
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