Littérature scientifique sur le sujet « IMMUNOESCAPE »
Créez une référence correcte selon les styles APA, MLA, Chicago, Harvard et plusieurs autres
Consultez les listes thématiques d’articles de revues, de livres, de thèses, de rapports de conférences et d’autres sources académiques sur le sujet « IMMUNOESCAPE ».
À côté de chaque source dans la liste de références il y a un bouton « Ajouter à la bibliographie ». Cliquez sur ce bouton, et nous générerons automatiquement la référence bibliographique pour la source choisie selon votre style de citation préféré : APA, MLA, Harvard, Vancouver, Chicago, etc.
Vous pouvez aussi télécharger le texte intégral de la publication scolaire au format pdf et consulter son résumé en ligne lorsque ces informations sont inclues dans les métadonnées.
Articles de revues sur le sujet "IMMUNOESCAPE"
Concha-Benavente, Fernando, Raghvendra M. Srivastava, Soldano Ferrone et Robert L. Ferris. « EGFR-mediated tumor immunoescape ». OncoImmunology 2, no 12 (décembre 2013) : e27215. http://dx.doi.org/10.4161/onci.27215.
Texte intégralQUESNEL, BRUNO. « Tumor dormancy and immunoescape ». APMIS 116, no 7-8 (juillet 2008) : 685–94. http://dx.doi.org/10.1111/j.1600-0463.2008.01163.x.
Texte intégralMazzolini, Guillermo. « Immunotherapy and immunoescape in colorectal cancer ». World Journal of Gastroenterology 13, no 44 (2007) : 5822. http://dx.doi.org/10.3748/wjg.v13.i44.5822.
Texte intégralVan hede, Dorien, Inge Langers, Philippe Delvenne et Nathalie Jacobs. « Origin and immunoescape of uterine cervical cancer ». La Presse Médicale 43, no 12 (décembre 2014) : e413-e421. http://dx.doi.org/10.1016/j.lpm.2014.09.005.
Texte intégralSauleda, Jaume, Francisco Javier Verdú, Sergio Scrimini, Ernest Sala et Jaume Pons. « Immunoescape the link between emphysema and lung cancer ? » Journal of Thoracic Disease 11, S3 (mars 2019) : S329—S330. http://dx.doi.org/10.21037/jtd.2018.12.133.
Texte intégralTakasu, Chie, Shoko Yamashita, Yuji Morine, Kozo Yoshikawa, Takuya Tokunaga, Masaaki Nishi, Hideya Kashihara, Toshiaki Yoshimoto et Mitsuo Shimada. « The role of the immunoescape in colorectal cancer liver metastasis ». PLOS ONE 16, no 11 (19 novembre 2021) : e0259940. http://dx.doi.org/10.1371/journal.pone.0259940.
Texte intégraldeCampos-Lima, Pedro-Otavio, Jelena Levitskaya, Teresa Frisan et Maria G. Masucci. « Strategies of immunoescape in Epstein-Barr virus persistence and pathogenesis ». Seminars in Virology 7, no 1 (février 1996) : 75–82. http://dx.doi.org/10.1006/smvy.1996.0009.
Texte intégralYaguchi, Tomonori, Hidetoshi Sumimoto, Chie Kudo-Saito, Nobuo Tsukamoto, Ryo Ueda, Tomoko Iwata-Kajihara, Hiroshi Nishio, Naoshi Kawamura et Yutaka Kawakami. « The mechanisms of cancer immunoescape and development of overcoming strategies ». International Journal of Hematology 93, no 3 (mars 2011) : 294–300. http://dx.doi.org/10.1007/s12185-011-0799-6.
Texte intégralGhiringhelli, François, Mélanie Bruchard, Fanny Chalmin et Cédric Rébé. « Production of Adenosine by Ectonucleotidases : A Key Factor in Tumor Immunoescape ». Journal of Biomedicine and Biotechnology 2012 (2012) : 1–9. http://dx.doi.org/10.1155/2012/473712.
Texte intégralWu, Lei, Yanquan Xu, Huakan Zhao, Yu Zhou, Yu Chen, Shuai Yang, Juan Lei et al. « FcγRIIB potentiates differentiation of myeloid-derived suppressor cells to mediate tumor immunoescape ». Theranostics 12, no 2 (2022) : 842–58. http://dx.doi.org/10.7150/thno.66575.
Texte intégralThèses sur le sujet "IMMUNOESCAPE"
Alves, Inês Sofia Moutinho. « Contribution of ER stress to tumor immunosuppressive microenvironment ». Master's thesis, Universidade de Aveiro, 2014. http://hdl.handle.net/10773/14290.
Texte intégralBreast cancer is the most prevalent cancer among women and also one of the oncologic pathologies that causes more deaths. In the last decades several studies have reported that solid tumors generate an immunosuppressive microenvironment. This microenvironment (acidosis, hypoxia, glucose deprivation and cytokines) is favourable to endoplasmic reticulum (ER) stress induction. ER stress is primarily a response towards the re-establishment of homeostasis; however if not resolved it usually results in cell death by apoptosis. Nevertheless, ER stress and unfolded protein response (UPR) play a paradoxical role in cancer physiopathology: the three branches of UPR, PERK, IRE1 and ATF6 actively contribute to signalling of survival and metastasis mechanisms. Recently it was reported a possible transmission of ER stress from tumor cells to immune cells, modulating the phenotype and function of recipient cells. Thus, the aim of the present work is to assess the ability and the respective mechanisms by which T-47D tumor cells transmit ER stress to THP-1 monocytes, and the consequences of this transmission. ER stress transmission was only observed when pharmacological ER stress inducers were used, such as tunicamycin, contrarily to physiological stimulation, as glucose deprivation. Additionally, it was found that tunicamycin seems to be transported within exosomes which, in turn, directly induces ER stress on monocytes. It was also observed that exosomes derived from glucose deprived T-47D cells do not transmit ER stress; however these exosomes conduct monocytes towards a particular proinflammatory profile, accompanied by the decrease of its maturation status. Overall, our results question the ER stress mechanism originally described, showing that pharmacological ER stress inducers can be transported within exosomes and directly inducing ER stress on recipient cells.
O cancro da mama é o cancro de maior incidência entre as mulheres, sendo também uma das situações oncológicas que mais mortes causa. Na última década inúmeros estudos têm demonstrado que os tumores sólidos geram um microambiente favorável à evasão/subversão do sistema imune. Esse microambiente (acidose, hipoxia, deprivação de glucose, citoquinas) é muita das vezes propicio à indução de stress do reticulo endoplasmático (RE). O stress do RE é primariamente uma resposta no sentido de restabelecer a homeostasia no entanto se não resolvido resulta normalmente na morte celular por apoptose. O stress do RE e a respetiva resposta às proteínas mal conformadas (UPR), desempenham um papel paradoxal na fisiopatologia do cancro: os três ramos da UPR, PERK, IRE1 e ATF6, contribuem ativamente para a sinalização de alguns mecanismos de sobrevivência e metastização. Recentemente, foi descrita uma possível transmissão do stress do RE das células tumorais para as células do sistema imunitário, modulando a ação destas. Desta forma, pretendeu avaliar-se com o presente trabalho a capacidade e os mecanismos pelos quais células tumorais T-47D transmitem o stress do RE para células monocíticas THP-1, e quais as consequências desta transmissão. A transmissão foi apenas observada aquando da utilização de indutores farmacológicos como a tunicamicina, não se registando para estímulos fisiológicos como a deprivação de glucose. Por outro lado, verificou-se que a tunicamicina parece ser transportada via exossomas e desta forma induzir diretamente stress do RE nos monócitos. Observou-se ainda que os exossomas provenientes das células T-47D em stress do RE por deprivação de glucose apesar de não transmitirem o referido stress conduzem os monócitos para um perfil pró-inflamatório específico diminuindo ainda a sua capacidade de maturação. Em geral, os nossos resultados questionam seriamente o mecanismo de transmissão de stress ER tal como originalmente descrito, mostrando que no uso de indutores farmacológicos o que parece ocorrer é o transporte do fármaco em vesículas e a indução direta nas células recetoras.
MAZZOCCO, Marta. « CONTROL OF CANCER IMMUNOEDITING BY AUTOLOGOUS CELLULAR VACCINE AND EFFICACY ASSESSMENT OF IFN-alpha-ENGINEERED MESENCHYMAL STROMAL CELLS (MSCs) IN A MOUSE PLASMACYTOMA MODEL ». Doctoral thesis, 2011. http://hdl.handle.net/11562/349009.
Texte intégralIn the mouse Balb/c-derived myeloma model represented by the Sp6 hybridoma, de novo expression of the B7-1 costimulatory molecule obtained by transfection of the relative cDNA (Sp6/B7 transfectants) inhibits tumor growth in vivo and activates a memory immune response mediated by cytotoxic T lymphocytes (CTLs), protective against wild type (WT) Sp6. In the Balb/c genetic background, the MHC-I H-2 Ld molecule is the restriction element presenting the immunodominant epitopes of the two most common mouse tumor associated antigens: P1A and gp70. WT Sp6 and Sp6/B7 show a downregulated cell surface expression of H-2 Ld, still maintaining normal expression levels of H-2 Kd and Dd. Sp6 cells are lysed in vitro by gp70-Ld-restricted CTLs (not by P1A-Ld-restricted), indicating that they are able to present gp70 epitopes in spite of the low Ld expression. Increase of H-2 Ld expression in WT Sp6 and Sp6/B7 by transfection of the relative cDNA (Sp6/Ld and Sp6/B7/Ld transfectants) drives the immune response towards H-2 Ld-restricted antigens, whilst the H-2 Ld-downregulated state of WT Sp6 and Sp6/B7 determines a shift of the immune response towards subdominant antigens presented by H-2 Kd. Nevertheless, the immune response elicited by in vivo immunization with the autologous B7-1 positive cellular vaccine, either Sp6/B7 or Sp6/B7/Ld, is never gp70-specific. Analysis of gp70 expression in peripheral lymphoid organs showed the presence of gp70 specific transcripts in both spleen and lymph nodes of animals immunized with Sp6/B7 and Sp6/B7/Ld, absent in naïve animals. Electron mycroscope analysis of WT Sp6 and transfectants showed the presence of virus-like particles in both cytoplasma and exocytosis vesicles. We may hypothesize that, during immunization phase, a CTL-dependent lysis of Sp6/B7 and/or Sp6/B7/Ld cells migrated to the draining lymph nodes results in the release of a high number of virions, rapidly infecting the whole resident B cell population. The subsequent presentation of the immunodominant viral antigen epitopes by a large number of infected B cells can generate an activation-induced cell death of high affinity TCR-T cells, leading to clonal deletion of gp70-specific CD8+ T cells. In conclusion, Sp6 tumor appears to carry out two immunoescape mechanisms: 1) induction of peripheral tolerance against the gp70 immunodominant antigen; 2) H-2 Ld downregulation, to escape the tumor-specific immune response against the Ld-restricted epitopes of previously subdominant antigens, that the established gp70-peripheral tolerance has eventually made dominant. Our data show that, when tumors adopt these immunoescape mechanisms, autologous whole tumor cell vaccines still remain a potent tool for generating anti-tumor immunity, because they allow to rescue and amplify the protective immune responses against subdominant tumor antigens. Then, we have analyzed the therapeutic potential of mesenchymal stromal cells (MSCs) as cellular vehicle for intra-tumoral delivery of active molecules. Bone marrow derived MSCs (BM-MSCs) may survive and proliferate in the presence of cycling neoplastic cells. Exogenously administered MSCs are actively incorporated in the tumor as stromal fibroblasts, thus competing with the local mesenchymal cell precursors. For this reason, MSCs have been suggested as a suitable carrier for gene therapy strategies, as they can be engineered with genes encoding for biologically active molecules, which can inhibit tumor cell proliferation and enhance the anti-tumor immune response. We used BM-MSCs engineered with the murine interferon-alpha (IFN-a) gene (BM-MSCs/IFN-a) to assess in the mouse myeloma model represented by Sp6 the efficacy of this approach towards neoplastic plasma cells. We found that IFN-a can be efficiently produced and delivered inside the tumor microenvironment. Subcutaneous multiple administration of BM-MSCs/IFN-a significantly hampered the tumor growth in vivo and prolonged the overall survival of mice. The anti-tumor effect was associated with enhanced apoptosis of tumor cells, reduction in microvessel density, and ischemic necrosis. By contrast, intravenous administration of BM-MSCs/IFN-a did not significantly modify the survival of mice, mainly as a consequence of an excessive entrapment of injected cells in the pulmonary vessels. In conclusion, BM-MSCs/IFN-a are effective in inhibiting neoplastic plasma cell growth; however, systemic administration of engineered MSCs still needs to be improved to make this approach potentially suitable for the treatment of multiple myeloma.
Actes de conférences sur le sujet "IMMUNOESCAPE"
Zhang, Yanyan, Shuyi Zhu, Peipei Qian, Xiumei Wang, Zhi Xu, Wenbo Sun et Yong Xu. « Abstract 2791 : RelB upregulates PD-L1 in advanced prostate cancer : An insight into tumor immunoescape ». Dans 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.sabcs18-2791.
Texte intégralZhang, Yanyan, Shuyi Zhu, Peipei Qian, Xiumei Wang, Zhi Xu, Wenbo Sun et Yong Xu. « Abstract 2791 : RelB upregulates PD-L1 in advanced prostate cancer : An insight into tumor immunoescape ». Dans 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.am2019-2791.
Texte intégralRapports d'organisations sur le sujet "IMMUNOESCAPE"
Barber, Glen. Identifying a Defective Pathway in Innate Immunity as an Immunoescape Mechanism for Breast Cancer Development. Fort Belvoir, VA : Defense Technical Information Center, avril 2012. http://dx.doi.org/10.21236/ada566916.
Texte intégral