Relevant bibliographies by topics / Escape mechanisms

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Escape mechanisms'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 February 2022

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Journal articles on the topic "Escape mechanisms"

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&NA;. "Mechanisms of Escape." Journal of Immunotherapy 26, no. 6 (2003): S43—S45. http://dx.doi.org/10.1097/00002371-200311000-00015.

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Wildes, Tyler, Kyle Dyson, Connor Francis, et al. "IMMU-13. MECHANISMS OF IMMUNOLOGICAL ESCAPE DURING ADOPTIVE CELLULAR THERAPY IN HIGH GRADE GLIOMA." Neuro-Oncology 21, Supplement_6 (2019): vi121—vi122. http://dx.doi.org/10.1093/neuonc/noz175.507.

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Abstract INTRODUCTION Immunotherapy is remarkably effective, yet tumor escape is common. Herein, we investigated tumor escape after adoptive cellular therapy (ACT) in intractable glioma models. These studies revealed multiple mechanisms of escape including a shift in immunogenic tumor antigens, downregulation of MHC-I, and upregulation of checkpoint molecules. Despite these changes, we HYPOTHESIZED that a new population of escape variant-specific polyclonal T cells could be generated to target immune-escaped tumors through using tumor escape variant RNA. METHODS We studied KR158B-luc glioma-bearing mice during treatment with ACT with polyclonal tumor-specific T cells. We tested the immunogenicity of primary and escaped tumors using T cell restimulation assays. We used flow cytometry and RNA profiling of whole tumors to further define escape mechanisms. To treat immune-escaped tumors, we generated escape variant-specific T cells through the use of escape variant total tumor RNA and administered these cells as ACT. RESULTS Escape mechanisms included a shift in immunogenic tumor antigens, downregulation of major histocompatibility complex (MHC) class I by 50%, and upregulation of checkpoint molecules. This included activated T cells and NK cells from tumor-draining lymph nodes expressing 50% and 30% PD-1 after ACT. Importantly, polyclonal T cells specific for escape variants displayed greater recognition of escaped tumors than primary tumors. When administered as ACT, these T cells prolonged median survival of escape variant-bearing mice by 60% (24 to 33 days, p=.0003). The rational combination of ACT with PD-1 blockade prolonged median survival of escape variant glioma-bearing mice by 110% and was dependent upon NK cells and T cells as determined by cell depletion experiments. To prevent escape from primary tumors, we combined ACT with PD-1 blockade to yield 71% long-term cures in KR158B-luc-bearing mice. CONCLUSIONS These findings suggest that the immune landscape of brain tumors is markedly different post-immunotherapy yet can still be targeted with immunotherapy.
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Oudejans, J. J. "Immune escape mechanisms in ALCL." Journal of Clinical Pathology 56, >6 (2003): 423–25. http://dx.doi.org/10.1136/jcp.56.6.423.

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Moore, T. E., and G. V. Khazanov. "Mechanisms of ionospheric mass escape." Journal of Geophysical Research: Space Physics 115, A12 (2010): n/a. http://dx.doi.org/10.1029/2009ja014905.

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Chan, Wing C. "Immune escape mechanisms for TCRLBCL." Blood 137, no. 10 (2021): 1274–76. http://dx.doi.org/10.1182/blood.2020008766.

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Hara, Hiroyuki. "Mechanisms of Immune Escape in Cancer." Journal of Nihon University Medical Association 75, no. 4 (2016): 152–55. http://dx.doi.org/10.4264/numa.75.4_152.

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Capone, Emily, Pramudita R. Prasetyanti, and Gianluca Sala. "HER-3: hub for escape mechanisms." Aging 7, no. 11 (2015): 899–900. http://dx.doi.org/10.18632/aging.100850.

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Niederkorn, Jerry Y. "Immune escape mechanisms of intraocular tumors." Progress in Retinal and Eye Research 28, no. 5 (2009): 329–47. http://dx.doi.org/10.1016/j.preteyeres.2009.06.002.

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Bröcker, E. B., W. Dummer, and J. C. Becker. "Immune escape mechanisms in human melanoma." Melanoma Research 4, no. 2 (1994): 25. http://dx.doi.org/10.1097/00008390-199409001-00039.

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Poppema, S., M. Potters, L. Visser, and A. M. van den Berg. "Immune escape mechanisms in Hodgkin’s disease." Annals of Oncology 9 (1998): s21—s24. http://dx.doi.org/10.1093/annonc/9.suppl_5.s21.

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Dissertations / Theses on the topic "Escape mechanisms"

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Lawrie, Alastair. "Mechanisms of immune escape by B-cell lymphoma." Thesis, University of Aberdeen, 2016. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=231642.

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Many cancers, including lymphoma, are associated with increased numbers of T cells with suppressive properties, and it has been suggested that immune subversion is important in cancer pathogenesis. The ability of lymphoma cells to induce conventional CD25- T cells to adopt a regulatory phenotype was evaluated, with the aim of elucidating the factors and pathways governing this process and determining the clinical relevance. Regulatory T cell phenotype in both peripheral blood and nodal material from patients with lymphoma and healthy controls was also assessed. Preferential representation of Tregs in nodal tissue was noted with higher percentages seen than in peripheral blood. Contrary to previous studies, minimal evidence to suggest that lymphoma induces a regulatory phenotype from CD4+CD25- T cells was found. Furthermore, nodal Tregs displayed high expression of Helios and FOXP3, indicating a thymically-derived rather than induced origin. PD-1 expressing T cells were present in greater numbers in PBMCs from patients compared with healthy controls, suggesting an alternative reason for the immunosuppression that may be exhibited in these patients. These data support recruitment and amplification as the mechanism for the high proportion of Tregs seen in lymphoma. Hodgkin lymphoma is typified by a prominent reactive infiltrate and is the archetype of immune subversion in lymphoma. Inherited predisposition is demonstrated through familial and twin studies. Susceptibility loci have been identified in a number of genes that affect immune response, with the strongest association seen with the HLA region. 5 individuals with classical Hodgkin lymphoma from a family originating in North East Scotland were evaluated by linkage analysis and exome sequencing. Novel, shared variants predicted to disrupt protein function were identified in 2 genes on chromosome 3. Proximity to a previously described gene in familial Hodgkin lymphoma implicates this region as an important susceptibility locus.
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Rieder, Martina. "Mechanisms of rabies virus to escape the IFN system." Diss., Ludwig-Maximilians-Universität München, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-160211.

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Norell, Håkan. "Immunological recognition and tumor escape mechanisms of ovarian carcinoma /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-830-4/.

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Malmberg, Karl-Johan. "Mechanisms of immune escape : implications for immunotherapy against cancer /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-436-4/.

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Patel, Shalin S. "Lymphocytic Infiltration and Immune Escape Mechanisms in Human Chordoma." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:15821593.

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Recent advances in immunotherapy for cancer have led to increasing interest in the role of the immune system in the pathogenesis and treatment of various tumors. Tumor-infiltrating lymphocytes have been associated with more favorable prognoses in a number of malignancies, though the mechanism of such outcomes remains unclear. This study, to our knowledge, is the first to describe lymphocytic infiltration in chordoma. Slides from 62 patients with chordoma were evaluated for lymphocyte infiltrates. Lymphocytic infiltration was found in 84% of tumors. Twenty-four tumors were selected for immunohistochemical (IHC) analysis. All of the tumors with lymphocytic infiltration that underwent IHC staining had CD4-positive lymphocytes present. CD8-positive lymphocytes were noted in 52% of tumors. HLA class I antigen defects were noted in 79% of chordoma tumors. These included negative membranous and/or cytoplasmic staining patterns, weakly positive staining, and heterogeneous combinations of these defects. Both heavy chain isoforms and beta-2-microglobulin components were affected. Our novel finding of intratumoral lymphocytes in chordoma tumors suggests that a patient’s immune system mounts a response against their tumor. The absence of HLA class I antigen components is compatible with the possibility that a patient’s immune response imposes selective pressure that facilitates the outgrowth of chordoma cell subpopulations that have developed escape mechanisms from host immune recognition. While the clinical significance requires further evaluation, these data have implications in optimally selecting patients for appropriate treatment regimens. We believe these data will spark further inquiry into the role of immunotherapy in the treatment of chordoma and other bone tumors.
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Shen, Lijun, and 沈立軍. "Immune escape mechanisms in EBV-associated nasal NK/T-Cell lymphoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31244713.

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Christiansson, Lisa. "Myeloid-Derived Suppressor Cells and Other Immune Escape Mechanisms in Chronic Leukemia." Doctoral thesis, Uppsala universitet, Klinisk immunologi, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-197604.

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Chronic myeloid leukemia (CML) is characterized by the Philadelphia chromosome, a minute chromosome that leads to the creation of the fusion gene BCR/ABL and the transcription of the fusion protein BCR/ABL in transformed cells. The constitutively active tyrosine kinase BCR/ABL confers enhanced proliferation and survival on leukemic cells. CML has in only a few decades gone from being a disease with very bad prognosis to being a disease that can be effectively treated with oral tyrosine kinase inhibitors (TKIs). TKIs are drugs inhibiting BCR/ABL as well as other tyrosine kinases. In this thesis, the focus has been on the immune system of CML patients, on immune escape mechanisms present in untreated patients and on how these are affected by TKI therapy. We have found that newly diagnosed, untreated CML patients exert different kinds of immune escape mechanisms. Patients belonging to the Sokal high-risk group had higher levels of myeloid-derived suppressor cells (MDSCs) as well as high levels of the programmed death receptor 1 (PD-1)-expressing cytotoxic T cells compared to control subjects. Moreover, CML patients had higher levels of myeloid cells expressing the ligand for PD-1, PD-L1. CML patients as well as patients with B cell malignacies had high levels of soluble CD25 in blood plasma. In B cell malignacies, sCD25 was found to be released from T regulatory cells (Tregs). Treatment with the TKIs imatinib or dasatinib decreased the levels of MDSCs in peripheral blood. Tregs on the other hand increased during TKI therapy. The immunostimulatory molecule CD40 as well as NK cells increased during therapy, indicating an immunostimulatory effect of TKIs. When evaluating immune responses, multiplex techniques for quantification of proteins such as cytokines and chemokines are becoming increasingly popular. With these techniques a lot of information can be gained from a small sample volume and complex networks can be more easily studied than when using for example the singleplex ELISA. When comparing different multiplex platforms we found that the absolute protein concentration measured by one platform rarely correlated with the absolute concentration measured by another platform. However, relative quantification was better correlated.
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Domogalla, Matthias Philipp [Verfasser]. "Nanocapsule-based vaccination for inhibition of tumor escape mechanisms / Matthias Philipp Domogalla." Mainz : Universitätsbibliothek Mainz, 2018. http://d-nb.info/1155549112/34.

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Frisan, Teresa. "Mechanisms of immune escape in EBV associated malignancies : Hodgkin's disease and Burkitt's lymphoma /." Stockholm : Karolinska institutet, 1999. http://diss.kib.ki.se/1999/91-628-3660-9/.

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Patton, John Thomas Jr. "Identifying and Targeting Immune Escape Mechanisms in Epstein-Barr Virus-Driven Lymphoproliferative Disease." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1461074032.

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Books on the topic "Escape mechanisms"

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Backert, Steffen, ed. Molecular Mechanisms of Inflammation: Induction, Resolution and Escape by Helicobacter pylori. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15138-6.

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Lanteigne, Marc. Catch comparison of lobster traps equipped with two types of escape mechanisms. Gulf Fisheries Centre, 1995.

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Goldblatt, Roy. Payment is extracted: Mechanisms of escape into America in immigrant and post-immigrant Jewish American fiction. University of Joensuu, 2002.

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C, Ochoa Augusto, ed. Mechanisms of tumor escape from the immune response. Taylor & Francis, 2003.

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Backert, Steffen. Molecular Mechanisms of Inflammation: Induction, Resolution and Escape by Helicobacter pylori. Springer, 2019.

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Ochoa, A. Mechanisms of Tumor Escape from the Immune Response (Tumor Immunology and Immunotherapyseries, 1). CRC, 2002.

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Luis, Roniger. Escape, Deportation, and Exile. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190693961.003.0002.

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This chapter traces how exile became an institutionalized mechanism of exclusion and underscores the paradoxical connection between citizenship and exclusionary modernity in the region. It stresses how these countries experienced policies of massive deterritorialization of citizens to counteract a widened involvement in public arenas and politics, and that the very drive of modernization generated new social forces, which these political systems were unable to include through democratic institutionalization. It discusses the cases of Paraguay, with its cycles of authoritarian rule and political turmoil generating massive exile and expatriation; Argentina and its recurrent waves of territorial displacements; Uruguay and the mass expatriation and exile of its citizens in the authoritarian period; and post-1973 Chile, also with massive exile and global dispersion.
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LaRoche, Cheryl Janifer. Introduction. University of Illinois Press, 2017. http://dx.doi.org/10.5406/illinois/9780252038044.003.0001.

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This book explores the free Black communities in Illinois, Indiana, and Ohio and their associations with the Underground Railroad. Focusing on the Black settlements in Rocky Fork and Miller Grove in Illinois, Lick Creek in Indiana, and Poke Patch in Ohio, it considers how the Underground Railroad movement secretly operated in conjunction with free Blacks and their historic Black churches. The book uses vital elements of what it calls the “geography of resistance” to examine the mechanisms of escape from slavery from an alternative perspective. By drawing on geography in combination with archaeology, community and church histories, and traditional Underground Railroad stories, the book makes visible unrecognized parallel connections between free Black communities and larger better-known abolitionist centers.
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Piehler, Timothy F. Coercion and Contagion in Child and Adolescent Peer Relationships. Edited by Thomas J. Dishion and James Snyder. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199324552.013.11.

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Peer relationships during adolescence play a powerful role in youth adjustment. This chapter summarizes research regarding two distinct yet related social processes that have been observed within adolescent peer interactions to be predictive of problem behaviors: coercion and contagion. The mechanisms underlying these two processes are outlined, including positive reinforcement involved in deviancy training (a form of contagion) as well as escape conditioning involved in coercion. The chapter details some of the commonalities between the two processes as seen in adolescence as well as key differences and risk factors unique to each. Several recent studies that simultaneously examined both coercion and contagion in peer interactions are highlighted. Finally, a number of future directions are outlined, including advancing analytic methods to better understand bidirectional effects and further investigating the role of these processes in internalizing symptoms in adolescence.
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Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.

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AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.
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Book chapters on the topic "Escape mechanisms"

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Capron, M., O. Duvaux-Miret, and A. Capron. "Escape Mechanisms in Schistosomiasis." In Progress in Immunology Vol. VIII. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_87.

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Kemp, W. M. "Parasite Immune Escape Mechanisms." In Parasitic and Related Diseases. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5027-9_3.

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Pawelec, Graham. "Escape Mechanisms in Tumour Immunity." In Cancer Immunology. Springer Netherlands, 2001. http://dx.doi.org/10.1007/978-94-017-0963-7_13.

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Visser, Lydia, Anke van den Berg, Sibrand Poppema, and Arjan Diepstra. "Microenvironment, Crosstalk, and Immune Escape Mechanisms." In Hodgkin Lymphoma. Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-12505-3_4.

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Visser, Lydia, Anke van den Berg, Sibrand Poppema, and Arjan Diepstra. "Microenvironment, Cross-Talk, and Immune Escape Mechanisms." In Hodgkin Lymphoma. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12780-9_4.

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Visser, Lydia, Johanna Veldman, Sibrand Poppema, Anke van den Berg, and Arjan Diepstra. "Microenvironment, Cross-Talk, and Immune Escape Mechanisms." In Hodgkin Lymphoma. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-32482-7_4.

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Lambert, P. H., J. A. Louis, and G. Del Giudice. "Can New Vaccines Overcome Parasite Escape Mechanisms?" In Progress in Immunology Vol. VIII. Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-51479-1_88.

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Soncin, Fabrice. "Role of Endothelial Cells in Tumor Escape from Immunity." In Molecular Mechanisms of Angiogenesis. Springer Paris, 2014. http://dx.doi.org/10.1007/978-2-8178-0466-8_15.

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Ethier, Wilfred J. "Escape and Entry Mechanisms in the Multilateral Trade System." In Challenges to the World Economy. Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-19018-6_19.

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Rivera, Lee, Melissa Pandika, and Gabriele Bergers. "Escape Mechanisms from Antiangiogenic Therapy: An Immune Cell’s Perspective." In Advances in Experimental Medicine and Biology. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-5915-6_4.

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Conference papers on the topic "Escape mechanisms"

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Derbel, Bilel, Geoffrey Pruvost, and Byung-Woo Hong. "Enhancing Moea/d with Escape Mechanisms." In 2021 IEEE Congress on Evolutionary Computation (CEC). IEEE, 2021. http://dx.doi.org/10.1109/cec45853.2021.9504957.

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Shipp, Margaret A. "Abstract IA6: Immune escape mechanisms in lymphoid malignancies." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-ia6.

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O'Brien, Siobhan, Liang Chen, Wenyan Zhong, Douglas Armellino, Maximillian Follettie, and Marc Damelin. "Abstract 1968: Breast cancer cells escape from chemotherapy and hypoxia by distinct mechanisms." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1968.

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Spring, Bryan Q., R. Bryan Sears, Lei Z. Zheng, et al. "Photodynamic therapy with simultaneous suppression of multiple treatment escape pathways (Conference Presentation)." In Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy XXV, edited by David H. Kessel and Tayyaba Hasan. SPIE, 2016. http://dx.doi.org/10.1117/12.2213828.

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Polyak, Kornelia. "Abstract IA005: Immune escape during breast tumor progression." In Abstracts: AACR Virtual Special Conference: The Evolving Tumor Microenvironment in Cancer Progression: Mechanisms and Emerging Therapeutic Opportunities; in association with the Tumor Microenvironment (TME) Working Group; January 11-12, 2021. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.tme21-ia005.

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Myronov, Alexander, Iga Niemiec, Katarzyna Gruba, et al. "Abstract 6541: Accounting for immune escape mechanisms in personalized and shared neoantigen cancer vaccine design." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-6541.

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Mori, Shoji, Lujie Shen, and Kunito Okuyama. "Effect of Cell Size of a Honeycomb Porous Plate Attached to a Heated Surface on CHF in Saturated Pool Boiling." In 2010 14th International Heat Transfer Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/ihtc14-22349.

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The critical heat flux (CHF) in a saturated pool boiling of water was investigated experimentally under the condition in which a honeycomb porous plate is attached to the heated surface. In a previous study, the CHF was shown experimentally to be approximately 2.5 times (approximately 2.51 MW/m2) compared to that of a plain surface for the case of a honeycomb porous plate with a vapor escape channel width of 1.4 mm and a channel height (plate thickness) of 1.0 mm (Mori and Okuyama (2009)). The enhancement is considered to result from the capillary supply of liquid onto the heated surface and the release of generated vapor through the channels. In the present paper, the vapor escape channel width was varied in the range of 1.4 mm to 7.9 mm, which was smaller than the Taylor instability wavelength (approximately 15.6 mm), and the effect of the channel width on the saturated pool boiling CHF of water has been investigated. The CHF values predicted by capillary limit models were compared with measured values. As a result, the main mechanisms for CHF enhancement using a honeycomb porous plate were shown to be due to liquid supply to the heated surface as a result of not only capillary suction but also the inflow of liquid through vapor escape channels from the top surface due to gravity. The ratio of the contribution in the mechanisms of the CHF enhancement was found to depend on the vapor escape channel widths. In particular, in the case of a larger cell width, the CHF was enhanced primarily due to the inflow of liquid through vapor escape channels from the top surface.
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Cieslik, Marcin P., Yi-Mi Wu, Lisha Wang, Xuhong Cao, Dan Robinson, and Arul M. Chinnaiyan. "Abstract B15: The landscape of immune infiltration and mechanisms of immune escape across 500 metastatic cancers." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-b15.

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Truffaux, Nathalene, Ludivine Le Dret, Stephanie Puget, Gilles Vassal, Birgit Geoerger, and Jacques Grill. "Abstract 2763: Activity of dasatinib and potential escape mechanisms in diffuse intrinsic pontine glioma (DIPG) models." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-2763.

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Abbott, Charles W., Sean M. Boyle, Eric Levy, Rena McClory, Sekwon Jang, and Richard Chen. "Abstract 905: Comprehensive immunogenomic profiling of anti-PD-1 treated melanoma patients reveals subject-specific tumor escape mechanisms." 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.sabcs18-905.

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Reports on the topic "Escape mechanisms"

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Coetzee, Gerhard A., Judd Rice, and Li Jia. Androgen Receptor-Mediated Escape Mechanisms from Androgen Ablation Therapy. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada461600.

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Coetzee, Gerhard A., Judd Rice, and Li Jia. Androgen Receptor-Mediated Escape Mechanism from Androgen Ablation Therapy. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada501983.

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