Academic literature on the topic 'Immune tumor microenvironment'
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Journal articles on the topic "Immune tumor microenvironment"
Pathania, Anup Singh. "Immune Microenvironment in Childhood Cancers: Characteristics and Therapeutic Challenges." Cancers 16, no. 12 (June 12, 2024): 2201. http://dx.doi.org/10.3390/cancers16122201.
Full textTillyashaykhov, Mirzagaleb, Elena Boyko, and Shakhnoza Jumaniyazova. "EXTRATUMOR MICROENVIRONMENT IN RENAL CELL CARCINOMA." UZBEK MEDICAL JOURNAL 2, no. 4 (April 30, 2021): 5–12. http://dx.doi.org/10.26739/2181-0664-2021-4-1.
Full textChew, Valerie, Han Chong Toh, and Jean-Pierre Abastado. "Immune Microenvironment in Tumor Progression: Characteristics and Challenges for Therapy." Journal of Oncology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/608406.
Full textSK, Deshmukh. "Immune Cells in the Tumor Microenvironment and Cancer Stem Cells: Interplay for Tumor Progression." Journal of Embryology & Stem Cell Research 2, no. 2 (2018): 1–2. http://dx.doi.org/10.23880/jes-16000109.
Full textMeo, Concetta, and Filomena de Nigris. "Clinical Potential of YY1-Hypoxia Axis for Vascular Normalization and to Improve Immunotherapy." Cancers 16, no. 3 (January 23, 2024): 491. http://dx.doi.org/10.3390/cancers16030491.
Full textKang, Minjeong, DaeYong Lee, Yifan Wang, Betty Kim, and Wen Jiang. "Abstract 3230: Tumor microenvironment modulation by immunotherapy sensitizes solid tumors to radiation." Cancer Research 83, no. 7_Supplement (April 4, 2023): 3230. http://dx.doi.org/10.1158/1538-7445.am2023-3230.
Full textGao, Zetian, Qiubo Zhang, Xie Zhang, and Yufei Song. "Advance of T regulatory cells in tumor microenvironment remodeling and immunotherapy in pancreatic cancer." European Journal of Inflammation 20 (January 2022): 1721727X2210929. http://dx.doi.org/10.1177/1721727x221092900.
Full textNoman, Muhammad Zaeem, Meriem Hasmim, Yosra Messai, Stéphane Terry, Claudine Kieda, Bassam Janji, and Salem Chouaib. "Hypoxia: a key player in antitumor immune response. A Review in the Theme: Cellular Responses to Hypoxia." American Journal of Physiology-Cell Physiology 309, no. 9 (November 1, 2015): C569—C579. http://dx.doi.org/10.1152/ajpcell.00207.2015.
Full textAhmad, Aamir. "Tumor microenvironment and immune surveillance." Microenvironment and Microecology Research 4, no. 1 (2022): 6. http://dx.doi.org/10.53388/mmr2022006.
Full textFerrone, Soldano, and Theresa L. Whiteside. "Tumor Microenvironment and Immune Escape." Surgical Oncology Clinics of North America 16, no. 4 (October 2007): 755–74. http://dx.doi.org/10.1016/j.soc.2007.08.004.
Full textDissertations / Theses on the topic "Immune tumor microenvironment"
Jiménez, Bernal Isabel. "Tumor immune microenvironment in B-cell lymphoid malignancies." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671173.
Full textEl microambiente inmune tumoral juega un papel fundamental en las etapas tempranas de la formación de los tumores y en la progresión de éstos. Terapias dirigidas a este microambiente ofrecen nuevas opciones terapéuticas y también sirven para mejorar las terapias actuales frente a muchos cánceres, incluyendo los que afectan a las células B. Sin embargo, son necesarias más investigaciones para entender en mayor profundidad los mecanismos de evasión del sistema inmune que favorecen la progresión de los tumores y diseñar inmunoterapias más precisas. Nuestros principales objetivos son aportar nuevas evidencias sobre mecanismos inmunes asociados a la progresión tumoral y las bases pre-clínicas para el desarrollo de nuevas estrategias terapéuticas con potencial inmuno-modulador. Para ello, nos centramos en la leucemia linfática crónica (LLC) y en el linfoma cerebral primario (LCP). Los mecanismos de progresión en LLC desde estadios tempranos no son conocidos en su totalidad. Aunque la adquisición de alteraciones moleculares es escasa sugiriendo que la LLC no progresa exclusivamente por mecanismos de evolución clonal, todavía no se ha llevado a cabo un análisis exhaustivo del microambiente inmune que demuestre que la progresión sí pueda deberse a cambios inmunes. Por ello, hemos realizado un estudio longitudinal abarcando tanto los escenarios genéticos como inmunológicos en pacientes de LLC sin tratar que han progresado clínicamente y en pacientes asintomáticos durante un largo periodo de tiempo. Nuestros resultados muestran que los pacientes que progresan experimentan un incremento de células T CD8+ efectoras de memoria y terminalmente exhaustas T-betmid/-EomeshiPDhi a la progresión. Este incremento no se observa en los pacientes de LLC que no han progresado. Además, las células T a la progresión adquieren un perfil transcripcional diferente. Esto va acompañado de un aumento en las propiedades inmunosupresoras de las células leucémicas a la progresión. Demostramos que las células de LLC en el momento de la progresión tienen mayor capacidad de inducir exhaustión tanto en células T CD8+ de LLC como aquellas procedentes de individuos sanos, y que lo hacen mediante un mecanismo dependiente de factores solubles que incluye IL-10. Los escasos cambios genéticos que encontramos tras secuenciar el exoma de nuestros pacientes nos permiten concluir que las variaciones inmunes que hemos identificado son fundamentales para la progresión de la LLC. El desenlace de los pacientes diagnosticados con LCP es normalmente desfavorable debido a la escasez de opciones terapéuticas efectivas. Las células malignas de LCP presentan con frecuencia una desregulación de la vía del receptor de la célula B (del inglés, BCR), pero su inhibición mediante ibrutinib muestra respuestas muy breves en pacientes. Sin embargo, la vía del BCR también puede bloquearse mediante la inhibición de la exportina nuclear XPO1 con selinexor. Selinexor atraviesa la barrera hemato-encefálica y ha mostrado actividad en un paciente diagnosticado con linfoma difuso de células grandes B con recaída en el sistema nervioso central. Por consiguiente, decidimos evaluar los efectos de selinexor en monoterapia y combinado con ibrutinib en modelos pre-clínicos murinos de LCP. Nuestro análisis muestra que selinexor bloquea el crecimiento tumoral y prolonga la supervivencia en un modelo de ratón bioluminiscente y la combinación con ibrutinib prolonga aún más la supervivencia. Demostramos que los linfomas cerebrales en ratón están infiltrados con macrófagos pro-tumorales M2 que expresan PD-1 y SIRPα. Además, el tratamiento con selinexor e ibrutinib favorece la respuesta inmune anti-tumoral induciendo un cambio en la polarización de los macrófagos hacia un perfil pro-inflamatorio y reduciendo la expresión de PD-1 y SIRPα en los macrófagos M2 asociados al tumor.
The tumor immune microenvironment (TIME) plays a critical role in the early formation of tumors and their progression. Targeting the TIME has offered new therapeutic approaches and improved current ones in several cancers, including B-cell malignancies. Nonetheless, further investigation is needed in order to more deeply understand immune evasion mechanisms that lead to tumor progression and to design therapies that modulate the immune system more precisely. Here, our main objectives are to provide new insights into immune mechanisms that favor tumor progression and a pre-clinical rationale for the design of new therapeutic strategies with immunomodulatory potential. To accomplish these goals our study will focus on chronic lymphocytic leukemia (CLL) and primary central nervous system lymphoma (PCNSL). Mechanisms driving the progression of CLL from its early stages are not fully understood. This hampers detecting progression in advance and developing therapies that could intervene in the early stages. Although the limited acquisition of molecular changes suggests that CLL progression is not mainly driven by clonal evolution, a deeper analysis of the immune microenvironment that demonstrates immune variations over time that contribute to progression has not been performed. Hence, we longitudinally studied the immune and genetic landscapes of untreated progressing and non-progressing patients. Our results show that progressed CLL patients experience an increase in effector memory and terminally exhausted T-betmid/-EomeshiPDhi CD8+ T cells over time, not observed in non-progressing patients. In addition, T cells at progression acquire a distinct transcriptional profile. This is accompanied by enhanced immunosuppressive properties in leukemic cells at progression. We prove that progressed CLL cells are intrinsically more capable of inducing CD8+ T-cell exhaustion in T cells affected by CLL and healthy T cells by a mechanism dependent on soluble factors including IL-10. In addition, the reduced genetic changes we found by whole-exome sequencing in our cohort indicate these immune variations are fundamental for progression in CLL. Patients diagnosed with PCNSL often face dismal outcomes due to the limited availability of therapeutic options. PCNSL cells frequently have deregulated B-cell receptor (BCR) signaling, but its inhibition using ibrutinib only offers a brief effective response in PCNSL patients. Nonetheless, the BCR pathway can also be blocked by inhibiting the nuclear exportin XPO1 using selinexor. Selinexor is able to cross the blood–brain barrier and has shown positive clinical activity in a patient with refractory diffuse large B-cell lymphoma in the CNS. Accordingly, we evaluated the effects of selinexor alone and also combined it with ibrutinib in pre-clinical mouse models of PCNSL. Our analysis shows that selinexor blocks tumor growth and prolongs survival in a bioluminescent mouse model and its combination with ibrutinib further increases survival. We demonstrate that CNS lymphomas in mice are infiltrated by tumor-promoting M2-like macrophages expressing PD-1 and SIRPα. Moreover, the treatment with selinexor and ibrutinib favors an anti-tumoral immune response by shifting macrophage polarization toward an inflammatory phenotype and diminishing the expression of PD-1 and SIRPα in M2 tumor-associated macrophages.
TANASKOVIC, OLGA. "LACK OF P21 EXPRESSION IN TUMOR-ASSOCIATED APCS TRIGGERS THE ACTIVATION OF A POTENT ANTI-TUMOR IMMUNE RESPONSE." Doctoral thesis, Università degli Studi di Milano, 2019. http://hdl.handle.net/2434/608993.
Full textGiallongo, Cesarina. "Immune escape mechanisms in hematological diseades: role of the myeloid derived suppressor cells and tumor microenvironment." Doctoral thesis, Università di Catania, 2017. http://hdl.handle.net/10761/3889.
Full textMa, Yuting. "The crosstalk between dying tumor cells and immune effectors within tumor microenvironment elicited by anti-cancer therapies dictates the therapeutic outcome." Phd thesis, Université Paris Sud - Paris XI, 2011. http://tel.archives-ouvertes.fr/tel-00636891.
Full textYuting, Ma. "The crosstalk between dying tumor cells and immune effectors within tumor microenvironment elicited by anti-cancer therapies dictates the therapeutic outcome." Thesis, Paris 11, 2011. http://www.theses.fr/2011PA11T033/document.
Full textBesides exerting cytostatic or cytotoxic effects on tumor cells, some anti-cancer therapies (anthracyclines, oxaliplatin, X-Rays) could trigger an immunogenic cell death modality, releasing danger signals to alert immune system. We have shown that tumor-specific IFN- producing CD8+ T cells (Tc1) are mandatory for the success of chemotherapy to prevent tumor outgrowth. Priming of Tc1 response depends on IL-1β secretion by DC confronted with anthracycline-treated tumor cells releasing ATP. To identify the inflammatory components which link innate and cognate immune responses, we analyzed the influence of immunogenic chemotherapy on tumor microenvironment. We found an upregulated Th1- and Th17-related gene expression pattern in growth-retarded tumor after anthracycline treatment. By interfering with IFN- or IL-17A pathways, therapeutic effect of doxorubicin and oxaliplatin was abolished and dying tumor cell-based vaccine lost its efficacy to protect mice from live tumor cell rechallenge. Interestingly, we discovered that distinct subsets of T lymphocytes (V4+ and V6+) colonized tumors shortly after chemotherapy, where they proliferated and became the dominant IL-17 producers within tumor beds. In three tumor models treated with chemotherapy or radiotherapy, a strong correlation between the presence of IL-17-producing T ( T17) and IFN--producing CD8+ TIL (Tc1) was discovered. IL-17A signaling acts as upstream of IFN- since defect in IL-17RA led to complete loss of antigen specific Tc1 priming. The contribution of T17 cells (V4+ and V6+) to chemotherapy is critical as V4/6-/- mice showed reduced sensitivity to chemotherapy and vaccination. Also, tumor infiltrating T17 and Tc1 cells were reduced to basal level in this strain. IL-1β/IL-1R, but not IL-23/IL-23R, is pivotal for IL-17 production by T cells and the success of chemotherapy. Importantly, adoptive transfer of T cells could restore the efficacy of chemotherapy in IL-17A-/- mice and ameliorate the effect of chemotherapy in wild type host, provided that they retain the expression of IL-1R and IL-17A. Our research suggest a DC (IL-1β) → T cells (IL-17) → Tc1 (IFN-) immune axis triggered by chemotherapy-induced dying tumor cells, which is critical for the favorable therapeutic response. To boost the immune system, we try to combine immunogenic chemotherapy with tumor vaccine in the presence of TLR3 agonist Poly (A:U). This sequential combined therapy, which we named VCT, could significantly retard tumor growth or even completely eradicate tumor and establish long-term protection against rechallenge in highly tumorigenic models. To dissect the effect of Poly (A:U) on immune system and that on TLR3 expressing-tumor cells, we performed VCT treatment in nude mice, TRIF-/- mice and with TRIF-silencing tumors. Interestingly, our results suggested that anti-tumor effect of VCT required T cells and intact TRIF signaling pathway at the level of the host and that of tumor cells. Poly (A:U) treatment could induce high level of CCL5 and CXCL10 production from tumor cells both in vitro and in vivo, which could negatively and positively influence the therapeutic outcome. By uncoupling the effect of CCL5 from that of CXCL10, the VCT treatment can be ameliorated. Our study emphasizes that both tumor and host derived inflammatory factors participate in regulating anti-tumor response. We also highlight that therapeutic application of TLR agonists can be optimized through regulating the profile of chemokines and their downstream signaling events
Khan, Sarwat Tahsin. "An Interleukin-12-Expressing Oncolytic-Virus Infected Autologous Tumor Cell Vaccine Generates Potent Anti-Tumor Immune Responses." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/37940.
Full textZhang, Yahan. "THE EFFECT OF PEGYLATION ON THE CELLULAR UPTAKE OF AN IMMUNOSTIMULATORY NANOPARTICLE IN THE TUMOR IMMUNE MICROENVIRONMENT." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1618916816447844.
Full textSullivan, Camille. "Epithelial and Macrophage RON Receptor Signaling Regulates the Antitumor Immune Response in Prostate Cancer." University of Cincinnati / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=ucin159524743258716.
Full textLima, Joanna Darck Carola Correia. "O papel do infiltrado inflamatório no tumor e sua contribuição para inflamação sistêmica e desenvolimento da caquexia." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42134/tde-12082016-100836/.
Full textCancer cachexia is characterized by severe weight loss and large metabolic imbalance.It is a result of the interaction between the host\'s cells and the tumour, which induces systemic inflammation.Understand the relationship is required for the discovery of diagnostic markers.The aim of the present study was to characterize differences in inflammatory tumour infiltrate and molecular aspects in order to assess whether the presence of cachexia is determined by the inflammatory tumour profile. The study involved patients diagnosed with colorectal cancer and then distributed into two groups: cancer without cachexia(WSC) and cancer cachexia(CC).Histopathological analysis showed that the presence of cachexia in patients with colo-rectal cancer was independent from tumour staging.Characterization of infiltrating macrophages revealed a lower percentage of M2 profile in CC.Protein expression of cytokines demonstrated lower of IL-13 in CC and pro-inflammatory cytokines is higher in CC. Correlation between macrophages and cytokines was shown positive with macrophages type M1.These results provide evidence that tumor has a different secretion profile between the groups with regard to inflammatory factors and different percentages of macrophage phenotype.
VENETIS, KONSTANTINOS. "BREAST CANCER DURING PREGNANCY AS A SPECIAL TYPE OF EARLY-ONSET BREAST CANCER: INSIGHTS INTO THE TUMOR MICROENVIRONMENT AND IMMUNE TRANSCRIPTOME." Doctoral thesis, Università degli Studi di Milano, 2023. https://hdl.handle.net/2434/951469.
Full textBooks on the topic "Immune tumor microenvironment"
Kalinski, Pawel, ed. Tumor Immune Microenvironment in Cancer Progression and Cancer Therapy. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-67577-0.
Full textObradovic, Aleksandar. Discovering Master Regulators of Single-Cell Transcriptional States in the Tumor Immune Microenvironment to Reveal Immuno-Therapeutic Targets and Synergistic Treatments. [New York, N.Y.?]: [publisher not identified], 2022.
Find full textReader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny, and Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.
Full textde Oliveira, Ana Karina, Jay William Fox, Mariane Tami Amano, Adriana Franco Paes Leme, and Rodrigo Nalio Ramos, eds. Tumor Microenvironment (TME) and Tumor Immune Microenvironment (TIME): New Perspectives for Prognosis and Therapy. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-83250-132-0.
Full textKalinski, Pawel. Tumor Immune Microenvironment in Cancer Progression and Cancer Therapy. Springer, 2018.
Find full textKalinski, Pawel. Tumor Immune Microenvironment in Cancer Progression and Cancer Therapy. Springer, 2019.
Find full textLi, Yongsheng, and Bo Zhu, eds. Metabolism of Cancer Cells and Immune Cells in the Tumor Microenvironment. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88945-785-4.
Full textTang, Yanyan, Shiv K. Gupta, and Zong Sheng Guo, eds. The Role of ncRNAs (non-coding RNAs) in Regulating Tumor Immune Microenvironment. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-957-5.
Full textWang, Xu, Tengchuan Jin, Christopher James Pirozzi, Xueli Zhang, and Shu-Heng Jiang, eds. Inflammatory Tumor Immune Microenvironment: Molecular Mechanisms and Signaling Pathways in Cancer Progression and Metastasis. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-754-2.
Full textPasello, Giulia, Emanuela Felley-Bosco, and Jordi Remon, eds. Understanding the Interplay Between the Tumor Immune Microenvironment and Genetic Alterations in Thoracic Malignancies. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-818-1.
Full textBook chapters on the topic "Immune tumor microenvironment"
Chellappa, Stalin, Einar M. Aandahl, and Kjetil Taskén. "Cancer Immunity and Immune Evasion Mechanisms." In Biomarkers of the Tumor Microenvironment, 195–220. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39147-2_8.
Full textBrekken, Rolf A., and Katarzyna Wnuk-Lipinska. "Drivers of EMT and Immune Evasion." In Biomarkers of the Tumor Microenvironment, 221–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39147-2_9.
Full textBrekken, Rolf A., and Katarzyna Wnuk-Lipinska. "Drivers of EMT and Immune Evasion." In Biomarkers of the Tumor Microenvironment, 183–94. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98950-7_11.
Full textJiang, Aimin, Katherine E. Stagliano, Steven M. Cuss, Ashley Triplett, Chunmei Fu, and Arthur A. Hurwitz. "Transcriptional Regulation of Dendritic Cells in the Tumor Microenvironment." In Tumor-Induced Immune Suppression, 263–93. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4899-8056-4_9.
Full textSpano, Daniela, and Massimo Zollo. "Immune Cells Within the Tumor Microenvironment." In Interaction of Immune and Cancer Cells, 1–23. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1300-4_1.
Full textDas, Chandan Kanta, Bikash Chandra Jena, Ranabir Majumder, Himadri Tanaya Panda, and Mahitosh Mandal. "The Interplay of Autophagy and the Immune System in the Tumor Microenvironment." In Autophagy in tumor and tumor microenvironment, 183–202. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6930-2_9.
Full textWhiteside, Theresa L. "Immune Cells in the Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 167–71. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5357-1_27.
Full textLi, Yongsheng, Yisong Y. Wan, and Bo Zhu. "Immune Cell Metabolism in Tumor Microenvironment." In Advances in Experimental Medicine and Biology, 163–96. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1170-6_5.
Full textHuang, Yin, Keli Liu, Qing Li, Yikun Yao, and Ying Wang. "Exosomes Function in Tumor Immune Microenvironment." In Advances in Experimental Medicine and Biology, 109–22. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-74470-4_7.
Full textBlake, Maja K., Patrick O’Connell, and Yasser A. Aldhamen. "Advances in Tumor Microenvironment Immune Profiling." In Handbook of Cancer and Immunology, 1–24. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-80962-1_85-1.
Full textConference papers on the topic "Immune tumor microenvironment"
Hoover, Ashley R., Kaili Liu, and Wei R. Chen. "Impact of local intervention-based photo-immunotherapy on tumor microenvironment." In Biophotonics and Immune Responses XVI, edited by Wei R. Chen. SPIE, 2021. http://dx.doi.org/10.1117/12.2583747.
Full textYamshchikov, P. S., and I. V. Larionova. "REVEALING IMMUNE COMPARTMENTS USING DENOISING PROCEDURE OF SPATIAL TRANSCRIPTOMICS DATA FROM 10X GENOMICS VISIUM." In OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-44.
Full textMorimoto, Mariko, Nicholas A. Till, and Carolyn R. Bertozzi. "1178 Tumor-immune cell targeting chimeras (TICTACs): targeted immune reprogramming of the tumor microenvironment." In SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.1178.
Full textMalta, Tathiane Maistro, Indrani Datta, Thais Sabedot, Ruicong She, AnaValeria Castro, Antonio Iavarone, Laila M. Poisson, and Houtan Noushmehr. "Abstract 2717: Glioma immune microenvironment change during tumor recurrence." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2717.
Full textChu, Tianqing, and Zhang Bei. "Abstract 2796: Pan-cancer characterization of tumor immune microenvironment." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2796.
Full textPolyak, 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.
Full textDownward, Julian. "Abstract IA06: Oncogenic Ras control of the tumor immune microenvironment." In Abstracts: AACR Special Conference on Targeting RAS-Driven Cancers; December 9-12, 2018; San Diego, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3125.ras18-ia06.
Full textMiller, George. "Abstract IA7: Innate immune signaling in the pancreatic tumor microenvironment." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-ia7.
Full textGregory Sawyer, W., Duy Nguyen, Ryan Smolchek, Jack Famiglietti, and Stephanie Warrington. "1229 Immunotherapy in three dimensions: the tumor microenvironment, immune cells, and tumor invasion." In SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1229.
Full textYan, Feng, Trisha I. Valerio, Chen Wang, Wei R. Chen, and Qinggong Tang. "Monitoring the microenvironment and microvasculature of primary pancreatic tumor under photothermal-induced immunotherapy by optical coherence tomography (Conference Presentation)." In Biophotonics and Immune Responses XVIII, edited by Wei R. Chen. SPIE, 2023. http://dx.doi.org/10.1117/12.2651195.
Full textReports on the topic "Immune tumor microenvironment"
Luo, Yunping, and Ralph A. Reisfeld. Priming the Tumor Immune Microenvironment Improves Immune Surveillance of Cancer Stem Cells and Prevents Cancer Recurrence. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada574527.
Full textReisfeld, Ralph R., Debbie Liao, and Yunping Luo. Priming the Tumor Immune Microenvironment Improves Immune Surveillance of Cancer Stem Cells and Prevents Cancer Recurrence. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada553886.
Full text