Gotowe bibliografie tematyczne / Immune tumor microenvironment

Gotowa bibliografia na temat „Immune tumor microenvironment”

Autor: Grafiati
Data publikacji: 25 maja 2024
Data aktualizacji: 6 lipca 2024

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Artykuły w czasopismach na temat "Immune tumor microenvironment"

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Pathania, Anup Singh. "Immune Microenvironment in Childhood Cancers: Characteristics and Therapeutic Challenges". Cancers 16, nr 12 (12.06.2024): 2201. http://dx.doi.org/10.3390/cancers16122201.

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The tumor immune microenvironment is pivotal in cancer initiation, advancement, and regulation. Its molecular and cellular composition is critical throughout the disease, as it can influence the balance between suppressive and cytotoxic immune responses within the tumor’s vicinity. Studies on the tumor immune microenvironment have enriched our understanding of the intricate interplay between tumors and their immunological surroundings in various human cancers. These studies illuminate the role of significant components of the immune microenvironment, which have not been extensively explored in pediatric tumors before and may influence the responsiveness or resistance to therapeutic agents. Our deepening understanding of the pediatric tumor immune microenvironment is helping to overcome challenges related to the effectiveness of existing therapeutic strategies, including immunotherapies. Although in the early stages, targeted therapies that modulate the tumor immune microenvironment of pediatric solid tumors hold promise for improved outcomes. Focusing on various aspects of tumor immune biology in pediatric patients presents a therapeutic opportunity that could improve treatment outcomes. This review offers a comprehensive examination of recent literature concerning profiling the immune microenvironment in various pediatric tumors. It seeks to condense research findings on characterizing the immune microenvironment in pediatric tumors and its impact on tumor development, metastasis, and response to therapeutic modalities. It covers the immune microenvironment’s role in tumor development, interactions with tumor cells, and its impact on the tumor’s response to immunotherapy. The review also discusses challenges targeting the immune microenvironment for pediatric cancer therapies.
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Tillyashaykhov, Mirzagaleb, Elena Boyko i Shakhnoza Jumaniyazova. "EXTRATUMOR MICROENVIRONMENT IN RENAL CELL CARCINOMA". UZBEK MEDICAL JOURNAL 2, nr 4 (30.04.2021): 5–12. http://dx.doi.org/10.26739/2181-0664-2021-4-1.

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The review is focused on studying the immunosuppressive mechanisms acting in the microenvironment of renal cell carcinoma tumors. The report contains a collection of basic literature materials on the study of tumor growth factors that boost tumor cell proliferation and metastasis. The tumor microenvironment (TME) limits the immune surveillance of tumor-associated antigens and the effectiveness of immune checkpoint inhibitors. Although renal cell carcinoma is one of several tumor types sensitive to immune checkpoint inhibitors, the efficacy of these agents is likely to be limited by different tumor-infiltrating myeloid cells of bone marrow that make up the TME. Several strategies aimed at eliminating the onset of these cells in tumor tissue or neutralizing their immunosuppressive function have shown encouraging results in animal tumor models and clinical trials.Keywords: cytotoxic T lymphocytes (CTL), immune checkpoint inhibitor (ICI), tumor microenvironment (MEV), myeloid-derived suppressor cells (MDSC), regulatory T cells (Tregs), renal cell carcinoma (RCC), tumor-associated macrophages (TAM), vascular endothelial growth factor (VEGF)
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Chew, Valerie, Han Chong Toh i 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.

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The tumor microenvironment plays a critical role in cancer development, progression, and control. The molecular and cellular nature of the tumor immune microenvironment influences disease outcome by altering the balance of suppressive versus cytotoxic responses in the vicinity of the tumor. Recent developments in systems biology have improved our understanding of the complex interactions between tumors and their immunological microenvironment in various human cancers. Effective tumor surveillance by the host immune system protects against disease, but chronic inflammation and tumor “immunoediting” have also been implicated in disease development and progression. Accordingly, reactivation and maintenance of appropriate antitumor responses within the tumor microenvironment correlate with a good prognosis in cancer patients. Improved understanding of the factors that shape the tumor microenvironment will be critical for the development of effective future strategies for disease management. The manipulation of these microenvironmental factors is already emerging as a promising tool for novel cancer treatments. In this paper, we summarize the various roles of the tumor microenvironment in cancer, focusing on immunological mediators of tumor progression and control, as well as the significant challenges for future therapies.
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SK, Deshmukh. "Immune Cells in the Tumor Microenvironment and Cancer Stem Cells: Interplay for Tumor Progression". Journal of Embryology & Stem Cell Research 2, nr 2 (2018): 1–2. http://dx.doi.org/10.23880/jes-16000109.

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Meo, Concetta, i Filomena de Nigris. "Clinical Potential of YY1-Hypoxia Axis for Vascular Normalization and to Improve Immunotherapy". Cancers 16, nr 3 (23.01.2024): 491. http://dx.doi.org/10.3390/cancers16030491.

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Abnormal vasculature in solid tumors causes poor blood perfusion, hypoxia, low pH, and immune evasion. It also shapes the tumor microenvironment and affects response to immunotherapy. The combination of antiangiogenic therapy and immunotherapy has emerged as a promising approach to normalize vasculature and unlock the full potential of immunotherapy. However, the unpredictable and redundant mechanisms of vascularization and immune suppression triggered by tumor-specific hypoxic microenvironments indicate that such combination therapies need to be further evaluated to improve patient outcomes. Here, we provide an overview of the interplay between tumor angiogenesis and immune modulation and review the function and mechanism of the YY1-HIF axis that regulates the vascular and immune tumor microenvironment. Furthermore, we discuss the potential of targeting YY1 and other strategies, such as nanocarrier delivery systems and engineered immune cells (CAR-T), to normalize tumor vascularization and re-establish an immune-permissive microenvironment to enhance the efficacy of cancer therapy.
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Kang, Minjeong, DaeYong Lee, Yifan Wang, Betty Kim i Wen Jiang. "Abstract 3230: Tumor microenvironment modulation by immunotherapy sensitizes solid tumors to radiation". Cancer Research 83, nr 7_Supplement (4.04.2023): 3230. http://dx.doi.org/10.1158/1538-7445.am2023-3230.

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Abstract Radiation therapy (RT) has been prevalently implemented to treat cancer in clinical settings by inducing DNA damage in tumor cells. However, tumor microenvironmental factors such as severe hypoxic conditions and vascular anomalies attenuate the therapeutic efficacy of RT, thus resulting in unsatisfactory outcomes in solid tumors. Recently, Immune checkpoint blockade (ICB) has improved immune recognition to tumor cells and normalized tumor vasculature to diminish hypoxia in solid tumors. Herein, we suggest that RT combined with ICB synergistically alters tumor microenvironments, thus facilitating the recruitment of cytotoxic immune cells into tumors as well as sensitizing radiation effectiveness. RT in combination with ICB not only normalized tumor vasculature to reduce hypoxia, but also increased anti-tumor effects from immune-mediated toxicity and DNA damage-mediated apoptosis in several solid tumor-bearing mouse models to a greater extent than did either monotreatment of RT or ICB. This study will provide mechanistic insight into synergistic effects conferred by RT and ICB as well as a strong preclinical rationale for combining the two therapeutic modalities in human cancers. Citation Format: Minjeong Kang, DaeYong Lee, Yifan Wang, Betty Kim, Wen Jiang. Tumor microenvironment modulation by immunotherapy sensitizes solid tumors to radiation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3230.
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Gao, Zetian, Qiubo Zhang, Xie Zhang i Yufei Song. "Advance of T regulatory cells in tumor microenvironment remodeling and immunotherapy in pancreatic cancer". European Journal of Inflammation 20 (styczeń 2022): 1721727X2210929. http://dx.doi.org/10.1177/1721727x221092900.

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Pancreatic ductal adenocarcinoma (PDAC) is highly aggressive, deadly, and is rarely diagnosed early. Regulatory T cells (Treg) are a multifunctional class of immunosuppressive T cells that help maintain immunologic homeostasis and participate in autoimmune diseases, transplants, and tumors. This cell type mediates immune homeostasis, tolerance, and surveillance and is associated with poor outcomes in PDAC. Tregs remodel the tumor immune microenvironment, mediate tumor immune escape, and promote tumor invasion and metastasis. A promising area of research involves regulating Tregs to reduce their infiltration into tumor tissues. However, the complexity of the immune microenvironment has limited the efficacy of immunotherapy in PDAC. Treg modulation combined with other treatments is emerging. This review summarizes the mechanisms of Tregs activity in tumor immune microenvironments in PDAC and the latest developments in immunotherapy and clinical trials.
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Noman, Muhammad Zaeem, Meriem Hasmim, Yosra Messai, Stéphane Terry, Claudine Kieda, Bassam Janji i 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, nr 9 (1.11.2015): C569—C579. http://dx.doi.org/10.1152/ajpcell.00207.2015.

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The tumor microenvironment is a complex system, playing an important role in tumor development and progression. Besides cellular stromal components, extracellular matrix fibers, cytokines, and other metabolic mediators are also involved. In this review we outline the potential role of hypoxia, a major feature of most solid tumors, within the tumor microenvironment and how it contributes to immune resistance and immune suppression/tolerance and can be detrimental to antitumor effector cell functions. We also outline how hypoxic stress influences immunosuppressive pathways involving macrophages, myeloid-derived suppressor cells, T regulatory cells, and immune checkpoints and how it may confer tumor resistance. Finally, we discuss how microenvironmental hypoxia poses both obstacles and opportunities for new therapeutic immune interventions.
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Ahmad, Aamir. "Tumor microenvironment and immune surveillance". Microenvironment and Microecology Research 4, nr 1 (2022): 6. http://dx.doi.org/10.53388/mmr2022006.

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Ferrone, Soldano, i Theresa L. Whiteside. "Tumor Microenvironment and Immune Escape". Surgical Oncology Clinics of North America 16, nr 4 (październik 2007): 755–74. http://dx.doi.org/10.1016/j.soc.2007.08.004.

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Rozprawy doktorskie na temat "Immune tumor microenvironment"

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Jiménez, Bernal Isabel. "Tumor immune microenvironment in B-cell lymphoid malignancies". Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/671173.

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El microambient immune tumoral juga un paper fonamental en les etapes inicials de la formació dels tumors i en la progressió d’aquests. Teràpies dirigides a aquest microambient ofereixen noves opcions terapèutiques i també serveixen per a millorar les teràpies actuals enfront de molts càncers, incloent els que afecten les cèl·lules B. No obstant això, són necessàries més recerques per a entendre en major profunditat els mecanismes d’evasió del sistema immune que afavoreixen la progressió dels tumors i dissenyar immunoteràpies més precises. Els nostres principals objectius són aportar noves evidències sobre mecanismes immunes associats a la progressió tumoral i les bases pre-clíniques per al desenvolupament de noves estratègies terapèutiques amb potencial immunomodulador. Per a això, ens centrem en la leucèmia limfàtica crònica (LLC) i en el limfoma cerebral primari (LCP). Els mecanismes de progressió en LLC des d’estadis inicials no són coneguts íntegrament. Encara que l’adquisició d’alteracions moleculars és escassa suggerint que la LLC no progressa exclusivament per mecanismes d’evolució clonal, encara no s’ha dut a terme una anàlisi exhaustiva del microambient immune que demostri que la progressió sí que pugui deure’s a canvis immunes. Per això, hem realitzat un estudi longitudinal abastant tant els escenaris genètics com immunològics en pacients de LLC sense tractar que han progressat clínicament i en pacients asimptomàtics durant un llarg període de temps. Els nostres resultats mostren que els pacients que progressen experimenten un increment de cèl·lules T CD8+ efectores de memòria i terminalment exhaustes T-betmid/-*EomeshiPDhi a la progressió. Aquest increment no s’observa en els pacients de LLC que no han progressat. A més, les cèl·lules T a la progressió adquireixen un perfil transcripcional diferent. Això va acompanyat d’un augment en les propietats immunosupressores de les cèl·lules leucèmiques a la progressió. Vam demostrar que les cèl·lules de LLC en el moment de la progressió tenen major capacitat d’induir exhaustió tant en cèl·lules T CD8+ de LLC com aquelles procedents d’individus sans, i que ho fan mitjançant un mecanisme dependent de factors solubles que inclou IL-10. Els escassos canvis genètics que trobem després de seqüenciar el exoma dels nostres pacients ens permeten concloure que les variacions immunes que hem identificat són fonamentals per a la progressió de la LLC. El desenllaç dels pacients diagnosticats amb LCP és normalment desfavorable a causa de l’escassetat d’opcions terapèutiques efectives. Les cèl·lules malignes de LCP presenten amb freqüència una desregulació de la via del receptor de la cèl·lula B (de l’anglès, BCR), però la seva inhibició mitjançant ibrutinib mostra respostes molt breus en pacients. No obstant això, la via del BCR també pot bloquejar-se mitjançant la inhibició de la exportina nuclear XPO1 amb selinexor. Selinexor travessa la barrera hemato-encefàlica i ha mostrat activitat en un pacient diagnosticat amb limfoma difús de cèl·lules grans B amb recaiguda en el sistema nerviós central. Per consegüent, decidim avaluar els efectes de selinexor en monoteràpia i combinat amb ibrutinib en models preclínics murinos de LCP. La nostra anàlisi mostra que selinexor bloqueja el creixement tumoral i prolonga la supervivència en un model de ratolí bioluminiscent i la combinació amb ibrutinib prolonga encara més la supervivència. Vam demostrar que els limfomes cerebrals en ratolí estan infiltrats amb macròfags pro-tumorals M2 que expressen PD-1 i SIRPα. A més, el tractament amb selinexor i ibrutinib afavoreix la resposta immune anti-tumoral induint un canvi en la polarització dels macròfags cap a un perfil pro-inflamatori i reduint l’expressió de PD-1 i SIRPα en els macròfags M2 associats al tumor.
El 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.
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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.

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Over the last decade, the cell-cycle inhibitor p21 has been shown to sustain leukaemia propagation with two distinct mechanisms. On one hand, p21 was shown to be critical for maintaining increased self-renewal capacities of leukaemia stem cells. Indeed, the absence of p21 in leukaemia stem cells leads to their functional exhaustion, which results in loss of leukaemia transplantability in syngeneic mice. On the other hand, p21 expression is crucial for evading the surveillance mechanisms of the immune system, thus ensuring tumor growth. Specifically, lack of p21 in the leukemic microenvironment activates a potent CD4+ T-cell mediated immunological response against tumor in syngeneic context (un-published data from the host laboratory). To translate the observed p21-dependent anti-tumoral immunity into novel immune-therapies against cancer, underlying mechanisms needed to be unrevealed. In my thesis work, I dissected the cellular bases of the p21-dependent anti-tumor immuni-ty. I disclosed a crucial role of the p21-/- tumor microenvironment in triggering activation of an anti-tumor immunological response. In particular, for the first time I identified rare iron-loaded CD68+ tumor-associated macrophages (iTAMs) in the p21-null context as key me-diators of a potent immunological mechanisms of cancer clearance. By unravelling crucial players of the p21-dependent anti-tumor immunity, my work set the basis for the future de-sign of novel anti-cancer vaccines. Such vaccines will grant more efficient and less toxic treatment for cancer patients. To further transpose such immunological mechanism of cancer clearance in humans, the us-age of a proper humanized mouse model is needed. Actually, humanized mice allow to study the interaction between human immune system and cancers of human origin. I gener-ated hCB-CD34+ NSG mice containing all the cellular components of human immunity. However, I showed that these mice are fully accessible to human tumor growth, demon-strating the inadequacy of hCB-CD34+ NSG model in immuno-oncology. Thus, the devel-opment of a proper humanized mouse model to study p21-dependent anti-tumoral immune response in human context remains necessary.
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Giallongo, 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.

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The interactions between the immune system and the tumor cells occur through complex events that lead to tumor eradication or immune evasion by cancer. Recently, the prognostic role of Myeloid derived suppressor cells (MDSC) accumulation has been documented for some hematological malignancies where they correlates with disease progression and persistence of minimal residual disease. We first evaluated the change of MDSC frequency in hematological patients during therapy founding a significant correlation between the number of persistent monocytic-MDSC and major molecular response (MMR) value in chronic myeloid leukemia patients treated with dasatinib. Moreover, our data demonstrated that tumor cells, through the release of soluble factors and exosomes, are able to expand monocytic-MDSC, creating an immunotolerant environment that results in T cell anergy and facilitates tumor growth. In addition, cancer cells are also able to promote immune dysfunction in MSC with their consequent commitment, via TLR4 signaling, toward an activated status promoting immune escape through the polarization of neutrophils in immunosuppressive cells.
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Ma, 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.

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Besides 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 (V4+ and V6+) 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 (V4+ and V6+) to chemotherapy is critical as V4/6-/- 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.
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Yuting, 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.

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En dehors des effets cytostatiques ou cytotoxiques sur les cellules tumorales, certaines thérapies anti-cancéreuses peuvent déclencher la mort cellulaire immunogénique, libérant les signaux de danger pour alerter le système immunitaire. Les cellules T CD8+ T (Tc1) productrices d’IFN- et spécifiques de la tumeur sont nécessaires pour le succès de la chimiothérapie et la diminution de la croissance tumorale. L’amorçage d’une réponse bénéfique Tc1 dépend de la sécrétion d'IL-1β par les cellules dendritiques confrontées à des cellules tumorales traitées avec de l’anthracycline libérant de l’ATP. Pour identifier les composants inflammatoires qui lient les réponses immunitaires innées et adaptatives, nous avons analysé l'influence de la chimiothérapie immunogène sur le microenvironnement de la tumeur. Nous avons identifié une up-régulation de gènes associés à la réponse Th1 et Th17 dans un modèle de tumeur répondant au traitement par les anthracyclines par un retard de croissance. En interférant avec les voies IFN- ou l'IL-17A, l'effet thérapeutique de la doxorubicine et l'oxaliplatine a été aboli et le vaccin à base de cellules tumorales mortes ne protège plus les souris de la réintroduction de cellules tumorales vivantes. Nous avons également découvert que des sous-populations distinctes de lymphocytes T  (V4+ et V6+) colonisent des tumeurs peu de temps après la chimiothérapie, où ils ont proliféré et sont devenus producteurs majeurs de l’IL-17 au sein de la tumeur. Nous avons constaté une forte corrélation entre la présence de lymphocytes T  producteurs d’IL-17 ( T17) et de TIL CD8+ (Tc1) dans trois modèles différents de tumeurs traitées par la chimiothérapie ou la radiothérapie. IL-17A agit sur la signalisation en amont de l'IFN- puisqu’un défaut d’expression d’IL-17RA conduit à la perte complète de la production des Tc1 spécifiques de l’antigène. La contribution des cellules  T17 (V4+ et V6+) dans l’effet bénéfique de la chimiothérapie est essentielle puisque les souris V4/6-/-. L’axe IL-1β/IL-1R, mais pas IL-23/IL-23R, est essentielle pour la production d'IL-17 par les cellules T et l’effet bénéfique de la chimiothérapie. Le transfert adoptif de lymphocytes  T peut rétablir l'efficacité de la chimiothérapie dans le modèle de souris IL-17A-/- et améliorer l'effet de la chimiothérapie chez la souris wt, s'ils conservent l'expression de l'IL-1R et de l'IL-17A. Nos résultats suggèrent l’existence d’un axe fonctionnel: DC (IL-1β) → cellules T (IL-17) → Tc1 (IFN-), déclenché par la chimiothérapie induisant la mort des cellules tumorales, phénomène essentiel pour une réponse thérapeutique favorable. Pour renforcer la réponse immunitaire, nous essayons de combiner la chimiothérapie « immunogène » avec le vaccin anti-tumoral en présence d’adjuvants (poly (A:U), l'agoniste de TLR3).Ce type de thérapie séquentielle combinée, appelé VCT, pourrait retarder considérablement la croissance des tumeurs, voire l’éradiquer complètement et établir une protection spécifique à long terme. Pour décortiquer l'effet de la poly (A:U) sur le système immunitaire et sur les cellules tumorales exprimant le TLR3, nous avons effectué un traitement VCT chez la souris nude, TRIF-/- et les souris présentant une diminution de l’expression de TRIF au niveau des cellules tumorales. Ainsi l'effet anti-tumoral de VCT requiert les lymphocytes T et la voie de signalisation TRIF intacte au niveau de l'hôte et des cellules tumorales. Le traitement poly (A:U) peut induire un niveau élevé de production de certaines chimiokines associées à la réponse de type Th1 (CCL5 et CXCL10 ) par les cellules tumorales in vitro et in vivo, ce qui peut influencer négativement et positivement les résultats thérapeutiques. Le découplage de l’action de CCL5 et de XCL10, pourrait améliorer le traitement par la VCT. Notre étude souligne ainsi le rôle des facteurs inflammatoires dérivés de la tumeur et de l’hôte dans la régulation de la réponse immunitaire anti-tumorale
Besides 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 (V4+ and V6+) 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 (V4+ and V6+) to chemotherapy is critical as V4/6-/- 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
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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.

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Zhang, 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.

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Sullivan, 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.

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Lima, 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/.

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A caquexia associada ao câncer é caracterizada pela perda de peso severa e um desequilíbrio metabólico.Acredita-se que resulta da interação entre o hospedeiro e tumor que induz a inflamação sistêmica,portanto compreender essa relação é fundamental para a descoberta de marcadores efetivos para diagnóstico.O objetivo do trabalho foi caracterizar diferenças nos infiltrados imunitários do tumor e analisar aspectos moleculares ligados à inflamação,a fim de avaliar se a presença da caquexia é determinada pelo perfil inflamatório do tumor.O estudo envolveu pacientes com câncer colorretal e posteriormente distribuídos em dois grupos:Câncer sem caquexia(WSC) e Câncer com caquexia (CC).A análise histopatológica mostrou que o estadiamento independende da caquexia e caracterização dos macrófagos infiltrantes resultou M2 menor em CC,já a expressão proteica de citocinas indicou IL-13 menor em CC e citocinas pró-iflamatórias estavam aumentadas em CC. A correlação de macrófagos com citocinas foi positiva com M1 e negativa com M2.Esses resultados fornecem evidências de que o tumor possui um perfil de secreção diferente entre os grupos no que diz respeito a fatores inflamatórios e diferentes percentuais de fenótipo de macrófagos.
Cancer 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.
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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.

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Breast cancer during pregnancy (PrBC) is a rare tumor with limited information on its immune landscape. Here, we sought to characterize the cellular composition of the tumor microenvironment (TME) and the immune transcriptome of PrBC to identify their differences from early-onset breast cancer (EOBC) in non-pregnant women. Eighty-three PrBC and 89 EOBC were selected and subjected to tumor-infiltrating lymphocytes (TILs) profiling and immunohistochemistry for CD4, CD8, forkhead box P3 (FOXP3), and programmed death-ligand 1 (PD-L1) (clone 22C3). A subset of 28 PrBC and 23 EOBC was selected for transcriptome profiling. RNA extracted from tumor (T) and corresponding normal (N) tissues was subjected to gene expression analysis using a next-generation sequencing assay (Oncomine™ Immune Response Research Assay) targeting 395 immune-related genes. A significantly lower frequency of hormone receptor (HR)-positive tumors was found in PrBC. The prevalence of low/null PD-L1 and CD8+TILs was higher in PrBC than in the controls, specifically in HR+/HER2– breast cancers. PrBC had a significantly higher risk of relapse and disease-related death, compared to EOBC. The presence of TILs and each TIL subpopulation were significantly associated with disease relapse. The death rate was higher in PrBC with CD8+ TILs. Twenty-three differentially expressed genes (DEGs) were found in the comparison between T (PrBC and EOBC), 3 (IFNA17, IFNB1, and PECAM1) upregulated and 20 downregulated. Compared to corresponding N, PrBCT had 46 upregulated and 18 downregulated genes. Four DEGs were PrBCT-specific, one (PECAM1) upregulated and 3 (CXCL1, CCL21, and HGF) downregulated. The TME and immune transcriptome of PrBC are characterized by specific patterns of TIL subpopulations and distinct gene expression patterns. Assessment of TILs and TILs subtyping in these patients might help to identify clinically relevant subsets of women with PrBC. Our findings suggest that immune regulation takes different genomic pathways in PrBC, and PrBCT has a unique immune transcriptome.
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Książki na temat "Immune tumor microenvironment"

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Kalinski, Pawel, red. 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.

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Obradovic, 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.

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Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny i Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.

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Ovarian adenocarcinoma is typified by detection at late stages with dissemination of cancer cells into the peritoneal cavity and frequent acquisition of chemoresistance. A number of studies show the importance of the tumor microenvironment and innate immune recognition in tumor progression. Ovarian cancer cells can regulate the composition of their stroma to promote the formation of ascitic fluid rich in cytokines and bioactive lipids such as PGE2, and to stimulate the differentiation of stromal cells into a pro-tumoral phenotype. In response, cancer-associated fibroblasts, cancer-associated mesenchymal stem cells, tumor-associated macrophages, and other peritoneal cells can act through direct and indirect mechanisms to regulate tumor growth, chemoresistance via alteration of class III β‎ tubulin, angiogenesis and dissemination. This chapter deciphers the current knowledge about the role of stromal cells, associated secreted factors, and the immune system on tumor progression. This suggests that targeting the microenvironment holds great potential to improve the prognosis of patients with ovarian adenocarcinoma.
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de Oliveira, Ana Karina, Jay William Fox, Mariane Tami Amano, Adriana Franco Paes Leme i Rodrigo Nalio Ramos, red. 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.

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Kalinski, Pawel. Tumor Immune Microenvironment in Cancer Progression and Cancer Therapy. Springer, 2018.

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Kalinski, Pawel. Tumor Immune Microenvironment in Cancer Progression and Cancer Therapy. Springer, 2019.

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Li, Yongsheng, i Bo Zhu, red. 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.

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Tang, Yanyan, Shiv K. Gupta i Zong Sheng Guo, red. 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.

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Wang, Xu, Tengchuan Jin, Christopher James Pirozzi, Xueli Zhang i Shu-Heng Jiang, red. 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.

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Pasello, Giulia, Emanuela Felley-Bosco i Jordi Remon, red. 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.

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Części książek na temat "Immune tumor microenvironment"

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Chellappa, Stalin, Einar M. Aandahl i Kjetil Taskén. "Cancer Immunity and Immune Evasion Mechanisms". W Biomarkers of the Tumor Microenvironment, 195–220. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39147-2_8.

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Brekken, Rolf A., i Katarzyna Wnuk-Lipinska. "Drivers of EMT and Immune Evasion". W Biomarkers of the Tumor Microenvironment, 221–39. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-39147-2_9.

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Brekken, Rolf A., i Katarzyna Wnuk-Lipinska. "Drivers of EMT and Immune Evasion". W Biomarkers of the Tumor Microenvironment, 183–94. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-98950-7_11.

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Jiang, Aimin, Katherine E. Stagliano, Steven M. Cuss, Ashley Triplett, Chunmei Fu i Arthur A. Hurwitz. "Transcriptional Regulation of Dendritic Cells in the Tumor Microenvironment". W 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.

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Spano, Daniela, i Massimo Zollo. "Immune Cells Within the Tumor Microenvironment". W Interaction of Immune and Cancer Cells, 1–23. Vienna: Springer Vienna, 2013. http://dx.doi.org/10.1007/978-3-7091-1300-4_1.

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Das, Chandan Kanta, Bikash Chandra Jena, Ranabir Majumder, Himadri Tanaya Panda i Mahitosh Mandal. "The Interplay of Autophagy and the Immune System in the Tumor Microenvironment". W Autophagy in tumor and tumor microenvironment, 183–202. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-6930-2_9.

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Whiteside, Theresa L. "Immune Cells in the Tumor Microenvironment". W 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.

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Li, Yongsheng, Yisong Y. Wan i Bo Zhu. "Immune Cell Metabolism in Tumor Microenvironment". W Advances in Experimental Medicine and Biology, 163–96. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-024-1170-6_5.

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Huang, Yin, Keli Liu, Qing Li, Yikun Yao i Ying Wang. "Exosomes Function in Tumor Immune Microenvironment". W 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.

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Blake, Maja K., Patrick O’Connell i Yasser A. Aldhamen. "Advances in Tumor Microenvironment Immune Profiling". W 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.

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Streszczenia konferencji na temat "Immune tumor microenvironment"

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Hoover, Ashley R., Kaili Liu i Wei R. Chen. "Impact of local intervention-based photo-immunotherapy on tumor microenvironment". W Biophotonics and Immune Responses XVI, redaktor Wei R. Chen. SPIE, 2021. http://dx.doi.org/10.1117/12.2583747.

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Yamshchikov, P. S., i I. V. Larionova. "REVEALING IMMUNE COMPARTMENTS USING DENOISING PROCEDURE OF SPATIAL TRANSCRIPTOMICS DATA FROM 10X GENOMICS VISIUM". W OpenBio-2023. ИПЦ НГУ, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-44.

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Ovarian cancer has worse prognosis among gynecological malignancies. Tumor immune microenvironment significantly impact on disease prognosis. 10x Genomics Visium enables analysis of tumor immune microenvironment in a context of parenchymal-stromal relationships. Visium data biased due to “drop-out” effect. In current study we define optimal denoising strategy to reveal immune compartments in tissue section of ovarian cancer.
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Morimoto, Mariko, Nicholas A. Till i Carolyn R. Bertozzi. "1178 Tumor-immune cell targeting chimeras (TICTACs): targeted immune reprogramming of the tumor microenvironment". W SITC 38th Annual Meeting (SITC 2023) Abstracts. BMJ Publishing Group Ltd, 2023. http://dx.doi.org/10.1136/jitc-2023-sitc2023.1178.

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Malta, Tathiane Maistro, Indrani Datta, Thais Sabedot, Ruicong She, AnaValeria Castro, Antonio Iavarone, Laila M. Poisson i Houtan Noushmehr. "Abstract 2717: Glioma immune microenvironment change during tumor recurrence". W 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.

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Chu, Tianqing, i Zhang Bei. "Abstract 2796: Pan-cancer characterization of tumor immune microenvironment". W 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.

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Polyak, Kornelia. "Abstract IA005: Immune escape during breast tumor progression". W 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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Downward, Julian. "Abstract IA06: Oncogenic Ras control of the tumor immune microenvironment". W 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.

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Miller, George. "Abstract IA7: Innate immune signaling in the pancreatic tumor microenvironment". W 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.

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Gregory Sawyer, W., Duy Nguyen, Ryan Smolchek, Jack Famiglietti i Stephanie Warrington. "1229 Immunotherapy in three dimensions: the tumor microenvironment, immune cells, and tumor invasion". W SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.1229.

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Yan, Feng, Trisha I. Valerio, Chen Wang, Wei R. Chen i Qinggong Tang. "Monitoring the microenvironment and microvasculature of primary pancreatic tumor under photothermal-induced immunotherapy by optical coherence tomography (Conference Presentation)". W Biophotonics and Immune Responses XVIII, redaktor Wei R. Chen. SPIE, 2023. http://dx.doi.org/10.1117/12.2651195.

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Raporty organizacyjne na temat "Immune tumor microenvironment"

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Luo, Yunping, i 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, październik 2012. http://dx.doi.org/10.21236/ada574527.

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Reisfeld, Ralph R., Debbie Liao i 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, październik 2011. http://dx.doi.org/10.21236/ada553886.

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