Littérature scientifique sur le sujet « Glioma, microenvironment, tumor associated macrophages »
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Articles de revues sur le sujet "Glioma, microenvironment, tumor associated macrophages"
Andersen, Johannes K., Hrvoje Miletic et Jubayer A. Hossain. « Tumor-Associated Macrophages in Gliomas—Basic Insights and Treatment Opportunities ». Cancers 14, no 5 (4 mars 2022) : 1319. http://dx.doi.org/10.3390/cancers14051319.
Texte intégralTamai, Sho, Toshiya Ichinose, Taishi Tsutsui, Shingo Tanaka, Farida Garaeva, Hemragul Sabit et Mitsutoshi Nakada. « Tumor Microenvironment in Glioma Invasion ». Brain Sciences 12, no 4 (15 avril 2022) : 505. http://dx.doi.org/10.3390/brainsci12040505.
Texte intégralKennedy, Benjamin C., Christopher R. Showers, David E. Anderson, Lisa Anderson, Peter Canoll, Jeffrey N. Bruce et Richard C. E. Anderson. « Tumor-Associated Macrophages in Glioma : Friend or Foe ? » Journal of Oncology 2013 (2013) : 1–11. http://dx.doi.org/10.1155/2013/486912.
Texte intégralRao, Rohit, Rong Han, Sean Ogurek, Lai Man Wu, Liguo Zhang, Jian Hu, Matthew Garrett, Tim Phoenix, Stephen N. Waggoner et Qing Richard Lu. « TAMI-31. GLIOBLASTOMA GENETIC DRIVERS DICTATE THE FUNCTION OF TUMOR-ASSOCIATED MACROPHAGES/MICROGLIA AND RESPONSES TO CSF1R INHIBITION ». Neuro-Oncology 23, Supplement_6 (2 novembre 2021) : vi204. http://dx.doi.org/10.1093/neuonc/noab196.815.
Texte intégralWang, Qiang-Wei, Li-Hua Sun, Ying Zhang, Zheng Wang, Zheng Zhao, Zhi-Liang Wang, Kuan-Yu Wang et al. « MET overexpression contributes to STAT4-PD-L1 signaling activation associated with tumor-associated, macrophages-mediated immunosuppression in primary glioblastomas ». Journal for ImmunoTherapy of Cancer 9, no 10 (octobre 2021) : e002451. http://dx.doi.org/10.1136/jitc-2021-002451.
Texte intégralPeng, Yichen, Feng Chen, Shenglan Li, Xiu Liu, Can Wang, Chunna Yu et Wenbin Li. « Tumor‐associated macrophages as treatment targets in glioma ». Brain Science Advances 6, no 4 (décembre 2020) : 306–23. http://dx.doi.org/10.26599/bsa.2020.9050015.
Texte intégralJang, Bum-Sup, et In Ah Kim. « Relationship between Macrophage and Radiosensitivity in Human Primary and Recurrent Glioblastoma : In Silico Analysis with Publicly Available Datasets ». Biomedicines 10, no 2 (27 janvier 2022) : 292. http://dx.doi.org/10.3390/biomedicines10020292.
Texte intégralKim, In Ah, et Bum Sup Jang. « TMIC-52. RELATIONSHIP BETWEEN MACROPHAGE AND RADIOSENSITIVITY IN HUMAN PRIMARY AND RECURRENT GLIOBLASTOMA : IN SILICO ANALYSIS WITH PUBLICLY AVAILABLE DATASETS ». Neuro-Oncology 24, Supplement_7 (1 novembre 2022) : vii283. http://dx.doi.org/10.1093/neuonc/noac209.1096.
Texte intégralRichard, Seidu A. « The Pivotal Immunoregulatory Functions of Microglia and Macrophages in Glioma Pathogenesis and Therapy ». Journal of Oncology 2022 (4 avril 2022) : 1–19. http://dx.doi.org/10.1155/2022/8903482.
Texte intégralWei, Jun, Konrad Gabrusiewicz et Amy Heimberger. « The Controversial Role of Microglia in Malignant Gliomas ». Clinical and Developmental Immunology 2013 (2013) : 1–12. http://dx.doi.org/10.1155/2013/285246.
Texte intégralThèses sur le sujet "Glioma, microenvironment, tumor associated macrophages"
Saavedra, López Elena. « Stimulation of Glioma-Associated Microglia/Macrophages effector phagocytic synapse towards tumor clearance in glioma ». Doctoral thesis, Universitat Autònoma de Barcelona, 2019. http://hdl.handle.net/10803/667801.
Texte intégralGlioblastoma (GBM) is the most aggressive form of glioma and currently has no cure. Given that around 30% of the cells within the tumor are microglia/macrophages (glioma- associated microglia/macrophages or GAMM from now on), we decided to study them in order to shed light in possible future immunotherapies. The first discovery during this investigation was the presence of GAMM in pseudopalisades (PPs) of human GBM. These structures are thought to be very important in the contribution of the tumor invasiveness, therefore the knowledge of the role of GAMMs here might be crucial. Particularly, GAMMs were found to be traveling through the PPs towards the necrotic focus, contrasting with the tumor cells. Moreover, the myeloid cells seem to gain cellular persistence with the hypoxic gradient and travel in a haptotactic manner using the gradient of glioma cells as a cue. When they reach the necrotic focus, they shift their phenotype and phagocytose tumor material, including GFAP+ fragments and nuclei. Secondly, by means of cell cultures we achieved to translocate p65 NF-κB and promote phagocytosis of tumor glioma cells (C6) by primary microglia. Moreover, using cell lines (BV-2 and GL261) we described the putative steps of phagocytosis and the distribution of some receptors (CD11b and CD16/32) involved in the process of phagocytosis. Importantly, the distribution of Iba-1 in interacting GAMMs was also defined in the animal models. Finally, we tested two immunotherapy strategies in a immunocompetent GBM animal model (C57/BL6 intracraneally inoculated with GL261 cells), and discovered that both immunotherapies have different outcomes: while CD47 neutralizing antibody seemed to be non-effective, neutralizing SIRP1α had a beneficial outcome. This way, anti-CD47 treated animals did not have any increase on survival rate than control groups; and they showed decreased bodyweight throughout the experiment, suggesting that the therapy had some systemic side effects. On the other hand, blocking SIRP1α allowed the increase of the bodyweight of the animals throughout the experiment, and decreased the cellularity of the tumor core by increasing the phagocytic activity of GAMM at the peripheral area of tumor invasion without interfering in their infiltration capacity. In all, this thesis contributes to a better understanding of the role of GAMMs in GBM and the intrinsic phagocytic capacity they can play, possibly helping in the development of immunotherapeutic tools to fight this fatal tumor.
Halin, Sofia. « Targeting the prostate tumor microenvironment and vasculature : the role of castration, tumor-associated macrophages and pigment epithelium-derived factor ». Doctoral thesis, Umeå universitet, Patologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-30300.
Texte intégralGurusamy, Devikala. « Epithelial and Stromal Ron Receptor Expression Promotes Tumor Growth in a Murine Model of Prostate Cancer ». University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1367929231.
Texte intégralEduardo, Rodrigo. « Exploring Tumor Macrophage Interaction in Anaplastic Thyroid Cancer ». Master's thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica António Xavier, 2019. http://hdl.handle.net/10362/130111.
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Mola, Silvia. « Tumor Associated Macrophages (TAMs) a pivotal orchestrator in cancer-related inflammation and a new important target in cancer-therapy ». Doctoral thesis, Università del Piemonte Orientale, 2021. https://hdl.handle.net/11579/127797.
Texte intégralFERRUCCI, VERONICA. « PRUNE-1 DRIVES THE RECRUITMENT AND THE POLARIZATION OF TUMOUR-ASSOCIATED MACROPHAGES (TAMS) PREPARING THE SOIL FOR LUNG METASTASES IN TRIPLE NEGATIVE BREAST CANCER ». Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/563230.
Texte intégralAlves, Alessandro Menna. « Carcinoma espinocelular de boca e inflamação : papel dos macrófagos no prognóstico e influência de citocinas inflamatórias no comportamento migratório ». reponame:Biblioteca Digital de Teses e Dissertações da UFRGS, 2016. http://hdl.handle.net/10183/152699.
Texte intégralOral squamous cell carcinoma (OSCC) is the most common malignant neoplasm of the oral cavity, corresponding to approximately 94% of the cases in this region. Despite the diverse molecular and cellular studies of OSCC, the patient survival rate is approximately 50%, mainly due to tumor size, regional lymph node metastasis, cell differentiation and anatomic site. The OSCC tumor microenvironment is extremely complex and diverse, with the main characteristic being an immunosuppressive chronic inflammatory state. This microenvironment is supported by the release of different inflammatory cytokines, such as IL-6, TNF- - and enhance the activities of both tumor and stromal cells. Among these activities, it has been reported in the literature that inflammatory cytokines are capable of increasing migration and invasiveness of tumor cells. Among stromal cells, macrophages are the most abundant and participate in the maintenance of the tumor microenvironment. According to the stimulus, macrophages can be polarized in M1, with pro-inflammatory and anti-tumoral role, and M2, with antiinflammatory and pro-tumoral role. Thus, the aim of this thesis was to evaluate the role of macrophages in the prognosis of OSCC and the influence of inflammatory cytokines IL-6, TNF- - OSCC cell lines. To assess the role of macrophages in the prognosis, a systematic review was conducted in which only studies using a sample of OSCC patients were evaluated and the prognosis was evaluated with macrophage markers. It was observed that higher concentrations of CD68 + and CD163 + macrophages were related to worse prognosis in patients with OSCC, although it was not possible to conclude which tumor region the presence of these cells is more important for the outcome. In order to analyze the role of the inflammatory cytokines IL-6, TNF- - atory 9 behavior of OSCC cells, in vitro assays using two cell lines, SCC25 and Cal27, were performed in migration-promoting conditions under the influence of these cytokines. It was observed that IL-6 was able to increase the speed migration and directionality of both SCC25 and Cal 27 and that this improvement in migratory capacity occurred through a crosstalk between the IL6-related signaling pathway (STAT3) and cell migration-related pathway, RhoGTPase Rac1. These data reinforce the role of the tumor microenvironment in the tumor progression process and suggest potential therapeutic targets such as the modulation of the profile of the macrophages population and the role of interleukins in the control of tissue invasion and metastasis.
Mota, José Mauricio Segundo Correia. « Progressão tumoral de melanoma B16 em camundongos sobreviventes à sepse. Possível papel de macrófagos associados ao tumor através da via CXCR4/CXCL12 ». Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17154/tde-19072016-165003/.
Texte intégralBackground: Survivors from sepsis present higher long-term mortality and increased risk of opportunistic infections. There is clinical and experimental evidence for an immunosuppressive immune dysregulation in post-sepsis. These alterations are similar to those found in tumor microenvironment. The present work assessed the role of tumorassociated macrophage (TAM) in a model of tumor progression in sepsis-surviving mice. Materials and Methods: C57/BL6 mice were submitted to cecal ligation and puncture (CLP) and treated with ertapenem (20 mg/kg, ip. - 6 h after CLP and then each 12 h for 3 days). Sepsis surviving mice were inoculated with B16-F10 melanoma cells (30,000, sc., 15 days after CLP). Naïve mice were used as controls. Tumor progression, survival and distant spontaneous metastasis were evaluated. Mice were killed at D+14 for TAM measurement through flow cytometry (CD45+F4/80+CD206+) and for cytokines (IFN-?, IL-10, TNF-?, TGF-?, CCL2, CXCL12) quantification by ELISA. Bone marrow-derived macrophage (BMDM) were isolated and co-inoculated together with B16 melanoma cells for tumor progression and survival evaluation. TAM from naïve or post-sepsis mice were isolated through Percoll gradient (70/30) followed by selective adhesion. The RNA was isolated for gene expression analysis using microarray assay. To evaluate the role of CXCL12/CXCR4, we used the specific antagonist AMD3100 (5 mg/kg, ip., at D+10 and D+14) and assessed tumor progression, survival and TAM accumulation at D+14. Results: Sepsis-surviving mice showed increased tumor progression (15, 30 or 60 days after CLP), higher metastatic burden (15 days after CLP), and less overall survival. TAM were increased in post-sepsis mice at D+14. We found increased serum levels of TGF-?, CXCL12, CCL2 e TNF-?. Naïve mice inoculated with BMDM from post-sepsis and B16 cells showed higher tumoral progression and less survival, when compared to the control group. TAM from post-sepsis showed decreased expression of MHC-II related genes and genes related to leukocyte activation. The inhibition of CXCL12/CXCR4 prevented the post-sepsis-induced tumor progression, with less TAM accumulation and reduced expression of Ki67 in TAM. Conclusions: The post-sepsis state promotes the progression of B16 melanoma in mice, which was associated with an increase in TAM accumulation. CXCL12/CXCR4 mediates TAM accumulation in this experimental model.
Kostine, Marie. « Defining the immune microenvironment in sarcoma : could immunotherapy be part of the treatment strategy in sarcoma patients ? » Thesis, Bordeaux, 2018. http://www.theses.fr/2018BORD0387/document.
Texte intégralLocal control with adequate surgery is the cornerstone of sarcoma treatment. However, most sarcoma lack effective systemic therapies in case of advanced disease, emphasizing an unmet medical need for new therapeutic targets. The recent success of immunotherapy in epithelial malignancies raises the question whether such therapies, and which ones, would be applicable in sarcomas. As a prerequisite for therapeutic applications, we characterized the immune microenvironment in three sarcoma subtypes potentially candidate to immunotherapy: 1) In chondrosarcoma, PD-L1 expression was exclusively found in nearly 50% of the dedifferentiated subtype, in association with immune-infiltrating cells and HLA class I expression. These data provide rationale for including such patients in clinical trials with PD-1/PD-L1-targeted therapies. 2) In osteosarcoma, we observed a high density of tumor-infiltrating T cells in metastatic lesions compared to primary tumors and local relapses. Furthermore, PD-L1 positivity in almost half of metastases while mainly negative in the associated primary tumors, emphasises the dynamics of an adaptive mechanism of immune escape. Enhancing the preexisting immune response in metastatic lesions using T-cell-based immunotherapy may offer clinical benefit. 3) In leiomyosarcoma, HLA class I molecules were strongly upregulated and PD-L1 expression found in 30% of high-grade tumors, which were also highly infiltrated with CD163+ immunosuppressive macrophages. CD163+ was found to be an independent poor prognostic factor for overall survival, indicating the need for assessing a macrophage-targeted approach in this tumor type, as single agent or in combination with anti PD-1/PD-L1agents
Elmously, Sherine mohamed Mohamed Kamel. « The role of the tumor microenvironment in cerebral glioma progression ». Doctoral thesis, 2016. http://hdl.handle.net/11562/944431.
Texte intégralBackground: The tumor associated macrophages (TAMs) are classified into pro-inflammatory M1 TAMs, and anti-inflammatory M2 TAMs. Glioma stem cells (GSCs) polarize TAMs into M2 phenotype which promote glioma progression. We aimed to study the implication of the total and differential TAM infiltration in low grade glioma (LGG) and high grade glioma (HGG). Also we investigated the effect of exosomes released from M1 TAMs on the fate of glioma cells. Methodolgy: Immunohistochemistry was performed on 11 paired specimens obtained from cases progressing from LGG to HGG. iNOS was used as a marker for M1 and CD163 as a marker for M2. In the in-vitro experiments, we polarized human monocytes U937 into M1 phenotype, then we isolated the exosomes from the M1conditioned medium by centrifugation and filtration. After adding M1 exosomes to U251 glioma cells, we studied the glioma cell activation by MTT assay and we studied the glioma cell apoptosis by flow-cytometry. We used Annexin V as a marker of early apoptosis and propidium iodide as a marker of late apoptosis. Results: immunohistochemistry showed an M1/M2 imbalance with the majority being M2 in either LGG and HGG. The higher M2 infiltration, the earlier was the progression. The in-vitro experiments revealed the anti-tumor effect of M1 exosomes which were able to inhibit the proliferation and to induce early and late apoptosis of glioma cells. Conclusion: our data confirmed the role of M2 TAMs in glioma progression and exhibited the tumoricidal role of M1 exosomes against gliomas.
Livres sur le sujet "Glioma, microenvironment, tumor associated macrophages"
Reader, Jocelyn, Sarah Lynam, Amy Harper, Gautam Rao, Maya Matheny et Dana M. Roque. Ovarian Tumor Microenvironment and Innate Immune Recognition. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0004.
Texte intégralChapitres de livres sur le sujet "Glioma, microenvironment, tumor associated macrophages"
Sica, Antonio, et Chiara Porta. « Role of Tumor-Associated Macrophages (TAM) in Cancer Related Inflammation ». Dans Tumor Microenvironment, 77–98. Chichester, UK : John Wiley & Sons, Ltd, 2010. http://dx.doi.org/10.1002/9780470669891.ch5.
Texte intégralAnfray, Clément, Aldo Ummarino, Alfonso Calvo, Paola Allavena et Fernando Torres Andón. « In Vivo Analysis of Tumor-Associated Macrophages in the Tumor Microenvironment ». Dans Methods in Molecular Biology, 93–108. New York, NY : Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2914-7_7.
Texte intégralMir, Manzoor Ahmad, Abrar Yousuf Mir et Tabasum Mushtaq. « Role of tumor-associated macrophages in the breast tumor microenvironment ». Dans Role of Tumor Microenvironment in Breast Cancer and Targeted Therapies, 137–69. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-443-18696-7.00003-8.
Texte intégralHughes, Russell, et Munitta Muthana. « The tumor microenvironment : The role of tumor-associated macrophages in cancer progression and responses to therapy ». Dans Tumor Immunology and Immunotherapy, 43–62. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199676866.003.0004.
Texte intégralTiwari, Meenakshi, Lokendra Kumar Sharma et Ajit Kumar Saxena. « Potential Role of Cancer Stem Cells in Glioblastoma : A Therapeutic Aspect ». Dans Glioblastoma - Current Evidences [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.106332.
Texte intégralHooda-Nehra, Anupama, Tracey L. Smith, Alejandra I. Ferrer, Fernanda I. Staquicini, Wadih Arap, Renata Pasqualini et Pranela Rameshwar. « Targeted Regulation and Cellular Imaging of Tumor-Associated Macrophages in Triple-Negative Breast Cancer : From New Mechanistic Insights to Candidate Translational Applications ». Dans Macrophages celebrating 140 years of discovery [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.105654.
Texte intégralPonnoor Anto, Nikhil, et Rashmi Mittal. « Evaluating Fate of Emerging Resistance Hitting the Brakes on Conventional Treatment Approach ». Dans Therapeutic Drug Targets and Phytomedicine For Triple Negative Breast Cancer, 99–122. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815079784123010008.
Texte intégralActes de conférences sur le sujet "Glioma, microenvironment, tumor associated macrophages"
Guerriero, Jennifer L., et Anthony Letai. « Abstract A17 : Modulation of tumor-associated macrophages towards an antitumor phenotype ». Dans Abstracts : AACR Special Conference on Cellular Heterogeneity in the Tumor Microenvironment ; February 26 — March 1, 2014 ; San Diego, CA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.chtme14-a17.
Texte intégralRabe, Daniel C., Casey Frankenberger, Russell Bainer, Devipriya Sankarasharma, Kiran Chada, Thomas Krausz, Yoav Gilad, Lev Becker et Marsha Rich Rosner. « Abstract A01 : Metastasis suppressors regulate the tumor microenvironment by blocking recruitment of pro-metastatic tumor-associated macrophages ». Dans Abstracts : AACR Special Conference on Tumor Metastasis ; November 30-December 3, 2015 ; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-a01.
Texte intégralRabe, Daniel C., Casey Frankenberger, Russell Bainer, Devipriya Sankarasharma, Kiran Chada, Thomas Krausz, Yoav Gilad, Lev Becker et Marsha Rich Rosner. « Abstract PR02 : Metastasis suppressors regulate the tumor microenvironment by blocking recruitment of pro-metastatic tumor-associated macrophages ». Dans Abstracts : AACR Special Conference on Tumor Metastasis ; November 30-December 3, 2015 ; Austin, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tummet15-pr02.
Texte intégralMiyauchi, Jeremy T., Danling Chen, Matthew K. Choi, Kenneth Shroyer, David Selwood et Stella E. Tsirka. « Abstract 4919 : Ablation of neuropilin 1 from glioma-associated microglia and macrophages slows tumor progression ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4919.
Texte intégralMiyauchi, Jeremy T., Danling Chen, Matthew Choi, Jillian Nissen, Kenneth Shroyer, David Selwood et Stella E. Tsirka. « Abstract A129 : Ablation of neuropilin 1 from glioma associated macrophages and microglia slows tumor progression ». Dans Abstracts : Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference : Translating Science into Survival ; September 25-28, 2016 ; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-a129.
Texte intégralZarif, Jelani C., James R. Hernandez et Kenneth J. Pienta. « Abstract B34 : Targeting M2-tumor associated macrophages (M2-TAMs) in prostate cancer ». Dans Abstracts : AACR Special Conference : The Function of Tumor Microenvironment in Cancer Progression ; January 7-10, 2016 ; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-b34.
Texte intégralMathsyaraja, Haritha, Katie Thies, David A. Taffany et Michael C. Ostrowski. « Abstract A27 : Micromanaging the microenvironment : The role of microRNA in metastatic mammary tumor-associated macrophages ». Dans Abstracts : AACR Special Conference on Tumor Invasion and Metastasis - January 20-23, 2013 ; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tim2013-a27.
Texte intégralKosoff, David, Jiaquan Yu, Jennifer L. Schehr, David J. Beebe et Joshua M. Lang. « Abstract 4922 : Microscale engineering of the tumor microenvironment for therapeutic targeting of tumor-associated macrophages in prostate cancer ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4922.
Texte intégralLow, Pin Yan, Yaw Chyn Lim, Wei Peng Yong, Bok Yan et Jimmy So. « Abstract C36 : Tumor-associated macrophages enhance tumor invasiveness and promote CD4+ T-cell recruitment in Gastric Cancer ». Dans Abstracts : AACR Special Conference : The Function of Tumor Microenvironment in Cancer Progression ; January 7-10, 2016 ; San Diego, CA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.tme16-c36.
Texte intégralTorroella-Kouri, Marta, Dayron Rodriguez, Risset Silvera, Mehrjad Nadji, Raul Caso, Gracielena Rodriguez, Ruben R. Gonzalez-Perez, Vijaya Iragavarapu-Charyulu et Roberto Carrio. « Abstract 398 : Tumor microenvironment imposes major alterations and profoundly shapes functional status of macrophages : peritoneal and tumor-associated macrophages from tumor hosts are two very different subpopulations ». Dans Proceedings : AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012 ; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-398.
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