Supplementary Table S4 from CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer

Supplementary Table S4 from CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer

<p>Table S4</p>

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Bibliografische gegevens
Hoofdauteur:	Erika Y. Faraoni (14844897) (author)
Andere auteurs:	Kanchan Singh (14844900) (author), Vidhi Chandra (14844903) (author), Olivereen Le Roux (14844906) (author), Yulin Dai (14844909) (author), Ismet Sahin (14844912) (author), Baylee J. O'Brien (14844915) (author), Lincoln N. Strickland (14844918) (author), Le Li (14844921) (author), Emily Vucic (14844924) (author), Amanda N. Warner (14844927) (author), Melissa Pruski (14844930) (author), Trent Clark (14844933) (author), George Van Buren (14844936) (author), Nirav C. Thosani (14844939) (author), John S. Bynon (14844942) (author), Curtis J. Wray (14844945) (author), Dafna Bar-Sagi (14844948) (author), Kyle L. Poulsen (14844951) (author), Lana A. Vornik (14844954) (author), Michelle I. Savage (14844957) (author), Shizuko Sei (14844960) (author), Altaf Mohammed (14844963) (author), Zhongming Zhao (12534149) (author), Powel H. Brown (14844966) (author), Tingting Mills (14844969) (author), Holger K. Eltzschig (14844972) (author), Florencia McAllister (14844975) (author), Jennifer M. Bailey-Lundberg (14844978) (author)
Gepubliceerd in:	2025
Onderwerpen:	Cancer Tumor Biology Immuno-oncology Methods and Technology Cancer Prevention Animal models of prevention Gastrointestinal Cancers Pancreatic cancer Immunology Immune responses to cancer Immunomodulation Immunotherapy Preclinical Models Animal models of cancer Tumor Heterogeneity Tumor Microenvironment Immune cells and the microenvironment
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Supplementary Table S1 from CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer
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Supplementary Table S3 from CD73-Dependent Adenosine Signaling through Adora2b Drives Immunosuppression in Ductal Pancreatic Cancer
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Supplementary Table from CDK2 Inhibition Enhances Antitumor Immunity by Increasing IFN Response to Endogenous Retroviruses
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Supplementary Table from CDK2 Inhibition Enhances Antitumor Immunity by Increasing IFN Response to Endogenous Retroviruses
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Supplementary Table from CDK2 Inhibition Enhances Antitumor Immunity by Increasing IFN Response to Endogenous Retroviruses
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Figure 1 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Figure 2 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Figure 3 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Figure 4 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Figure 5 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Figure 6 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Figure 7 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Gepubliceerd in: (2025)

Supplementary Table S1 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
door: Ernesto Gargiulo (15134961)
Gepubliceerd in: (2025)

Supplementary Table S2 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
door: Ernesto Gargiulo (15134961)
Gepubliceerd in: (2025)

Supplementary Table S3 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Gepubliceerd in: (2025)

Supplementary Table S4 from Extracellular Vesicle Secretion by Leukemia Cells <i>In Vivo</i> Promotes CLL Progression by Hampering Antitumor T-cell Responses
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Suppl video 4 from Neutrophil Conversion to a Tumor-Killing Phenotype Underpins Effective Microbial Therapy
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Supplementary Table 1 from Neutrophil Conversion to a Tumor-Killing Phenotype Underpins Effective Microbial Therapy
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Supplementary Figure 2 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Figure 4 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Figure 5 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Figure 6 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Figure7 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Table 1 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Table 2 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Supplementary Table 3 from BAFF Attenuates Immunosuppressive Monocytes in the Melanoma Tumor Microenvironment
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Table S9 from Cross-talk between Myeloid and B Cells Shapes the Distinct Microenvironments of Primary and Secondary Liver Cancer
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Supplementary table S3 from SMAD4 Loss Induces c-MYC–Mediated NLE1 Upregulation to Support Protein Biosynthesis, Colorectal Cancer Growth, and Metastasis
door: Leon P. Loevenich (14963948)
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Supplementary table S4 from SMAD4 Loss Induces c-MYC–Mediated NLE1 Upregulation to Support Protein Biosynthesis, Colorectal Cancer Growth, and Metastasis
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