Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.0685
Mythili Koneru, J. Vera, Shukaib Arslan, Hongtao Liu, Margarida Magalhaes-Silverma, N. Bejanyan, Antonio DiStasi, B. Oran, J. Hsu, Robin McCallum, Silvia Quintero, Gerald Garrett, Karrie Wang, E. Smith, T. Hoang, T. Shahim, J. Crisostomo, A. Wilga-Savitski, J. Pickering, Laura Angelo, Anastasiya Smith
{"title":"685 Preliminary results of MT-401 in post-transplant MRD+AML patients","authors":"Mythili Koneru, J. Vera, Shukaib Arslan, Hongtao Liu, Margarida Magalhaes-Silverma, N. Bejanyan, Antonio DiStasi, B. Oran, J. Hsu, Robin McCallum, Silvia Quintero, Gerald Garrett, Karrie Wang, E. Smith, T. Hoang, T. Shahim, J. Crisostomo, A. Wilga-Savitski, J. Pickering, Laura Angelo, Anastasiya Smith","doi":"10.1136/jitc-2022-sitc2022.0685","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.0685","url":null,"abstract":"","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129048711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.0084
N. Malinga, B. Rapoport, Siwele Shalete, H. Steel, L. Kwofie, P. Meyer, R. Anderson, M. Kgokolo, T. Smit
{"title":"84 Systemic levels of the soluble co-inhibitory and co-stimulatory immune checkpoint molecules in basal cell carcinoma","authors":"N. Malinga, B. Rapoport, Siwele Shalete, H. Steel, L. Kwofie, P. Meyer, R. Anderson, M. Kgokolo, T. Smit","doi":"10.1136/jitc-2022-sitc2022.0084","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.0084","url":null,"abstract":"","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129245412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.1050
K. Tomczak, Carlos Ramos, Nathaniel Deboever, N. Zhou, Jacqueline Liszeth Oliva, Changping Wu, C. Strange, A. Weissferdt, D. Rice, R. Mehran, Jianjun Zhang, M. Altan, A. Tsao, B. Sepesi, C. Haymaker
Background Malignant pleural mesothelioma (MPM) is a rare and aggressive cancer associated with exposure to asbestos that lacks effective treatment options. 1 Immunotherapy approaches remain challenging with a current paucity of knowledge on the tumor-infiltrating lymphocyte (TIL) land-scape. 2 We aimed to generate a reference transcriptomic and epigenomic atlas of MPM T cell subpopulations that could inform on cellular features and states of propagated ex vivo cells to allow new immunotherapy design. IL9R-Tcells, five CD8-MKI67 and CD8-TOX), four gamma-delta T cell clusters (?d-TRDC), and one unique cluster (MALAT1). scATAC-seq analysis of the MPM TIL paired with their transcriptomic clusters validated the presence of existing cell states with trajectory analysis confirming the separation of the distinct cell states. Activation and inhibitory markers showed heterogenous pattern. Upregulation of activation markers OX40 ( TNFRSF4*** ) and ICOS*** was present in CD4-CD40LG and OX40 ( TNFRSF4*** ) marker in IL9R-Tcells. Moreover, CD4-CD40LG showed high upregulation of CTLA4*** and GITR ( TNFRSF18*** ), whereas, among CD8+ subsets, GITR *** expression was observed only in gd -TRDC and IL9R-Tcells. gd -TRDC also displayed heterogenous upregulation of other inhibitory markers LAG3 and TOX.
{"title":"1050 Single cell transcriptome and epigenome profiling reveals the diversity of T cell states inex vivogrown tumor-infiltrating lymphocytes from malignant pleural mesothelioma","authors":"K. Tomczak, Carlos Ramos, Nathaniel Deboever, N. Zhou, Jacqueline Liszeth Oliva, Changping Wu, C. Strange, A. Weissferdt, D. Rice, R. Mehran, Jianjun Zhang, M. Altan, A. Tsao, B. Sepesi, C. Haymaker","doi":"10.1136/jitc-2022-sitc2022.1050","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.1050","url":null,"abstract":"Background Malignant pleural mesothelioma (MPM) is a rare and aggressive cancer associated with exposure to asbestos that lacks effective treatment options. 1 Immunotherapy approaches remain challenging with a current paucity of knowledge on the tumor-infiltrating lymphocyte (TIL) land-scape. 2 We aimed to generate a reference transcriptomic and epigenomic atlas of MPM T cell subpopulations that could inform on cellular features and states of propagated ex vivo cells to allow new immunotherapy design. IL9R-Tcells, five CD8-MKI67 and CD8-TOX), four gamma-delta T cell clusters (?d-TRDC), and one unique cluster (MALAT1). scATAC-seq analysis of the MPM TIL paired with their transcriptomic clusters validated the presence of existing cell states with trajectory analysis confirming the separation of the distinct cell states. Activation and inhibitory markers showed heterogenous pattern. Upregulation of activation markers OX40 ( TNFRSF4*** ) and ICOS*** was present in CD4-CD40LG and OX40 ( TNFRSF4*** ) marker in IL9R-Tcells. Moreover, CD4-CD40LG showed high upregulation of CTLA4*** and GITR ( TNFRSF18*** ), whereas, among CD8+ subsets, GITR *** expression was observed only in gd -TRDC and IL9R-Tcells. gd -TRDC also displayed heterogenous upregulation of other inhibitory markers LAG3 and TOX.","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"48 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124564732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.1305
Shelley M Herbrich, Swetha Anandhan, P. Sharma
Background Clonal hematopoiesis (CH) is an age-related phenomenon characterized by the overrepresentation of blood cells arising from a single, mutant clone and is detectable in 10-20% of individuals over 70.1 CH has now been implicated in a variety of non-hematological disorders, such as cardiovascular diseases and Covid-19 infections, by exacerbating the innate inflammatory response.2-4 However, the impact of CH in solid tumors and response to immune checkpoint blockade (ICB) is unknown. Methods To assess the prevalence and role of CH in patients with solid tumors, we analyzed publicly available data from the MSKCC-IMPACT study.5, 6 To mechanistically study CH in solid tumors, we established an orthotopic model of pancreatic adenocarcinoma (PDAC) in mice with Tet2+/- CH. CH and WT mice were treated with either ICB (aCTLA-4 + aPD-1) or vehicle control. Single-cell (sc-) RNAseq was performed on tumor infiltrating lymphocytes (n=3/group) while remaining mice were observed for disease progression and overall survival (n=10/group). Results Analyzing CH frequencies in a cohort of patients with solid tumors, we observed that the prevalence of CH was approximately 5 times higher in patients with cancer when compared to healthy age-matched controls. Further, patients with detectable CH clones had significantly worse overall survival (figure 1A). In vivo, sc-RNAseq data revealed that myeloid cells present within the pancreatic tumors of mice with Tet2+/- CH were significantly enriched for both type I and type II interferon (IFN) signaling (figure 1B). Further, these IFN+ myeloid cells were ablated after ICB therapy in Tet2+/+ WT mice but persisted in mice with Tet2+/- CH (figure 1C). PDAC tumors from mice with Tet2+/- CH had approximately half the total number of infiltrating CD8 T cells at baseline when compared to those from Tet2+/+ WT mice. Upon ICB treatment, CD8 effector cells only expanded in the tumors from Tet2+/+ WT mice. Functionally, this translated to more rapidly progressing tumors, resistance to ICB, and reduced overall survival in mice with Tet2+/- CH (figure 1D). Conclusions CH is present in upwards of 30% of patients with solid tumors and is associated with significantly worsened prognosis. Modeling PDAC in the presence of Tet2+/- CH in vivo revealed distinct alterations in the tumor microenvironment that ultimately influenced tumor progression and response to ICB. This proposed research bridges the fields of solid tumor immunology and clonal hematopoiesis to address novel mechanisms of immunotherapy resistance that will span cancer type and, ultimately, improve patient care.
{"title":"1305 Impact of Tet2-mutant clonal hematopoiesis on solid tumor immunology and response to checkpoint blockade","authors":"Shelley M Herbrich, Swetha Anandhan, P. Sharma","doi":"10.1136/jitc-2022-sitc2022.1305","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.1305","url":null,"abstract":"Background Clonal hematopoiesis (CH) is an age-related phenomenon characterized by the overrepresentation of blood cells arising from a single, mutant clone and is detectable in 10-20% of individuals over 70.1 CH has now been implicated in a variety of non-hematological disorders, such as cardiovascular diseases and Covid-19 infections, by exacerbating the innate inflammatory response.2-4 However, the impact of CH in solid tumors and response to immune checkpoint blockade (ICB) is unknown. Methods To assess the prevalence and role of CH in patients with solid tumors, we analyzed publicly available data from the MSKCC-IMPACT study.5, 6 To mechanistically study CH in solid tumors, we established an orthotopic model of pancreatic adenocarcinoma (PDAC) in mice with Tet2+/- CH. CH and WT mice were treated with either ICB (aCTLA-4 + aPD-1) or vehicle control. Single-cell (sc-) RNAseq was performed on tumor infiltrating lymphocytes (n=3/group) while remaining mice were observed for disease progression and overall survival (n=10/group). Results Analyzing CH frequencies in a cohort of patients with solid tumors, we observed that the prevalence of CH was approximately 5 times higher in patients with cancer when compared to healthy age-matched controls. Further, patients with detectable CH clones had significantly worse overall survival (figure 1A). In vivo, sc-RNAseq data revealed that myeloid cells present within the pancreatic tumors of mice with Tet2+/- CH were significantly enriched for both type I and type II interferon (IFN) signaling (figure 1B). Further, these IFN+ myeloid cells were ablated after ICB therapy in Tet2+/+ WT mice but persisted in mice with Tet2+/- CH (figure 1C). PDAC tumors from mice with Tet2+/- CH had approximately half the total number of infiltrating CD8 T cells at baseline when compared to those from Tet2+/+ WT mice. Upon ICB treatment, CD8 effector cells only expanded in the tumors from Tet2+/+ WT mice. Functionally, this translated to more rapidly progressing tumors, resistance to ICB, and reduced overall survival in mice with Tet2+/- CH (figure 1D). Conclusions CH is present in upwards of 30% of patients with solid tumors and is associated with significantly worsened prognosis. Modeling PDAC in the presence of Tet2+/- CH in vivo revealed distinct alterations in the tumor microenvironment that ultimately influenced tumor progression and response to ICB. This proposed research bridges the fields of solid tumor immunology and clonal hematopoiesis to address novel mechanisms of immunotherapy resistance that will span cancer type and, ultimately, improve patient care.","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"25 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124668185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.0564
J. Hays, Tianhong Li, H. Chen, G. Zahrah, Richard Frank, J. Hamm, M. Markham, Thomas George, E. Whitman, Mark Goldstein, Kai He, Rohit Joshi, Daniel S Chen, Yang Liu, P. Zheng, D. O’Malley
{"title":"564 Safety and clinical activities of the acid pH-sensitive anti-CTLA-4 mAb ONC-392 in ovarian cancer patients","authors":"J. Hays, Tianhong Li, H. Chen, G. Zahrah, Richard Frank, J. Hamm, M. Markham, Thomas George, E. Whitman, Mark Goldstein, Kai He, Rohit Joshi, Daniel S Chen, Yang Liu, P. Zheng, D. O’Malley","doi":"10.1136/jitc-2022-sitc2022.0564","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.0564","url":null,"abstract":"","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124677523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.0015
R. Seager, M. Senosain, Erik Van Roey, S. Gao, M. Nesline, J. Conroy, S. Pabla
Background Many individual biomarkers describe the idiosyn-crasies of each tumor and its interactions with the tumor microenvironment (TME). However, tumors often evade immunotherapy through multiple immune escape mechanisms. Here, we present a method of integrating immune and neo-plastic biomarkers that classify tumor and immune activity in the TME. Methods Standard-of-care comprehensive genomic and immune profiling was performed on 5450 FFPE tumors representing 39 histologic types, assessing expression levels of 395 immune genes and >500 tumor-associated genes. From this data, three previously published gene expression signatures were calcu-lated: cell proliferation (CP), tumor immunogenic signature (TIGS), and cancer testis antigen burden (CTAB). PD-L1 status of each tumor was assessed by IHC, and tumor mutational burden (TMB) was calculated. Principle component analysis (PCA) and unsupervised clustering revealed four distinct bio-logical groups. Subsequently, a nearest neighbor method was used to classify an immune checkpoint inhibitor (ICI) treated 242-patient validation cohort (Lung cancer, melanoma and renal cell carcinoma) into these groups, the association between these groups and ICI treatment response was deter-mined by overrepresentation analysis, and overall survival was assessed using Kaplan-Meyer and CoxPH analyses. Results PCA and clustering generated four groups: 1) Tumor-dominant, exhibiting high CTAB, TMB, and CP, and low PD-L1 and TIGS; 2) Proliferative, exhibiting high CP and low TIGS, PD-L1, CTAB, and TMB; 3) Inflamed, exhibiting high TIGS and low CP, PD-L1, CTAB, and TMB; and 4) Checkpoint, exhibiting high PD-L1, TIGS, and TMB,
{"title":"15 Integration of multiple immune-associated biomarkers facilitates classification of solid tumors by primary immune escape mode and prediction of patient outcomes","authors":"R. Seager, M. Senosain, Erik Van Roey, S. Gao, M. Nesline, J. Conroy, S. Pabla","doi":"10.1136/jitc-2022-sitc2022.0015","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.0015","url":null,"abstract":"Background Many individual biomarkers describe the idiosyn-crasies of each tumor and its interactions with the tumor microenvironment (TME). However, tumors often evade immunotherapy through multiple immune escape mechanisms. Here, we present a method of integrating immune and neo-plastic biomarkers that classify tumor and immune activity in the TME. Methods Standard-of-care comprehensive genomic and immune profiling was performed on 5450 FFPE tumors representing 39 histologic types, assessing expression levels of 395 immune genes and >500 tumor-associated genes. From this data, three previously published gene expression signatures were calcu-lated: cell proliferation (CP), tumor immunogenic signature (TIGS), and cancer testis antigen burden (CTAB). PD-L1 status of each tumor was assessed by IHC, and tumor mutational burden (TMB) was calculated. Principle component analysis (PCA) and unsupervised clustering revealed four distinct bio-logical groups. Subsequently, a nearest neighbor method was used to classify an immune checkpoint inhibitor (ICI) treated 242-patient validation cohort (Lung cancer, melanoma and renal cell carcinoma) into these groups, the association between these groups and ICI treatment response was deter-mined by overrepresentation analysis, and overall survival was assessed using Kaplan-Meyer and CoxPH analyses. Results PCA and clustering generated four groups: 1) Tumor-dominant, exhibiting high CTAB, TMB, and CP, and low PD-L1 and TIGS; 2) Proliferative, exhibiting high CP and low TIGS, PD-L1, CTAB, and TMB; 3) Inflamed, exhibiting high TIGS and low CP, PD-L1, CTAB, and TMB; and 4) Checkpoint, exhibiting high PD-L1, TIGS, and TMB,","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"115 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124693526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.0262
H. Quinn, Justin Bianchini, Liam Campion, Katherine E. Santostefano, T. Nishimura, Sydney Bucher, Buddha Gurung, Shelby Keating, Rebecca Genovese, Steven DeLuca, Bruno Bonanno, D. Walker, M. Beqiri, Christopher M Dower, Kaitlin Idank, Tomas Aramburu, Michael Naso, Luis Borges, Mark A. Wallet
Background CAR-T cell therapies have proven safe and effica-cious for hematologic malignancies, but there remains a signif-icant unmet need for effective cell therapy options for solid tumors. CAR-engineered induced pluripotent stem cell (iPSC)-derived effector cells allow for the treatment of cancer as an off-the-shelf allogeneic cell therapy. Gamma delta ( gd ) T cells exhibit the cytolytic features of conventional alpha beta ( ab ) CD8 + T cells with additional capabilities for innate recognition of tumors. For example, expression of CD16 on gd T cells can mediate antibody-dependent cellular cytotoxicity (ADCC) against tumors. Here we describe development of an iPSC-derived CAR gd T cell platform which can target solid tumors through both CAR-mediated recognition and ADCC when combined with a therapeutic antibody. process yielding >90% pure CAR + gd T cells. The TiPSCs contained the rearranged gd TCR gene and upon differentiation to T cells, uniformly expressed a V g 9V d 2 TCR and expressed high levels of CD16. CAR gd T cells were effective in killing SKOV-3 spheroids. When cultured with SKOV-3 spheroids in an ADCC assay, CAR gd T cells exhibited enhanced cytotoxicity in the presence of trastuzumab but not isotype control antibody. Activity of the gd T cells was not reliant on additional exogenous cytokine due to the engineered form of membrane-associated IL-15. Conclusions We have demonstrated that iPSC-derived gd T cells mediate anti-tumor activity in human solid tumor models through multiple pathways. The combination of two modes of tumor recognition (CAR and CD16/antibody) enabled more potent killing of solid tumor spheroids. The ability to manu-facture large batches of iPSC derived CAR gd T cells will enable a true off-the-shelf allogenic cell therapy for solid tumors.
{"title":"262 Multiple targeting of solid tumors with iPSC-derived gamma delta CAR T cells in combination with therapeutic antibodies","authors":"H. Quinn, Justin Bianchini, Liam Campion, Katherine E. Santostefano, T. Nishimura, Sydney Bucher, Buddha Gurung, Shelby Keating, Rebecca Genovese, Steven DeLuca, Bruno Bonanno, D. Walker, M. Beqiri, Christopher M Dower, Kaitlin Idank, Tomas Aramburu, Michael Naso, Luis Borges, Mark A. Wallet","doi":"10.1136/jitc-2022-sitc2022.0262","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.0262","url":null,"abstract":"Background CAR-T cell therapies have proven safe and effica-cious for hematologic malignancies, but there remains a signif-icant unmet need for effective cell therapy options for solid tumors. CAR-engineered induced pluripotent stem cell (iPSC)-derived effector cells allow for the treatment of cancer as an off-the-shelf allogeneic cell therapy. Gamma delta ( gd ) T cells exhibit the cytolytic features of conventional alpha beta ( ab ) CD8 + T cells with additional capabilities for innate recognition of tumors. For example, expression of CD16 on gd T cells can mediate antibody-dependent cellular cytotoxicity (ADCC) against tumors. Here we describe development of an iPSC-derived CAR gd T cell platform which can target solid tumors through both CAR-mediated recognition and ADCC when combined with a therapeutic antibody. process yielding >90% pure CAR + gd T cells. The TiPSCs contained the rearranged gd TCR gene and upon differentiation to T cells, uniformly expressed a V g 9V d 2 TCR and expressed high levels of CD16. CAR gd T cells were effective in killing SKOV-3 spheroids. When cultured with SKOV-3 spheroids in an ADCC assay, CAR gd T cells exhibited enhanced cytotoxicity in the presence of trastuzumab but not isotype control antibody. Activity of the gd T cells was not reliant on additional exogenous cytokine due to the engineered form of membrane-associated IL-15. Conclusions We have demonstrated that iPSC-derived gd T cells mediate anti-tumor activity in human solid tumor models through multiple pathways. The combination of two modes of tumor recognition (CAR and CD16/antibody) enabled more potent killing of solid tumor spheroids. The ability to manu-facture large batches of iPSC derived CAR gd T cells will enable a true off-the-shelf allogenic cell therapy for solid tumors.","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"59 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124723426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.1420
J. Mandula, Shiun Chang, Eslam Mohamed, Rachel Jiminez, Rosa Sierra-Mondragon, Darwin Chang, Alyssa N. Obermayer, Carlos Moran-Segura, Das Satyajit, J. Vázquez-Martínez, Karol Pierto, Ann J Chen, K. Smalley, B. Czerniecki, P. Forsyth, R. Koya, B. Ruffell, J. Cubillos-Ruiz, D. Munn, Timothy I. Shaw, J. Conejo-Garcia, P. Rodriguez
{"title":"1420 Targeting endoplasmic reticulum stress-responsive PERK in melanoma elicits paraptosis-mediated immunogenic cell death and induction of type I interferon-dependent adaptive antitumor immunity","authors":"J. Mandula, Shiun Chang, Eslam Mohamed, Rachel Jiminez, Rosa Sierra-Mondragon, Darwin Chang, Alyssa N. Obermayer, Carlos Moran-Segura, Das Satyajit, J. Vázquez-Martínez, Karol Pierto, Ann J Chen, K. Smalley, B. Czerniecki, P. Forsyth, R. Koya, B. Ruffell, J. Cubillos-Ruiz, D. Munn, Timothy I. Shaw, J. Conejo-Garcia, P. Rodriguez","doi":"10.1136/jitc-2022-sitc2022.1420","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.1420","url":null,"abstract":"","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"83 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124741616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.0310
Heather Lin, R. Freeman, A. Evans, Tenzin Passang Fnu, Tongrui Liu, Elyse Christensen, Raymond Fei, Tanisha Sinha, S. Ravindranathan, Lily Yang, Edmund Waller, S. Rafiq
{"title":"310 Engineering optimal CAR T cells to overcome pancreatic tumors with secreted antagonistic peptides","authors":"Heather Lin, R. Freeman, A. Evans, Tenzin Passang Fnu, Tongrui Liu, Elyse Christensen, Raymond Fei, Tanisha Sinha, S. Ravindranathan, Lily Yang, Edmund Waller, S. Rafiq","doi":"10.1136/jitc-2022-sitc2022.0310","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.0310","url":null,"abstract":"","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"55 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129455153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2022-11-01DOI: 10.1136/jitc-2022-sitc2022.1085
I. Hamaidi, Lin Zhang, P. Cheng, Minhsuan Wang, E. Johnson, Bin Fang, Sungjune Kim
{"title":"1085 The NAD+dependent deacetylase Sirt2 is a negative regulator of the JAK/STAT pathway in effector t cells","authors":"I. Hamaidi, Lin Zhang, P. Cheng, Minhsuan Wang, E. Johnson, Bin Fang, Sungjune Kim","doi":"10.1136/jitc-2022-sitc2022.1085","DOIUrl":"https://doi.org/10.1136/jitc-2022-sitc2022.1085","url":null,"abstract":"","PeriodicalId":398566,"journal":{"name":"Regular and Young Investigator Award Abstracts","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130317893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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