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1. Human chimeric antigen receptor macrophages for cancer immunotherapy

Author

Klichinsky, Michael, Ruella, Marco, Shestova, Olga, Lu, Xueqing Maggie, Best, Andrew, Zeeman, Martha, Schmierer, Maggie, Gabrusiewicz, Konrad, Anderson, Nicholas R., Petty, Nicholas E., Cummins, Katherine D., Shen, Feng, Shan, Xinhe, Veliz, Kimberly, Blouch, Kristin, Yashiro-Ohtani, Yumi, Kenderian, Saad S., Kim, Miriam Y., O’Connor, Roddy S., Wallace, Stephen R., Kozlowski, Miroslaw S., Marchione, Dylan M., Shestov, Maksim, Garcia, Benjamin A., June, Carl H., and Gill, Saar

Published
2020
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2. Abstract 6071: Whole-exome RNA sequencing of metastatic synovial sarcomas reveals heterogeneous transcriptomic profile and targetable co-alterations: Cohort study from the French Sarcoma Group

Author

Vanacker, Helene, primary, Brahmi, Mehdi, additional, Meitour, Yannick Le, additional, Bollard, Julien, additional, Attignon, Valery, additional, Meurgey, Alexandra, additional, Jean-Denis, Myriam, additional, Tonon, Laurie, additional, Pokras, Shibani, additional, Klohe, Erika, additional, Nathenson, Michael, additional, Blouch, Kristin, additional, Eleftheriadou, Ioanna, additional, Blay, Jean-Yves, additional, Tirode, Franck, additional, and Dufresne, Armelle, additional

Published
2023
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3. Study design of a global molecular disease characterization initiative (MDCI) in oncology clinical trials.

Author

Downs, David, primary, Weker, Rob, additional, Johnson, Melissa Lynne, additional, Sacher, Adrian G., additional, Butler, Marcus O., additional, Zarour, Hassane M., additional, Weber, Jeffrey S., additional, Garon, Edward B., additional, Carbone, David Paul, additional, Dokus, Ann, additional, Taylor, Jessica, additional, Dhar, Arindam, additional, Metcalf, Marilyn, additional, Messina, Cristina, additional, Yonchuk, John, additional, Blouch, Kristin, additional, and Martin, Anne-Marie, additional

Published
2022
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5. 390 A global, molecular disease characterization initiative (MDCI) in oncology clinical trials

Author

Johnson, Melissa, primary, Sacher, Adrian, additional, Butler, Marcus, additional, Zarour, Hassane, additional, Weber, Jeffrey, additional, Garon, Edward, additional, Carbone, David, additional, Dhar, Arindam, additional, Messina, Cristina, additional, Patel, Roma, additional, Blouch, Kristin, additional, Hoos, Axel, additional, and Martin, Anne-Marie, additional

Published
2021
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6. Open-label pilot study of genetically engineered NY-ESO-1–specific t cells (GSK3377794) alone or in combination with pembrolizumab in relapsed/refractory multiple myeloma.

Author

Rapoport, Aaron, primary, Hoffman, James Edward, additional, Kaufman, Jonathan L., additional, Blouch, Kristin, additional, Butler, Emily, additional, Deyoung, Maurice Phillip, additional, Farsaci, Benedetto, additional, Hasan, Aisha N., additional, Holmes, Andrew P., additional, Huff, Anne, additional, Jain, Amit, additional, Chisamore, Michael Jon, additional, and Nishihori, Taiga, additional

Published
2020
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7. Abstract PR07: Human chimeric antigen receptor (CAR) macrophages for cancer immunotherapy

Author

Klichinsky, Michael, primary, Ruella, Marco, additional, Shestova, Olga, additional, Best, Andrew, additional, Blouch, Kristin, additional, Lu, Xueqing M., additional, Kenderian, Saad S., additional, Kim, Miriam Y., additional, O'Connor, Roddy, additional, Wallace, Stephen, additional, Kozlowski, Miroslaw, additional, Marchione, Dylan M., additional, Shestov, Maksim, additional, Garcia, Benjamin A., additional, June, Carl, additional, and Gill, Saar, additional

Published
2020
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8. Open-Label Pilot Study of Genetically Engineered NY-ESO-1 Specific T Cells (GSK3377794) Alone or in Combination with Pembrolizumab in Relapsed and Refractory Multiple Myeloma

Author

Nishihori, Taiga, primary, Kaufman, Jonathan L., additional, Hoffman, James E., additional, Blouch, Kristin, additional, Pandit, Sunil, additional, Butler, Emily, additional, Jain, Amit, additional, Wu, Yuehui, additional, DeYoung, M. Phillip, additional, Hasan, Aisha N., additional, Farsaci, Benedetto, additional, Chisamore, Michael, additional, and Rapoport, Aaron P., additional

Published
2020
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9. Open-Label Pilot Study of Genetically Engineered NY-ESO-1 Specific T Cells (GSK3377794) Alone or in Combination with Pembrolizumab in Relapsed and Refractory Multiple Myeloma

Author

Nishihori, Taiga, primary, Kaufman, Jonathan L., additional, Hoffman, James E., additional, Blouch, Kristin, additional, Pandit, Sunil, additional, Butler, Emily, additional, Jain, Amit, additional, Wu, Yuehui, additional, DeYoung, M. Phillip, additional, Hasan, Aisha N., additional, and Rapoport, Aaron P., additional

Published
2019
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10. Checkpoint Blockade Reverses Anergy in IL-13Rα2 Humanized scFv-Based CAR T Cells to Treat Murine and Canine Gliomas

Author

Yin, Yibo, primary, Boesteanu, Alina C., additional, Binder, Zev A., additional, Xu, Chong, additional, Reid, Reiss A., additional, Rodriguez, Jesse L., additional, Cook, Danielle R., additional, Thokala, Radhika, additional, Blouch, Kristin, additional, McGettigan-Croce, Bevin, additional, Zhang, Logan, additional, Konradt, Christoph, additional, Cogdill, Alexandria P., additional, Panjwani, M. Kazim, additional, Jiang, Shuguang, additional, Migliorini, Denis, additional, Dahmane, Nadia, additional, Posey, Avery D., additional, June, Carl H., additional, Mason, Nicola J., additional, Lin, Zhiguo, additional, O’Rourke, Donald M., additional, and Johnson, Laura A., additional

Published
2018
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18. Different Modes of Retrovirus Restriction by Human APOBEC3A and APOBEC3G In Vivo.

Author

Stavrou, Spyridon, Crawford, Daniel, Blouch, Kristin, Browne, Edward P., Kohli, Rahul M., and Ross, Susan R.

Subjects
RETROVIRUS genetics, APOLIPOPROTEIN B, CYTIDINE deaminase, RNA viruses, INFECTION
Abstract

The apolipoprotein B editing complex 3 (A3) cytidine deaminases are among the most highly evolutionarily selected retroviral restriction factors, both in terms of gene copy number and sequence diversity. Primate genomes encode seven A3 genes, and while A3F and 3G are widely recognized as important in the restriction of HIV, the role of the other genes, particularly A3A, is not as clear. Indeed, since human cells can express multiple A3 genes, and because of the lack of an experimentally tractable model, it is difficult to dissect the individual contribution of each gene to virus restriction in vivo. To overcome this problem, we generated human A3A and A3G transgenic mice on a mouse A3 knockout background. Using these mice, we demonstrate that both A3A and A3G restrict infection by murine retroviruses but by different mechanisms: A3G was packaged into virions and caused extensive deamination of the retrovirus genomes while A3A was not packaged and instead restricted infection when expressed in target cells. Additionally, we show that a murine leukemia virus engineered to express HIV Vif overcame the A3G-mediated restriction, thereby creating a novel model for studying the interaction between these proteins. We have thus developed an in vivo system for understanding how human A3 proteins use different modes of restriction, as well as a means for testing therapies that disrupt HIV Vif-A3G interactions. [ABSTRACT FROM AUTHOR]

Published
2014
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19. DDX41 Recognizes RNA/DNA Retroviral Reverse Transcripts and Is Critical for In VivoControl of Murine Leukemia Virus Infection

Author

Stavrou, Spyridon, Aguilera, Alexya N., Blouch, Kristin, and Ross, Susan R.

Abstract

ABSTRACTHost recognition of viral nucleic acids generated during infection leads to the activation of innate immune responses essential for early control of virus. Retrovirus reverse transcription creates numerous potential ligands for cytosolic host sensors that recognize foreign nucleic acids, including single-stranded RNA (ssRNA), RNA/DNA hybrids, and double-stranded DNA (dsDNA). We and others recently showed that the sensors cyclic GMP-AMP synthase (cGAS), DEAD-box helicase 41 (DDX41), and members of the Aim2-like receptor (ALR) family participate in the recognition of retroviral reverse transcripts. However, why multiple sensors might be required and their relative importance in in vivocontrol of retroviral infection are not known. Here, we show that DDX41 primarily senses the DNA/RNA hybrid generated at the first step of reverse transcription, while cGAS recognizes dsDNA generated at the next step. We also show that both DDX41 and cGAS are needed for the antiretroviral innate immune response to murine leukemia virus (MLV) and HIV in primary mouse macrophages and dendritic cells (DCs). Using mice with cell type-specific knockout of the Ddx41gene, we show that DDX41 sensing in DCs but not macrophages was critical for controlling in vivoMLV infection. This suggests that DCs are essential in vivotargets for infection, as well as for initiating the antiviral response. Our work demonstrates that the innate immune response to retrovirus infection depends on multiple host nucleic acid sensors that recognize different reverse transcription intermediates.IMPORTANCEViruses are detected by many different host sensors of nucleic acid, which in turn trigger innate immune responses, such as type I interferon (IFN) production, required to control infection. We show here that at least two sensors are needed to initiate a highly effective innate immune response to retroviruses—DDX41, which preferentially senses the RNA/DNA hybrid generated at the first step of retrovirus replication, and cGAS, which recognizes double-stranded DNA generated at the second step. Importantly, we demonstrate using mice lacking DDX41 or cGAS that both sensors are needed for the full antiviral response needed to control in vivoMLV infection. These findings underscore the need for multiple host factors to counteract retroviral infection.

Published
2018
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20. In Vivo Examination of Mouse APOBEC3- and Human APOBEC3Aand APOBEC3G-Mediated Restriction of Parvovirus and Herpesvirus Infection in Mouse Models.

Author

Yuki Nakaya, Stavrou, Spyridon, Blouch, Kristin, Tattersall, Peter, and Ross, Susan R.

Subjects
*PARVOVIRUS diseases, *HERPESVIRUS diseases, *CYTIDINE deaminase, *VIRAL proteins, *LABORATORY mice
Abstract

APOBEC3 knockout and human APOBEC3A and -3G transgenic mice were tested for their ability to be infected by the herpesviruses herpes simplex virus 1 and murine herpesvirus 68 and the parvovirus minute virus of mice (MVM). Knockout, APOBEC3A and APOBEC3G transgenic, and wild-type mice were equally infected by the herpesviruses, while APOBEC3A but not mouse APOBEC3 conferred resistance to MVM. No viruses showed evidence of cytidine deamination by mouse or human APOBEC3s. These data suggest that in vitro studies implicating APOBEC3 proteins in virus resistance may not reflect their role in vivo. [ABSTRACT FROM AUTHOR]

Published
2016
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21. Different Modes of Retrovirus Restriction by Human APOBEC3A and APOBEC3G In Vivo.

Author

Stavrou, Spyridon, Crawford, Daniel, Blouch, Kristin, Browne, Edward P., Kohli, Rahul M., and Ross, Susan R.

Subjects
*RETROVIRUS genetics, *APOLIPOPROTEIN B, *CYTIDINE deaminase, *RNA viruses, *INFECTION
Abstract

The apolipoprotein B editing complex 3 (A3) cytidine deaminases are among the most highly evolutionarily selected retroviral restriction factors, both in terms of gene copy number and sequence diversity. Primate genomes encode seven A3 genes, and while A3F and 3G are widely recognized as important in the restriction of HIV, the role of the other genes, particularly A3A, is not as clear. Indeed, since human cells can express multiple A3 genes, and because of the lack of an experimentally tractable model, it is difficult to dissect the individual contribution of each gene to virus restriction in vivo. To overcome this problem, we generated human A3A and A3G transgenic mice on a mouse A3 knockout background. Using these mice, we demonstrate that both A3A and A3G restrict infection by murine retroviruses but by different mechanisms: A3G was packaged into virions and caused extensive deamination of the retrovirus genomes while A3A was not packaged and instead restricted infection when expressed in target cells. Additionally, we show that a murine leukemia virus engineered to express HIV Vif overcame the A3G-mediated restriction, thereby creating a novel model for studying the interaction between these proteins. We have thus developed an in vivo system for understanding how human A3 proteins use different modes of restriction, as well as a means for testing therapies that disrupt HIV Vif-A3G interactions. [ABSTRACT FROM AUTHOR]

Published
2014
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