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48 results on '"Gohil, Satyen H."'

1. Baseline immune state and T-cell clonal kinetics are associated with durable response to CAR-T therapy in large B-cell lymphoma

Author

Maurer, Katie, Grabski, Isabella N., Houot, Roch, Gohil, Satyen H., Miura, Shogo, Redd, Robert, Lyu, Haoxiang, Lu, Wesley, Arihara, Yohei, Budka, Justin, McDonough, Mikaela, Ansuinelli, Michela, Reynolds, Carol, Jacene, Heather, Li, Shuqiang, Livak, Kenneth J., Ritz, Jerome, Miles, Brodie, Mattie, Mike, Neuberg, Donna S., Irizarry, Rafael A., Armand, Philippe, Wu, Catherine J., and Jacobson, Caron

Published
2024
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2. Longitudinal Single-Cell Dynamics of Chromatin Accessibility and Mitochondrial Mutations in Chronic Lymphocytic Leukemia Mirror Disease History

Author

Penter, Livius, Gohil, Satyen H, Lareau, Caleb, Ludwig, Leif S, Parry, Erin M, Huang, Teddy, Li, Shuqiang, Zhang, Wandi, Livitz, Dimitri, Leshchiner, Ignaty, Parida, Laxmi, Getz, Gad, Rassenti, Laura Z, Kipps, Thomas J, Brown, Jennifer R, Davids, Matthew S, Neuberg, Donna S, Livak, Kenneth J, Sankaran, Vijay G, and Wu, Catherine J

Subjects
Clinical Research, Hematology, Human Genome, Cancer, Lymphoma, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Chromatin, Clonal Evolution, Clone Cells, DNA Copy Number Variations, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Mutation, Oncology and Carcinogenesis
Abstract

While cancers evolve during disease progression and in response to therapy, temporal dynamics remain difficult to study in humans due to the lack of consistent barcodes marking individual clones in vivo. We employ mitochondrial single-cell assay for transposase-accessible chromatin with sequencing to profile 163,279 cells from 9 patients with chronic lymphocytic leukemia (CLL) collected across disease course and utilize mitochondrial DNA (mtDNA) mutations as natural genetic markers of cancer clones. We observe stable propagation of mtDNA mutations over years in the absence of strong selective pressure, indicating clonal persistence, but dramatic changes following tight bottlenecks, including disease transformation and relapse posttherapy, paralleled by acquisition of copy-number variants and changes in chromatin accessibility and gene expression. Furthermore, we link CLL subclones to distinct chromatin states, providing insight into nongenetic sources of relapse. mtDNA mutations thus mirror disease history and provide naturally occurring genetic barcodes to enable patient-specific study of cancer subclonal dynamics.SignificanceSingle-cell multi-omic profiling of CLL reveals the utility of somatic mtDNA mutations as in vivo barcodes, which mark subclones that can evolve over time along with changes in accessible chromatin and gene expression profiles to capture dynamics of disease evolution. See related commentary by Hilton and Scott, p. 2965. This article is highlighted in the In This Issue feature, p. 2945.

Published
2021

4. Multifunctional barcoding with ClonMapper enables high-resolution study of clonal dynamics during tumor evolution and treatment

Author

Gutierrez, Catherine, Al’Khafaji, Aziz M, Brenner, Eric, Johnson, Kaitlyn E, Gohil, Satyen H, Lin, Ziao, Knisbacher, Binyamin A, Durrett, Russell E, Li, Shuqiang, Parvin, Salma, Biran, Anat, Zhang, Wandi, Rassenti, Laura, Kipps, Thomas J, Livak, Kenneth J, Neuberg, Donna, Letai, Anthony, Getz, Gad, Wu, Catherine J, and Brock, Amy

Subjects
Cancer, Biotechnology, Hematology, Human Genome, Emerging Infectious Diseases, Genetics, Cell Line, Clone Cells, Genomics, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Transcriptome
Abstract

Lineage-tracing methods have enabled characterization of clonal dynamics in complex populations, but generally lack the ability to integrate genomic, epigenomic and transcriptomic measurements with live-cell manipulation of specific clones of interest. We developed a functionalized lineage-tracing system, ClonMapper, which integrates DNA barcoding with single-cell RNA sequencing and clonal isolation to comprehensively characterize thousands of clones within heterogeneous populations. Using ClonMapper, we identified subpopulations of a chronic lymphocytic leukemia cell line with distinct clonal compositions, transcriptional signatures and chemotherapy survivorship trajectories; patterns that were also observed in primary human chronic lymphocytic leukemia. The ability to retrieve specific clones before, during and after treatment enabled direct measurements of clonal diversification and durable subpopulation transcriptional signatures. ClonMapper is a powerful multifunctional approach to dissect the complex clonal dynamics of tumor progression and therapeutic response.

Published
2021

5. A hotspot mutation in transcription factor IKZF3 drives B cell neoplasia via transcriptional dysregulation

Author

Lazarian, Gregory, Yin, Shanye, Ten Hacken, Elisa, Sewastianik, Tomasz, Uduman, Mohamed, Font-Tello, Alba, Gohil, Satyen H, Li, Shuqiang, Kim, Ekaterina, Joyal, Heather, Billington, Leah, Witten, Elizabeth, Zheng, Mei, Huang, Teddy, Severgnini, Mariano, Lefebvre, Valerie, Rassenti, Laura Z, Gutierrez, Catherine, Georgopoulos, Katia, Ott, Christopher J, Wang, Lili, Kipps, Thomas J, Burger, Jan A, Livak, Kenneth J, Neuberg, Donna S, Baran-Marszak, Fanny, Cymbalista, Florence, Carrasco, Ruben D, and Wu, Catherine J

Subjects
Biochemistry and Cell Biology, Biological Sciences, Biotechnology, Cancer, Lymphatic Research, Hematology, Lymphoma, Rare Diseases, Genetics, 2.1 Biological and endogenous factors, 5.1 Pharmaceuticals, Animals, B-Lymphocytes, Humans, Ikaros Transcription Factor, Leukemia, Lymphocytic, Chronic, B-Cell, Mice, Mice, Inbred C57BL, Mice, Inbred NOD, Mutation, NF-kappa B, Receptors, Antigen, B-Cell, Signal Transduction, Transcription, Genetic, BCR signaling, CLL, IKZF3, NF-κB, murine mode, Neurosciences, Oncology and Carcinogenesis, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

Hotspot mutation of IKZF3 (IKZF3-L162R) has been identified as a putative driver of chronic lymphocytic leukemia (CLL), but its function remains unknown. Here, we demonstrate its driving role in CLL through a B cell-restricted conditional knockin mouse model. Mutant Ikzf3 alters DNA binding specificity and target selection, leading to hyperactivation of B cell receptor (BCR) signaling, overexpression of nuclear factor κB (NF-κB) target genes, and development of CLL-like disease in elderly mice with a penetrance of ~40%. Human CLL carrying either IKZF3 mutation or high IKZF3 expression was associated with overexpression of BCR/NF-κB pathway members and reduced sensitivity to BCR signaling inhibition by ibrutinib. Our results thus highlight IKZF3 oncogenic function in CLL via transcriptional dysregulation and demonstrate that this pro-survival function can be achieved by either somatic mutation or overexpression of this CLL driver. This emphasizes the need for combinatorial approaches to overcome IKZF3-mediated BCR inhibitor resistance.

Published
2021

6. Distinct evolutionary paths in chronic lymphocytic leukemia during resistance to the graft-versus-leukemia effect

Author

Bachireddy, Pavan, Ennis, Christina, Nguyen, Vinhkhang N, Gohil, Satyen H, Clement, Kendell, Shukla, Sachet A, Forman, Juliet, Barkas, Nikolaos, Freeman, Samuel, Bavli, Natalie, Elagina, Liudmila, Leshchiner, Ignaty, Mohammad, Arman W, Mathewson, Nathan D, Keskin, Derin B, Rassenti, Laura Z, Kipps, Thomas J, Brown, Jennifer R, Getz, Gad, Ho, Vincent T, Gnirke, Andreas, Neuberg, Donna, Soiffer, Robert J, Ritz, Jerome, Alyea, Edwin P, Kharchenko, Peter V, and Wu, Catherine J

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Immunology, Orphan Drug, Stem Cell Research - Nonembryonic - Human, Regenerative Medicine, Cancer, Stem Cell Research, Human Genome, Hematology, Lymphoma, Clinical Research, Rare Diseases, Lymphatic Research, Transplantation, Genetics, Graft vs Host Disease, Graft vs Leukemia Effect, HLA Antigens, Hematopoietic Stem Cell Transplantation, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Transplantation, Homologous, Biological Sciences, Medical and Health Sciences, Medical biotechnology, Biomedical engineering
Abstract

Leukemic relapse remains a major barrier to successful allogeneic hematopoietic stem cell transplantation (allo-HSCT) for aggressive hematologic malignancies. The basis for relapse of advanced lymphoid malignancies remains incompletely understood and may involve escape from the graft-versus-leukemia (GvL) effect. We hypothesized that for patients with chronic lymphocytic leukemia (CLL) treated with allo-HSCT, leukemic cell-intrinsic features influence transplant outcomes by directing the evolutionary trajectories of CLL cells. Integrated genetic, transcriptomic, and epigenetic analyses of CLL cells from 10 patients revealed that the clinical kinetics of post-HSCT relapse are shaped by distinct molecular dynamics. Early relapses after allo-HSCT exhibited notable genetic stability; single CLL cell transcriptional analysis demonstrated a cellular heterogeneity that was static over time. In contrast, CLL cells relapsing late after allo-HSCT displayed notable genetic evolution and evidence of neoantigen depletion, consistent with marked single-cell transcriptional shifts that were unique to each patient. We observed a greater rate of epigenetic change for late relapses not seen in early relapses or relapses after chemotherapy alone, suggesting that the selection pressures of the GvL bottleneck are unlike those imposed by chemotherapy. No selective advantage for human leukocyte antigen (HLA) loss was observed, even when present in pretransplant subpopulations. Gain of stem cell modules was a common signature associated with leukemia relapse regardless of posttransplant relapse kinetics. These data elucidate the biological pathways that underlie GvL resistance and posttransplant relapse.

Published
2020

7. Distinct cellular dynamics associated with response to CAR-T therapy for refractory B cell lymphoma

Author

Haradhvala, Nicholas J., Leick, Mark B., Maurer, Katie, Gohil, Satyen H., Larson, Rebecca C., Yao, Ning, Gallagher, Kathleen M. E., Katsis, Katelin, Frigault, Matthew J., Southard, Jackson, Li, Shuqiang, Kann, Michael C., Silva, Harrison, Jan, Max, Rhrissorrakrai, Kahn, Utro, Filippo, Levovitz, Chaya, Jacobs, Raquel A., Slowik, Kara, Danysh, Brian P., Livak, Kenneth J., Parida, Laxmi, Ferry, Judith, Jacobson, Caron, Wu, Catherine J., Getz, Gad, and Maus, Marcela V.

Published
2022
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10. Mapping the evolution of T cell states during response and resistance to adoptive cellular therapy

Author

Bachireddy, Pavan, Azizi, Elham, Burdziak, Cassandra, Nguyen, Vinhkhang N., Ennis, Christina S., Maurer, Katie, Park, Cameron Y., Choo, Zi-Ning, Li, Shuqiang, Gohil, Satyen H., Ruthen, Neil G., Ge, Zhongqi, Keskin, Derin B., Cieri, Nicoletta, Livak, Kenneth J., Kim, Haesook T., Neuberg, Donna S., Soiffer, Robert J., Ritz, Jerome, Alyea, Edwin P., Pe’er, Dana, and Wu, Catherine J.

Published
2021
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12. Progressive immune dysfunction with advancing disease stage in renal cell carcinoma

Author

Braun, David A., Street, Kelly, Burke, Kelly P., Cookmeyer, David L., Denize, Thomas, Pedersen, Christina B., Gohil, Satyen H., Schindler, Nicholas, Pomerance, Lucas, Hirsch, Laure, Bakouny, Ziad, Hou, Yue, Forman, Juliet, Huang, Teddy, Li, Shuqiang, Cui, Ang, Keskin, Derin B., Steinharter, John, Bouchard, Gabrielle, Sun, Maxine, Pimenta, Erica M., Xu, Wenxin, Mahoney, Kathleen M., McGregor, Bradley A., Hirsch, Michelle S., Chang, Steven L., Livak, Kenneth J., McDermott, David F., Shukla, Sachet A., Olsen, Lars R., Signoretti, Sabina, Sharpe, Arlene H., Irizarry, Rafael A., Choueiri, Toni K., and Wu, Catherine J.

Published
2021
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15. Personal neoantigen vaccines induce persistent memory T cell responses and epitope spreading in patients with melanoma

Author

Hu, Zhuting, Leet, Donna E., Allesøe, Rosa L., Oliveira, Giacomo, Li, Shuqiang, Luoma, Adrienne M., Liu, Jinyan, Forman, Juliet, Huang, Teddy, Iorgulescu, J. Bryan, Holden, Rebecca, Sarkizova, Siranush, Gohil, Satyen H., Redd, Robert A., Sun, Jing, Elagina, Liudmila, Giobbie-Hurder, Anita, Zhang, Wandi, Peter, Lauren, Ciantra, Zoe, Rodig, Scott, Olive, Oriol, Shetty, Keerthi, Pyrdol, Jason, Uduman, Mohamed, Lee, Patrick C., Bachireddy, Pavan, Buchbinder, Elizabeth I., Yoon, Charles H., Neuberg, Donna, Pentelute, Bradley L., Hacohen, Nir, Livak, Kenneth J., Shukla, Sachet A., Olsen, Lars Rønn, Barouch, Dan H., Wucherpfennig, Kai W., Fritsch, Edward F., Keskin, Derin B., Wu, Catherine J., and Ott, Patrick A.

Published
2021
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16. A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors

Author

Slyper, Michal, Porter, Caroline B. M., Ashenberg, Orr, Waldman, Julia, Drokhlyansky, Eugene, Wakiro, Isaac, Smillie, Christopher, Smith-Rosario, Gabriela, Wu, Jingyi, Dionne, Danielle, Vigneau, Sébastien, Jané-Valbuena, Judit, Tickle, Timothy L., Napolitano, Sara, Su, Mei-Ju, Patel, Anand G., Karlstrom, Asa, Gritsch, Simon, Nomura, Masashi, Waghray, Avinash, Gohil, Satyen H., Tsankov, Alexander M., Jerby-Arnon, Livnat, Cohen, Ofir, Klughammer, Johanna, Rosen, Yanay, Gould, Joshua, Nguyen, Lan, Hofree, Matan, Tramontozzi, Peter J., Li, Bo, Wu, Catherine J., Izar, Benjamin, Haq, Rizwan, Hodi, F. Stephen, Yoon, Charles H., Hata, Aaron N., Baker, Suzanne J., Suvà, Mario L., Bueno, Raphael, Stover, Elizabeth H., Clay, Michael R., Dyer, Michael A., Collins, Natalie B., Matulonis, Ursula A., Wagle, Nikhil, Johnson, Bruce E., Rotem, Asaf, Rozenblatt-Rosen, Orit, and Regev, Aviv

Published
2020
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18. Mapping the evolution of T cell states during response and resistance to adoptive cellular therapy

Author

Bachireddy, Pavan, primary, Azizi, Elham, additional, Burdziak, Cassandra, additional, Nguyen, Vinhkhang N., additional, Ennis, Christina S., additional, Maurer, Katie, additional, Park, Cameron Y., additional, Choo, Zi-Ning, additional, Li, Shuqiang, additional, Gohil, Satyen H., additional, Ruthen, Neil G., additional, Ge, Zhongqi, additional, Keskin, Derin B., additional, Cieri, Nicoletta, additional, Livak, Kenneth J., additional, Kim, Haesook T., additional, Neuberg, Donna S., additional, Soiffer, Robert J., additional, Ritz, Jerome, additional, Alyea, Edwin P., additional, Pe’er, Dana, additional, and Wu, Catherine J., additional

Published
2023
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19. Data from Longitudinal Single-Cell Dynamics of Chromatin Accessibility and Mitochondrial Mutations in Chronic Lymphocytic Leukemia Mirror Disease History

Author

Penter, Livius, primary, Gohil, Satyen H., primary, Lareau, Caleb, primary, Ludwig, Leif S., primary, Parry, Erin M., primary, Huang, Teddy, primary, Li, Shuqiang, primary, Zhang, Wandi, primary, Livitz, Dimitri, primary, Leshchiner, Ignaty, primary, Parida, Laxmi, primary, Getz, Gad, primary, Rassenti, Laura Z., primary, Kipps, Thomas J., primary, Brown, Jennifer R., primary, Davids, Matthew S., primary, Neuberg, Donna S., primary, Livak, Kenneth J., primary, Sankaran, Vijay G., primary, and Wu, Catherine J., primary

Published
2023
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20. Supplementary Data from Longitudinal Single-Cell Dynamics of Chromatin Accessibility and Mitochondrial Mutations in Chronic Lymphocytic Leukemia Mirror Disease History

Author

Penter, Livius, primary, Gohil, Satyen H., primary, Lareau, Caleb, primary, Ludwig, Leif S., primary, Parry, Erin M., primary, Huang, Teddy, primary, Li, Shuqiang, primary, Zhang, Wandi, primary, Livitz, Dimitri, primary, Leshchiner, Ignaty, primary, Parida, Laxmi, primary, Getz, Gad, primary, Rassenti, Laura Z., primary, Kipps, Thomas J., primary, Brown, Jennifer R., primary, Davids, Matthew S., primary, Neuberg, Donna S., primary, Livak, Kenneth J., primary, Sankaran, Vijay G., primary, and Wu, Catherine J., primary

Published
2023
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21. Table S2 from Longitudinal Single-Cell Dynamics of Chromatin Accessibility and Mitochondrial Mutations in Chronic Lymphocytic Leukemia Mirror Disease History

Author

Penter, Livius, primary, Gohil, Satyen H., primary, Lareau, Caleb, primary, Ludwig, Leif S., primary, Parry, Erin M., primary, Huang, Teddy, primary, Li, Shuqiang, primary, Zhang, Wandi, primary, Livitz, Dimitri, primary, Leshchiner, Ignaty, primary, Parida, Laxmi, primary, Getz, Gad, primary, Rassenti, Laura Z., primary, Kipps, Thomas J., primary, Brown, Jennifer R., primary, Davids, Matthew S., primary, Neuberg, Donna S., primary, Livak, Kenneth J., primary, Sankaran, Vijay G., primary, and Wu, Catherine J., primary

Published
2023
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22. P004 Infective complications in patients with secondary haemophagocytic lymphohistiocytosis: a case series from a large central London teaching hospital

Author

Saha, Pratyasha, primary, McCann, Naina, additional, Brown, Michael, additional, Stone, Neil, additional, Sanchez, Emilie, additional, Carpenter, Ben, additional, Laurence, Arian, additional, Hutchinson, Matthew, additional, Jones, Alexis, additional, Gohil, Satyen H, additional, and Manson, Jessica, additional

Published
2023
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23. OA22 Management of haemophagocytic lymphohistiocytosis: service evaluation of a national multi-disciplinary meeting

Author

Shah, Neal S, primary, Hutchinson, Matthew, additional, Clark, Samuel, additional, Sanchez, Emilie, additional, Brown, Michael, additional, Stone, Neil, additional, Carr, Aisling S, additional, Carpenter, Ben, additional, Laurence, Arian, additional, Gohil, Satyen H, additional, Tattersall, Rachel S, additional, Manson, Jessica J, additional, and Jones, Alexis, additional

Published
2023
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24. Author Correction: A single-cell and single-nucleus RNA-Seq toolbox for fresh and frozen human tumors

Author

Slyper, Michal, Porter, Caroline B. M., Ashenberg, Orr, Waldman, Julia, Drokhlyansky, Eugene, Wakiro, Isaac, Smillie, Christopher, Smith-Rosario, Gabriela, Wu, Jingyi, Dionne, Danielle, Vigneau, Sébastien, Jané-Valbuena, Judit, Tickle, Timothy L., Napolitano, Sara, Su, Mei-Ju, Patel, Anand G., Karlstrom, Asa, Gritsch, Simon, Nomura, Masashi, Waghray, Avinash, Gohil, Satyen H., Tsankov, Alexander M., Jerby-Arnon, Livnat, Cohen, Ofir, Klughammer, Johanna, Rosen, Yanay, Gould, Joshua, Nguyen, Lan, Hofree, Matan, Tramontozzi, Peter J., Li, Bo, Wu, Catherine J., Izar, Benjamin, Haq, Rizwan, Hodi, F. Stephen, Yoon, Charles H., Hata, Aaron N., Baker, Suzanne J., Suvà, Mario L., Bueno, Raphael, Stover, Elizabeth H., Clay, Michael R., Dyer, Michael A., Collins, Natalie B., Matulonis, Ursula A., Wagle, Nikhil, Johnson, Bruce E., Rotem, Asaf, Rozenblatt-Rosen, Orit, and Regev, Aviv

Published
2020
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25. Acquired Glanzmann's thrombasthenia with IgG and IgA against activated αIIbβ3.

Author

Constantinescu‐Bercu, Adela, McCann, Sabina, Hmaid, Amjad, de Groot, Rens, Singh, Deepak, Gohil, Satyen H., Thomas, Mari, Scully, Marie, and Westwood, John‐Paul

Subjects
IMMUNOGLOBULIN G, MENORRHAGIA, ANTIPHOSPHOLIPID syndrome, MUCOSA-associated lymphoid tissue lymphoma, POST-acute COVID-19 syndrome
Abstract

The level of detection was highest when platelets were gated using the CD42b marker, suggesting a competition between patient autoantibodies and CD41/CD61, which stain for integrin SB IIb sb SB 3 sb . To investigate whether the patient had anti-platelet autoantibodies, we isolated platelets from healthy controls ( I n i = 8) as previously described[14] and incubated these with either control or patient plasma, in the presence/absence of platelet inhibitors (apyrase and prostaglandin E1) or collagen. Flow cytometry results clearly indicated that the patient presented both IgG and IgA against platelets. Glanzmann's thrombasthenia (GT) is a rare haemostatic disorder characterised by an impaired function of integrin SB IIb sb SB 3 sb . [Extracted from the article]

Published
2023
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26. Single-cell analysis reveals immune dysfunction from the earliest stages of CLL that can be reversed by ibrutinib

Author

Purroy, Noelia, Tong, Yuzhou Evelyn, Lemvigh, Camilla K., Cieri, Nicoletta, Li, Shuqiang, Parry, Erin M., Zhang, Wandi, Rassenti, Laura Z., Kipps, Thomas J., Slager, Susan L., Kay, Neil E., Lesnick, Connie, Shanafelt, Tait D., Ghia, Paolo, Scarfò, Lydia, Livak, Kenneth J., Kharchenko, Peter V., Neuberg, Donna S., Olsen, Lars Rønn, Fan, Jean, Gohil, Satyen H., and Wu, Catherine J.

Published
2022
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27. Distinct cellular dynamics associated with response to CAR-T therapy for refractory B-cell lymphoma

Author

Haradhvala, Nicholas J., primary, Leick, Mark B., additional, Maurer, Katie, additional, Gohil, Satyen H., additional, Larson, Rebecca C., additional, Yao, Ning, additional, Gallagher, Kathleen M. E., additional, Katsis, Katelin, additional, Frigault, Matthew J., additional, Southard, Jackson, additional, Li, Shuqiang, additional, Kann, Michael C., additional, Silva, Harrison, additional, Jan, Max, additional, Rhrissorrakrai, Kahn, additional, Utro, Filippo, additional, Levovitz, Chaya, additional, Jacobs, Raquel A., additional, Slowik, Kara, additional, Danysh, Brian P., additional, Livak, Kenneth J., additional, Parida, Laxmi, additional, Ferry, Judith, additional, Jacobson, Caron, additional, Wu, Catherine J., additional, Getz, Gad, additional, and Maus, Marcela V., additional

Published
2022
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30. Low seropositivity and suboptimal neutralisation rates in patients fully vaccinated against COVID‐19 with B‐cell malignancies

Author

Fox, Thomas A., primary, Kirkwood, Amy A., additional, Enfield, Louise, additional, O'Reilly, Maeve, additional, Arulogun, Suzanne, additional, D'Sa, Shirley, additional, O'Nions, Jenny, additional, Kavi, Janki, additional, Vitsaras, Evan, additional, Townsend, William, additional, Burns, Siobhan O., additional, Gohil, Satyen H., additional, Cwynarski, Kate, additional, Thomson, Kirsty J., additional, Noursadeghi, Mahdad, additional, Heyderman, Robert S., additional, Rampling, Tommy, additional, Ardeshna, Kirit M., additional, McCoy, Laura E., additional, and Morris, Emma C., additional

Published
2021
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31. Baseline Immune State and T Cell Clonal Kinetics Are Associated with Response to CAR-T Therapy in Large B-Cell Lymphoma

Author

Maurer, Katie, Grabski, Isabella N., Houot, Roch, Gohil, Satyen H, Miura, Shogo, Redd, Robert A., Lyu, Haoxiang, Lu, Wesley S, Miles, Brodie, Mattie, Mike, Arihara, Yohei, McDonough, Mikaela M., Reynolds, Carol, Ansuinelli, Michela, Li, Shuqiang, Livak, Kenneth J., Ritz, Jerome, Rodig, Scott, Irizarry, Rafael A., Armand, Philippe, Wu, Catherine J, and Jacobson, Caron A.

Published
2023
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32. Bendamustine Plus Brentuximab Has Superior Efficacy to Brentuximab Monotherapy As Third-Line Treatment for Classical Hodgkin Lymphoma: A Real-World, Multicentre UK Analysis

Author

Shotton, Rohan, Kirkwood, Amy A, Northend, Michael, Fathoala, Dina, Burton, Kieran, Ferguson, Graeme, Aiken, Laura, Shrubsole, Caroline, Henry, Lauren, Owen, Mary, Oliver, Rebecca, Martinez-Calle, Nicolas, Etherington, Astrid, Gallop-Evans, Eve, Burton, Cathy, Miall, Fiona, Osborne, Wendy, Le Dieu, Rifca, McKay, Pamela, Gohil, Satyen H, Collins, Graham P., and Phillips, Elizabeth H

Published
2023
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35. Massively parallel single-cell mitochondrial DNA genotyping and chromatin profiling

Author

Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Lareau, Caleb A, Ludwig, Leif S, Muus, Christoph, Gohil, Satyen H, Zhao, Tongtong, Chiang, Zachary, Pelka, Karin, Verboon, Jeffrey M, Luo, Wendy, Christian, Elena, Rosebrock, Daniel, Getz, Gad, Boland, Genevieve M, Chen, Fei, Buenrostro, Jason D, Hacohen, Nir, Wu, Catherine J, Aryee, Martin J, Regev, Aviv, Sankaran, Vijay G, Massachusetts Institute of Technology. Department of Biology, Koch Institute for Integrative Cancer Research at MIT, Lareau, Caleb A, Ludwig, Leif S, Muus, Christoph, Gohil, Satyen H, Zhao, Tongtong, Chiang, Zachary, Pelka, Karin, Verboon, Jeffrey M, Luo, Wendy, Christian, Elena, Rosebrock, Daniel, Getz, Gad, Boland, Genevieve M, Chen, Fei, Buenrostro, Jason D, Hacohen, Nir, Wu, Catherine J, Aryee, Martin J, Regev, Aviv, and Sankaran, Vijay G

Abstract

© 2020, The Author(s), under exclusive licence to Springer Nature America, Inc. Natural mitochondrial DNA (mtDNA) mutations enable the inference of clonal relationships among cells. mtDNA can be profiled along with measures of cell state, but has not yet been combined with the massively parallel approaches needed to tackle the complexity of human tissue. Here, we introduce a high-throughput, droplet-based mitochondrial single-cell assay for transposase-accessible chromatin with sequencing (scATAC-seq), a method that combines high-confidence mtDNA mutation calling in thousands of single cells with their concomitant high-quality accessible chromatin profile. This enables the inference of mtDNA heteroplasmy, clonal relationships, cell state and accessible chromatin variation in individual cells. We reveal single-cell variation in heteroplasmy of a pathologic mtDNA variant, which we associate with intra-individual chromatin variability and clonal evolution. We clonally trace thousands of cells from cancers, linking epigenomic variability to subclonal evolution, and infer cellular dynamics of differentiating hematopoietic cells in vitro and in vivo. Taken together, our approach enables the study of cellular population dynamics and clonal properties in vivo.

Published
2021

37. Local and Systemic Effects of Immune Checkpoint Blockade on Relapsed Myeloid Malignancies Following Allogeneic Hematopoietic Stem Cell Transplantation

Author

Penter, Livius, primary, Zhang, Yi, additional, Savell, Alexandra, additional, Ranasinghe, Srinika, additional, Huang, Teddy, additional, Cieri, Nicoletta, additional, Gohil, Satyen H, additional, Zhang, Wandi, additional, Li, Shuqiang, additional, Zeiser, Robert, additional, Kim, Haesook T., additional, Livak, Kenneth J., additional, Ritz, Jerome, additional, Neuberg, Donna S., additional, Soiffer, Robert J., additional, Liu, X. Shirley, additional, Davids, Matthew S., additional, Bachireddy, Pavan, additional, and Wu, Catherine J., additional

Published
2020
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38. Massively parallel single-cell mitochondrial DNA genotyping and chromatin profiling

Author

Lareau, Caleb A., primary, Ludwig, Leif S., additional, Muus, Christoph, additional, Gohil, Satyen H., additional, Zhao, Tongtong, additional, Chiang, Zachary, additional, Pelka, Karin, additional, Verboon, Jeffrey M., additional, Luo, Wendy, additional, Christian, Elena, additional, Rosebrock, Daniel, additional, Getz, Gad, additional, Boland, Genevieve M., additional, Chen, Fei, additional, Buenrostro, Jason D., additional, Hacohen, Nir, additional, Wu, Catherine J., additional, Aryee, Martin J., additional, Regev, Aviv, additional, and Sankaran, Vijay G., additional

Published
2020
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39. Distinct evolutionary paths in chronic lymphocytic leukemia during resistance to graft-versus-leukemia

Author

Bachireddy, Pavan, primary, Ennis, Christina, additional, Nguyen, Vinhkhang N., additional, Clement, Kendell, additional, Gohil, Satyen H., additional, Shukla, Sachet A., additional, Forman, Juliet, additional, Barkas, Nikolas, additional, Freeman, Samuel, additional, Bavli, Natalie, additional, Elagina, Liudmila, additional, Leshchiner, Ignaty, additional, Mohammad, Arman W., additional, Rassenti, Laura Z, additional, Kipps, Thomas J, additional, Brown, Jennifer R., additional, Getz, Gad A., additional, Ho, Vincent T., additional, Gnirke, Andreas, additional, Neuberg, Donna, additional, Soiffer, Robert J., additional, Ritz, Jerome, additional, Alyea, Edwin P., additional, Kharchenko, Peter V., additional, and Wu, Catherine J., additional

Published
2020
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40. T Cell Determinants of Response and Resistance to PD-1 Blockade in Richter's Transformation

Author

Parry, Erin, primary, Lemvigh, Camilla K, primary, Anandappa, Annabelle J, primary, Li, Shuqiang, primary, Werner, Lillian, primary, Lako, Ana, primary, Purroy, Noelia, primary, Gohil, Satyen H, primary, Oliveira, Giacomo, primary, Bachireddy, Pavan, primary, Huang, Teddy, primary, Leshchiner, Ignaty, primary, Martinez, Aina Zurita, primary, Olsen, Lars Ronn, primary, Livak, Kenneth, primary, Getz, Gad, primary, Neuberg, Donna S, primary, Rodig, Scott J, primary, Wierda, William G., primary, Kharchenko, Peter, primary, Jain, Nitin, primary, and Wu, Catherine J., primary

Published
2019
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41. Distinct Evolutionary Patterns in Chronic Lymphocytic Leukemia (CLL) during Resistance to Graft-Versus-Leukemia (GvL)

Author

Bachireddy, Pavan, primary, Ennis, Christina, primary, Nguyen, Vinhkhang N, primary, Barkas, Nikolas, primary, Shukla, Sachet, primary, Clement, Kendell, primary, Freeman, Samuel, primary, Gohil, Satyen H, primary, Bavli, Natalie, primary, Elagina, Liudmila, primary, Leshchiner, Ignaty, primary, Brown, Jennifer R., primary, Getz, Gad, primary, Ho, Vincent T., primary, Neuberg, Donna S, primary, Soiffer, Robert J., primary, Ritz, Jerome, primary, Alyea, Edwin P., primary, Kharchenko, Peter, primary, and Wu, Catherine J., primary

Published
2019
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42. A single-cell and single-nucleus RNA-seq toolbox for fresh and frozen human tumors

Author

Slyper, Michal, primary, Porter, Caroline B. M., additional, Ashenberg, Orr, additional, Waldman, Julia, additional, Drokhlyansky, Eugene, additional, Wakiro, Isaac, additional, Smillie, Christopher, additional, Smith-Rosario, Gabriela, additional, Wu, Jingyi, additional, Dionne, Danielle, additional, Vigneau, Sébastien, additional, Jané-Valbuena, Judit, additional, Napolitano, Sara, additional, Su, Mei-Ju, additional, Patel, Anand G., additional, Karlstrom, Asa, additional, Gritsch, Simon, additional, Nomura, Masashi, additional, Waghray, Avinash, additional, Gohil, Satyen H., additional, Tsankov, Alexander M., additional, Jerby-Arnon, Livnat, additional, Cohen, Ofir, additional, Klughammer, Johanna, additional, Rosen, Yanay, additional, Gould, Joshua, additional, Li, Bo, additional, Nguyen, Lan, additional, Wu, Catherine J., additional, Izar, Benjamin, additional, Haq, Rizwan, additional, Hodi, F. Stephen, additional, Yoon, Charles H., additional, Hata, Aaron N., additional, Baker, Suzanne J., additional, Suvà, Mario L., additional, Bueno, Raphael, additional, Stover, Elizabeth H., additional, Matulonis, Ursula A., additional, Clay, Michael R., additional, Dyer, Michael A., additional, Collins, Natalie B., additional, Wagle, Nikhil, additional, Rotem, Asaf, additional, Johnson, Bruce E., additional, Rozenblatt-Rosen, Orit, additional, and Regev, Aviv, additional

Published
2019
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44. Cytotoxic CD4+ Cells in Chronic Lymphocytic Leukaemia: An Extended Immunophenotypic Analysis Examining Their Association with Cytomegalovirus Serostatus and Similarities with Cytotoxic CD8+ Cells

Author

Marzolini, Maria A V, primary, Akarca, Ayse, additional, Teng, Karen, additional, Marafioti, Teresa, additional, Gohil, Satyen H, additional, Nathwani, Amit C, additional, Newell, Evan, additional, Quezada, Sergio A, additional, and Peggs, Karl S, additional

Published
2018
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46. Acquired Glanzmann's thrombasthenia with IgG and IgA against activated αIIbβ3.

Author

Constantinescu‐Bercu, Adela, McCann, Sabina, Hmaid, Amjad, de Groot, Rens, Singh, Deepak, Gohil, Satyen H., Thomas, Mari, Scully, Marie, and Westwood, John‐Paul

Subjects
*IMMUNOGLOBULIN G, *MENORRHAGIA, *ANTIPHOSPHOLIPID syndrome, *MUCOSA-associated lymphoid tissue lymphoma, *POST-acute COVID-19 syndrome
Abstract

The level of detection was highest when platelets were gated using the CD42b marker, suggesting a competition between patient autoantibodies and CD41/CD61, which stain for integrin SB IIb sb SB 3 sb . To investigate whether the patient had anti-platelet autoantibodies, we isolated platelets from healthy controls ( I n i = 8) as previously described[14] and incubated these with either control or patient plasma, in the presence/absence of platelet inhibitors (apyrase and prostaglandin E1) or collagen. Flow cytometry results clearly indicated that the patient presented both IgG and IgA against platelets. Glanzmann's thrombasthenia (GT) is a rare haemostatic disorder characterised by an impaired function of integrin SB IIb sb SB 3 sb . [Extracted from the article]

Published
2023
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47. Single cell analysis reveals immune dysfunction from the earliest stages of CLL that can be reversed by ibrutinib

Author

Noelia Purroy, Yuzhou Evelyn Tong, Camilla K. Lemvigh, Nicoletta Cieri, Shuqiang Li, Erin M. Parry, Wandi Zhang, Laura Z. Rassenti, Thomas J. Kipps, Susan L. Slager, Neil E. Kay, Connie Lesnick, Tait D. Shanafelt, Paolo Ghia, Lydia Scarfò, Kenneth J. Livak, Peter V. Kharchenko, Donna S. Neuberg, Lars Rønn Olsen, Jean Fan, Satyen H. Gohil, Catherine J. Wu, Purroy Zuriguel, Noelia, Tong, Yuzhou Evelyn, Lemvigh, Camilla K, Cieri, Nicoletta, Li, Shuqiang, Parry, Erin M, Zhang, Wandi, Rassenti, Laura Z, Kipps, Thomas J, Slager, Susan L, Kay, Neil E, Lesnick, Connie, Shanafelt, Tait D, Ghia, Paolo, Scarfò, Lydia, Livak, Kenneth J, Kharchenko, Peter V, Neuberg, Donna, Olsen, Lars Ronn, Fan, Jean, Gohil, Satyen H, and Wu, Catherine J

Subjects
Piperidines, Adenine, Immunology, Humans, Cell Biology, Hematology, Single-Cell Analysis, Letter to Blood, Biochemistry, Leukemia, Lymphocytic, Chronic, B-Cell, Protein Kinase Inhibitors
Published
2022

48. Tracking Rare Single Donor and Recipient Immune and Leukemia Cells after Allogeneic Hematopoietic Cell Transplantation Using Mitochondrial DNA Mutations.

Author

Penter L, Cieri N, Maurer K, Kwok M, Lyu H, Lu WS, Oliveira G, Gohil SH, Leshchiner I, Lareau CA, Ludwig LS, Neuberg DS, Kim HT, Li S, Bullinger L, Ritz J, Getz G, Garcia JS, Soiffer RJ, Livak KJ, and Wu CJ

Subjects
Humans, Male, Female, Adult, Middle Aged, Leukemia genetics, Leukemia therapy, Leukemia immunology, Single-Cell Analysis methods, Tissue Donors, Hematopoietic Stem Cell Transplantation methods, DNA, Mitochondrial genetics, Mutation, Transplantation, Homologous
Abstract

Combined tracking of clonal evolution and chimeric cell phenotypes could enable detection of the key cellular populations associated with response following therapy, including after allogeneic hematopoietic stem cell transplantation (HSCT). We demonstrate that mitochondrial DNA (mtDNA) mutations coevolve with somatic nuclear DNA mutations at relapse post-HSCT and provide a sensitive means to monitor these cellular populations. Furthermore, detection of mtDNA mutations via single-cell assay for transposase-accessible chromatin with select antigen profiling by sequencing (ASAP-seq) simultaneously determines not only donor and recipient cells but also their phenotype at frequencies of 0.1% to 1%. Finally, integration of mtDNA mutations, surface markers, and chromatin accessibility profiles enables the phenotypic resolution of leukemic populations from normal immune cells, thereby providing fresh insights into residual donor-derived engraftment and short-term clonal evolution following therapy for post-transplant leukemia relapse. As throughput evolves, we envision future development of single-cell sequencing-based post-transplant monitoring as a powerful approach for guiding clinical decision-making. Significance: mtDNA mutations enable single-cell tracking of leukemic clonal evolution and donor-recipient origin following allogeneic HSCT. This provides unprecedented insight into chimeric cellular phenotypes of early immune reconstitution, incipient relapse, and quality of donor engraftment with immediate translational potential for future clinical post-transplant monitoring and decision-making., (©2024 American Association for Cancer Research.)

Published
2024
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