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6. Oligoclonal T-cell expansion in a patient with bone marrow failure after CD19 CAR-T therapy for Richter-transformed DLBCL

Author

Rejeski, Kai, primary, Wu, Zhijie, additional, Blumenberg, Viktoria, additional, Kunz, Wolfgang G., additional, Müller, Susanna, additional, Kajigaya, Sachiko, additional, Gao, Shouguo, additional, Bücklein, Veit L., additional, Frölich, Lisa, additional, Schmidt, Christian, additional, von Bergwelt-Baildon, Michael, additional, Feng, Xingmin, additional, Young, Neal S., additional, and Subklewe, Marion, additional

Published
2022
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11. Myelodysplasia and Bone Marrow Manifestations of Somatic UBA1 Mutated Autoinflammatory Disease

Author

Obiorah, Ifeyinwa Emmanuela, primary, Beck, David B., additional, Wang, Weixin, additional, Ombrello, Amanda, additional, Ferrada, Marcela A, additional, Wu, Zhijie, additional, Sikora, Keith A, additional, Trick, Megan A, additional, Dulau-Florea, Alina, additional, Patel, Bhavisha A, additional, Groarke, Emma, additional, Burgess, Shawn M., additional, Werner, Achim A, additional, Aksentijevich, Ivona A, additional, Young, Neal S., additional, Kastner, Daniel L, additional, Grayson, Peter C, additional, and Calvo, Katherine R., additional

Published
2020
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12. Somatic Mutations in a Single Residue of UBA1 Cause Vexas, a Severe Adult-Onset Rheumatic Disease Associated with Myeloid Dysplasia

Author

Beck, David B., primary, Wu, Zhijie, additional, Patel, Bhavisha A, additional, Ferrada, Marcela A, additional, Sikora, Keith A, additional, Ombrello, Amanda, additional, Dulau Florea, Alina E., additional, Wang, Weixin, additional, Groarke, Emma M., additional, Burgess, Shawn M., additional, Aksentijevich, Ivona A, additional, Werner, Achim A, additional, Young, Neal S., additional, Calvo, Katherine R., additional, Kastner, Daniel L, additional, and Grayson, Peter C, additional

Published
2020
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15. Single-Cell RNA Sequencing Reveals a Distinct Transcriptome Signature of Hematopoiesis in GATA2 Deficiency

Author

Wu, Zhijie, primary, Gao, Shouguo, additional, Kajigaya, Sachiko, additional, Chen, Jinguo, additional, Shi, Rongye, additional, Diamond, Carrie, additional, Palmer, Cindy, additional, Hsu, Amy P., additional, Calvo, Katherine R., additional, Hickstein, Dennis D., additional, Holland, Steven M., additional, and Young, Neal S., additional

Published
2019
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16. Eltrombopag Improves Hematopoiesis in Patients with Low to Intermediate-2 Risk Myelodysplastic Syndrome (MDS)

Author

Vicente, Alana, primary, Gutierrez-Rodrigues, Fernanda, additional, Giudice, Valentina, additional, Wu, Zhijie, additional, Kajigaya, Sachiko, additional, Fernandez Ibanez, Maria del Pilar, additional, Albitar, Maher, additional, Weinstein, Barbara, additional, Calvo, Katherine R., additional, Townsley, Danielle M., additional, Scheinberg, Phillip, additional, Dunbar, Cynthia E., additional, Young, Neal S., additional, and Winkler, Thomas, additional

Published
2018
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21. Single-Cell RNA-Seq Reveals the Differentiation Hierarchy of Normal Human Bone Marrow and a Distinct Transcriptome Signature of Monosomy 7 Cells

Author

Zhao, Xin, primary, Gao, Shouguo, additional, Feng, Xingmin, additional, Liu, Delong, additional, Kajigaya, Sachiko, additional, Wu, Zhijie, additional, Liu, Qingguo, additional, Keyvanfar, Keyvan, additional, Desierto, Marie J., additional, Townsley, Danielle M., additional, Wang, Xujing, additional, and Young, Neal S., additional

Published
2016
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24. Myelodysplasia and Bone Marrow Manifestations of Somatic UBA1Mutated Autoinflammatory Disease

Author

Obiorah, Ifeyinwa Emmanuela, Beck, David B., Wang, Weixin, Ombrello, Amanda, Ferrada, Marcela A, Wu, Zhijie, Sikora, Keith A, Trick, Megan A, Dulau-Florea, Alina, Patel, Bhavisha A, Groarke, Emma, Burgess, Shawn M., Werner, Achim A, Aksentijevich, Ivona A, Young, Neal S., Kastner, Daniel L, Grayson, Peter C, and Calvo, Katherine R.

Abstract

Somatic mutations in UBA1in hematopoietic stem cells and myeloid cells have recently been described and are associated with adult-onset severe autoinflammatory diseases including relapsing polychondritis, Sweet syndrome, polyarteritis nodosa, and giant cell arteritis. This newly defined syndrome is named VEXAS (vacuoles, E1, X-linked, autoinflammatory, somatic). We performed clinicopathologic, cytogenetic, flow cytometric and molecular bone marrow assessment of 15 patients diagnosed with VEXAS and peripheral cytopenias. All patients were male, with a median age of 64y (IQR 45-80) and all had somatic missense mutations affecting the p.Met41 residue in UBA1with variant allele frequencies (VAF) over 20% from peripheral blood or bone marrow samples and with lineage restriction to mature myeloid cells. Germline mutations at this residue are not reported in any public databases. Peripheral blood findings included macrocytic anemia in all patients (100%), thrombocytopenia in 9/15, and neutropenia in 1/15. All bone marrow aspirates (15/15; 100%) showed prominent vacuolization of both myeloid and erythroid precursors with few vacuoles noted in mature cells. Of the 9 patients tested for serum copper levels all were normal or borderline low. Marrow was hypercellular with granulocytic and megakaryocytic hyperplasia in 12/15 (80%). Definitive WHO criteria for MDS was met in 5/15 (40%) with 3 cases of MDS-MLD, and 2 of MDS-SLD. The remaining cases were suspicious for MDS with low or borderline levels of dyspoiesis that did not exceed greater than 10% of cells in respective lineages meeting criteria for clonal cytopenia of undetermined significance (CCUS). Of the MDS cases, dysplasia was seen in megakaryocytes (5/5), myeloid (2/5) and erythroid (1/5) precursors. Cytogenetic abnormalities were detected in 2/5 MDS patients involving t(3;12)(q21;q13) in one case, and del (5q)/del (13q) in another case. Next generation sequencing analyses were performed in 9/15 patients and showed mutations in DNMT3Ain 2/5 MDS cases (VAF 43% and 44%), CSF1Rin 1/5 MDS (VAF 3.1%), GNA11in 1/5 MDS (VAF3.3%) and EZH2mutation (VAF 22%) in one of the patients without overt MDS. Clonal plasma cell or B-cell populations were diagnosed in 6/15 patients with 3 plasma cell dyscrasias, and 2 cases of monoclonal B-cell lymphocytosis. The most common abnormalities detected by bone marrow flow cytometry analysis were severely reduced or absent B-cell precursors, inverted CD4:CD8 ratios and abnormal expression of CD56 on monocytes.

Published
2020
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26. Crispr/Cas9-Induced DNMT3AMutations in the K562 Human Leukemic Cell Line As a Model of DNMT3A-Mutated Leukemogenesis

Author

Banaszak, Lauren G., Giudice, Valentina, Zhao, Xin, Wu, Zhijie, Hosokawa, Kohei, Keyvanfar, Keyvan, Townsley, Danielle, Kajigaya, Sachiko, and Young, Neal S.

Abstract

Background:DNA methyltransferase 3A(DNMT3A) is a member of the DNA methyltransferase family primarily involved in de novogene methylation. Mutations in DNMT3Aare associated with a wide range of hematological malignancies, most frequently acute myeloid leukemia (AML). DNMT3Amutations are thought to produce a pre-leukemic state, rendering cells vulnerable to secondary oncogenic mutations and malignant transformation. Mutations in DNMT3Aoften coexist with secondary lesions in leukemia-related genes such as NPM1and FLT3(Ley T et al., N Engl J Med, 2010). Furthermore, healthy individuals harboring DNMT3A-driven clonal hematopoiesis are at increased risk of future hematologic malignancies and all-cause mortality (Jaiswal S et al., N Engl J Med, 2014). Despite these important clinical associations, the mechanisms by which DNMT3Amutations contribute to malignant transformation have not been well-defined. Dnmt3a-knockout (KO)mouse hematopoietic stem cells (HSCs) preferentially self-renew rather than undergo differentiation, leading to their accumulation in the bone marrow (Challen GA et al., Nat Genet, 2011). DNMT3Aloss has also been shown to drive hypomethylation and subsequent activation of leukemia-related genes (Lu R et al., Cancer Cell, 2016; Yang L et al., Cancer Cell, 2016). However, these findings have not been recapitulated using human tissue. The goals of this study were thus to determine the transcriptional and biological effects of DNMT3Amutations which contribute towards malignant transformation in human cells.

Published
2016
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