5 results on '"Wenbin Xiao"'
Search Results
2. ETV6-FLT3–positive myeloid/lymphoid neoplasm with eosinophilia presenting in an infant: an entity distinct from JMML
- Author
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Ryma Benayed, Nancy Bouvier, Filemon S. Dela Cruz, Mikhail Roshal, Glorymar D. Ibanez Sanchez, Yanming Zhang, Neerav Shukla, Alina Markova, Barbara Spitzer, Andrew L. Kung, Wenbin Xiao, and M. Irene Rodriguez-Sanchez
- Subjects
Adult ,Oncology ,medicine.medical_specialty ,Myeloid ,Lymphoma ,hemic and lymphatic diseases ,Internal medicine ,Eosinophilia ,medicine ,Humans ,Lymphoid neoplasms ,Leukemia ,Myeloproliferative Disorders ,Juvenile myelomonocytic leukemia ,business.industry ,Infant ,Hematopoietic stem cell ,Hematology ,medicine.disease ,ETV6 ,medicine.anatomical_structure ,Leukemia, Myelomonocytic, Juvenile ,fms-Like Tyrosine Kinase 3 ,Exceptional Case Report ,medicine.symptom ,business ,Ex vivo - Abstract
Myeloid/lymphoid neoplasm with eosinophilia (MLN-Eo) is a World Health Organization (WHO) established category of hematologic malignancies primarily arising in adults. We discuss an 8-month-old infant who presented with clinical features similar to those of juvenile myelomonocytic leukemia (JMML) but who was diagnosed with MLN-Eo driven by an ETV6-FLT3 fusion. Results of patient-derived leukemia ex vivo studies demonstrated increased sensitivity to type I FLT3 inhibitors as compared with type II inhibitors. Treatment with the type I inhibitor gilteritinib resulted in complete immunophenotypic and cytogenetic remission. This patient subsequently underwent a hematopoietic stem cell transplant and remains in complete remission 1 year later. This is the youngest patient reported with an ETV6-FLT3 fusion and adds to the mounting reports of FLT3-rearranged MLN-Eo, supporting its addition to the WHO classification. Furthermore, this case highlights the clinical utility of ex vivo drug testing of targeted therapies.
- Published
- 2021
3. Clinical and molecular predictors of response and survival following venetoclax therapy in relapsed/refractory AML
- Author
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Anthony F. Daniyan, Maximilian Stahl, Martin S. Tallman, Alexander Chan, Aaron D. Viny, Sheng F. Cai, Christopher Famulare, Eytan M. Stein, Kamal Menghrajani, Jacob L. Glass, Bernadette M. Cuello, Mikhail Roshal, Omar Abdel-Wahab, Troy Z. Horvat, Aaron D. Goldberg, Andriy Derkach, Amber C. King, Wenbin Xiao, and Ross L. Levine
- Subjects
Oncology ,medicine.medical_specialty ,Myeloid ,Combination therapy ,Azacitidine ,Decitabine ,chemistry.chemical_compound ,Internal medicine ,Antineoplastic Combined Chemotherapy Protocols ,Humans ,Medicine ,Retrospective Studies ,Sulfonamides ,Myeloid Neoplasia ,business.industry ,Venetoclax ,Hematology ,Bridged Bicyclo Compounds, Heterocyclic ,medicine.disease ,Transplantation ,Leukemia, Myeloid, Acute ,Leukemia ,medicine.anatomical_structure ,chemistry ,Cytarabine ,business ,Nucleophosmin ,medicine.drug - Abstract
Azacitidine + venetoclax, decitabine + venetoclax, and low-dose cytarabine + venetoclax are now standard treatments for newly diagnosed older or unfit patients with acute myeloid leukemia (AML). Although these combinations are also commonly used in relapsed or refractory AML (RR-AML), clinical and molecular predictors of response and survival in RR-AML are incompletely understood. We retrospectively analyzed clinical and molecular characteristics and outcomes for 86 patients with RR-AML who were treated with venetoclax combinations. The complete remission (CR) or CR with incomplete hematologic recovery (CRi) rate was 24%, and the overall response rate was 31% with the inclusion of a morphologic leukemia-free state. Azacitidine + venetoclax resulted in higher response rates compared with low-dose cytarabine + venetoclax (49% vs 15%; P = .008). Median overall survival (OS) was 6.1 months, but it was significantly longer with azacitidine + venetoclax compared with low-dose cytarabine + venetoclax (25 vs 3.9 months; P = .003). This survival advantage of azacitidine + venetoclax over low-dose cytarabine + venetoclax persisted when patients were censored for subsequent allogeneic stem cell transplantation (8.1 vs 3.9 months; P = .035). Mutations in NPM1 were associated with higher response rates, whereas adverse cytogenetics and mutations in TP53, KRAS/NRAS, and SF3B1 were associated with worse OS. Relapse was driven by diverse mechanisms, including acquisition of novel mutations and an increase in cytogenetic complexity. Venetoclax combination therapy is effective in many patients with RR-AML, and pretreatment molecular characteristics may predict outcomes. Trials that evaluate novel agents in combination with venetoclax therapy in patients with RR-AML that have adverse risk genomic features are warranted.
- Published
- 2021
4. A JAK2/IDH1-mutant MPN clone unmasked by ivosidenib in an AML patient without antecedent MPN
- Author
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Martin S. Tallman, Robert L. Bowman, Ross L. Levine, Helen S. Tian, Yanming Zhang, Vidushi Durani, Tanmay Mishra, Menglei Zhu, Linde A. Miles, Sarah E. Stump, Wenbin Xiao, Sheng F. Cai, and Nicole L. DelGaudio
- Subjects
0301 basic medicine ,IDH1 ,Pyridines ,business.industry ,Antecedent (logic) ,fungi ,Mutant ,Glycine ,Clone (cell biology) ,food and beverages ,Hematology ,Janus Kinase 2 ,Isocitrate Dehydrogenase ,Clone Cells ,Microbiology ,Leukemia, Myeloid, Acute ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,hemic and lymphatic diseases ,030220 oncology & carcinogenesis ,Humans ,Medicine ,Exceptional Case Report ,business - Abstract
Key Points Myeloid neoplasm (MPN) clones can evolve from acute myeloid leukemia to gain dominance with isocitrate dehydrogenase inhibition. Pro-differentiation agents such as ivosidenib can unmask MPN sequelae.
- Published
- 2020
5. Clonal hematopoiesis in angioimmunoblastic T-cell lymphoma with divergent evolution to myeloid neoplasms
- Author
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Yanming Zhang, Ahmet Dogan, Kseniya Petrova-Drus, Ross L. Levine, Alison J. Moskowitz, Sarah Huet, Steven M. Horwitz, Anita A Kumar, Zachary D. Epstein-Peterson, Allison E. Sigler, Mikhail Roshal, Maria E. Arcila, Natasha Lewis, Wenbin Xiao, Qi Gao, Neval Ozkaya, and Jeeyeon Baik
- Subjects
Angioimmunoblastic T-cell lymphoma ,Mutation ,Myeloid ,Lymphoid Neoplasia ,Cell ,Clone (cell biology) ,Hematology ,T-Lymphocytes, Helper-Inducer ,Biology ,medicine.disease ,medicine.disease_cause ,Lymphoma, T-Cell ,Haematopoiesis ,medicine.anatomical_structure ,Immunoblastic Lymphadenopathy ,medicine ,Cancer research ,T-cell lymphoma ,Humans ,Bone marrow ,Clonal Hematopoiesis - Abstract
TET2 and DNMT3A mutations are frequently identified in T-cell lymphomas of T follicular helper cell origin (TCL-TFH), clonal hematopoiesis (CH), and myeloid neoplasms (MNs). The relationships among these 3 entities, however, are not well understood. We performed comprehensive genomic studies on paired bone marrow and tissue samples as well as on flow cytometry–sorted bone marrow and peripheral blood subpopulations from a cohort of 22 patients with TCL-TFH to identify shared CH-type mutations in various hematopoietic cell compartments. Identical mutations were detected in the neoplastic T-cell and myeloid compartments of 15 out of 22 patients (68%), including TET2 (14/15) and DNMT3A (10/15). Four patients developed MNs, all of which shared CH-type mutations with their TCL-TFH; additional unique genetic alterations were also detected in each patient’s TCL-TFH and MN. These data demonstrate that CH is prevalent in patients with TCL-TFH and that divergent evolution of a CH clone may give rise to both TCL-TFH and MNs.
- Published
- 2020
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