In vivo ablation of NF-κB cascade effectors alleviates disease burden in myeloproliferative neoplasms. Blood. 2024; 143:2414-2424.
.Metabolic reprogramming regulated by TRAF6 contributes to the leukemia progression. Leukemia. 2024; 38:1032-1045.
.ASXL1 mutations are associated with a response to alvocidib and 5-azacytidine combination in myelodysplastic neoplasms. Haematologica: the hematology journal. 2024; 109:1426-1438.
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. Abstract 1464: Smoking carcinogen-induced inflammation promotes lung carcinogenesis via IRAK4 activation. Cancer Research.2024; 84:3092.
. Abstract 3092: MICRO-TAG: A novel fluorescence-based real-time cellular target engagement platform for drug discovery. Cancer Research.2024; 3:1339870.
. Research and clinical updates on IRAK4 and its roles in inflammation and malignancy: themes and highlights from the 1st symposium on IRAK4 in cancer.2023; 142:2762.
. UBE2N Regulates Oncoprotein Networks in Myeloid Malignancies. Blood.2023; 142:1410.
. The Mechanism of Therapy Resistance By Lineage Plasticity in AML and How to Overcome It. Blood.2023; 142:1544.
. Therapeutic Targeting of FLT3 Gate Keeper Mutation with E2082-0047 in Traditional and a Novel Immunocompetent Murine Adoptive Transfer Model of AML. Blood.2023; 142:1391.
. The Zymogen Form of Caspase-1 Is Required to Fine Tune Excessive Cell-Intrinsic Inflammation in Acute Myeloid Leukemia. Blood.2023; 142:4152.
. Kme-0584, a Highly Potent IRAK1/IRAK4/panFLT3 Inhibitor, Is a Promising Clinical Candidate for Hypomethylating Agent Plus Venetoclax Resistant AML/MDS Patients. Blood.2023; 142:5765.
. Targeting CREB-Binding Protein (CREBBP) Overcomes Resistance to Azacitidine and Venetoclax Therapy in Acute Myeloid Leukemia (AML). Blood.2023; 142:1394.
. Defective Necroptosis Mediates Chemotherapy Resistance in AML. Blood.2023; 142:991.
. In Vivo Ablation of NFκB Cascade Effectors Alleviates Disease Burden in Myeloproliferative Neoplasms. Blood.2023; 142:45.
. Synthetic Lethal Interactions with IRAK4 Inhibition in Myeloid Malignancies. Blood.2023; 142:1370.
. Regulation of Metabolic Homeostasis By TRAF6 Contributes to the Leukemia Progression. Blood.Classification, risk stratification and response assessment in myelodysplastic syndromes/neoplasms (MDS): A state-of-the-art report on behalf of the International Consortium for MDS (icMDS). Blood Reviews. 2023; 62:101128.
.Are DDX41 variants of unknown significance and pathogenic variants created equal?. Haematologica: the hematology journal. 2023; 108:2883-2885.
.Discordant pathologic diagnoses of myelodysplastic neoplasms and their implications for registries and therapies. Blood Advances. 2023; 7:6120-6129.
.Inactivation of p53 provides a competitive advantage to del(5q) myelodysplastic syndrome hematopoietic stem cells during inflammation. Haematologica: the hematology journal. 2023; 108:2715-2729.
.Paralog-specific signaling by IRAK1/4 maintains MyD88-independent functions in MDS/AML. Blood. 2023; 142:989-1007.
.Repression of TRIM13 by chromatin assembly factor CHAF1B is critical for AML development. Blood Advances. 2023; 7:4822-4837.
.RUNX1 mutations mitigate quiescence to promote transformation of hematopoietic progenitors in Fanconi anemia. Leukemia. 2023; 37:1698-1708.
.Current landscape of translational and clinical research in myelodysplastic syndromes/neoplasms (MDS): Proceedings from the 1st International Workshop on MDS (iwMDS) Of the International Consortium for MDS (icMDS). Blood Reviews. 2023; 60:101072.
.An agenda to advance research in myelodysplastic syndromes: a TOP 10 priority list from the first international workshop in MDS. Blood Advances. 2023; 7:2709-2714.
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. Abstract A46: Heterozygous mutations in DDX41 cause erythroid progenitor cell defects and cooperate with p53 mutations to cause hematologic malignancy.2023; 83:2759.
. Abstract 2759: Real-time cellular target engagement and protein quantification for drug discovery. Cancer Research.2023; 124:s35.
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.Finding consistency in classifications of myeloid neoplasms: a perspective on behalf of the International Workshop for Myelodysplastic Syndromes. Leukemia. 2022; 36:2939-2946.
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. TRIM13 Is a Novel Cell Cycle Hub Regulated By CHAF1B to Promote Acute Myeloid Leukemogenesis. Blood.2022; 140:2240-2241.
. IRAK1 Contributes to IRAK4 Inhibitor Resistance Via Non-Canonical Signaling Mechanisms in MDS/AML. Blood.2022; 140:5830.
. UBE2N Is a Druggable Target and an Essential Ubiquitin-Conjugating Enzyme in Myeloid Malignancies. Blood.2022; 140:9749-9750.
. ASXL1 Mutations Are Associated with a Response to the Combination of Alvocidib and 5-Azacytidine in Higher-Risk Myelodysplastic Syndromes. Blood.2022; 140:5949-5950.
. Inhibition of Both IRAK1 and IRAK4 Is Required for Complete Suppression of NF-Kb Signaling across Multiple Receptor-Mediated Pathways in MDS and AML. Blood.2022; 140:975-976.
. A Circulating Microbial Metabolite Drives the Clonal Expansion of Pre-Leukemic Cells. Blood.The Impact of Inflammation-Induced Tumor Plasticity during Myeloid Transformation. Cancer Discovery. 2022; 12:2392-2413.
.Activation of targetable inflammatory immune signaling is seen in myelodysplastic syndromes with SF3B1 mutations. eLife. 2022; 11.
.IKAROS and MENIN in synergy in AML. Nature Cancer. 2022; 3:528-529.
.Blocking UBE2N abrogates oncogenic immune signaling in acute myeloid leukemia. Science Translational Medicine. 2022; 14:eabb7695.
.Momelotinib is a highly potent inhibitor of FLT3-mutant AML. Blood Advances. 2022; 6:1186-1192.
.TRAF6 functions as a tumor suppressor in myeloid malignancies by directly targeting MYC oncogenic activity. Cell Stem Cell. 2022; 29:298-314.e9.
.The deubiquitinase USP15 modulates cellular redox and is a therapeutic target in acute myeloid leukemia. Leukemia. 2022; 36:438-451.
.IRAK1 and IRAK4 as emerging therapeutic targets in hematologic malignancies. Current Opinion in Hematology. 2022; 29:8-19.
.Mitochondrial Fragmentation Triggers Ineffective Hematopoiesis in Myelodysplastic Syndromes. Cancer Discovery. 2022; 12:250-269.
.Germline DDX41 mutations cause ineffective hematopoiesis and myelodysplasia. Cell Stem Cell. 2021; 28:1966-1981.e6.
.TNF-α-induced alterations in stromal progenitors enhance leukemic stem cell growth via CXCR2 signaling. Cell Reports. 2021; 36:109386.
.Innate immune pathways and inflammation in hematopoietic aging, clonal hematopoiesis, and MDS. The Journal of Experimental Medicine. 2021; 218.
.Sequential CRISPR gene editing in human iPSCs charts the clonal evolution of myeloid leukemia and identifies early disease targets. Cell Stem Cell. 2021; 28:1074-1089.e7.
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. Systemic inflammation recruits fast-acting anti-inflammatory innate myeloid progenitors from BM into lymphatics. eLife.Inflammation rapidly recruits mammalian GMP and MDP from bone marrow into regional lymphatics. eLife. 2021; 10.
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. 81030 Utilizing a synergistic drug combination to target relapsed/refractory FLT3 mutant AML. Journal of Clinical and Translational Science.TNFAIP3 Plays a Role in Aging of the Hematopoietic System. Frontiers in Immunology. 2020; 11:536442.
.FBXO11 is a candidate tumor suppressor in the leukemic transformation of myelodysplastic syndrome. Blood Cancer Journal. 2020; 10:98.
.HHEX expression drives AML development. Blood. 2020; 136:1575-1576.
.TIFA and TIFAB: FHA-domain proteins involved in inflammation, hematopoiesis, and disease. Experimental Hematology. 2020; 90:18-29.
.Adaptive response to inflammation contributes to sustained myelopoiesis and confers a competitive advantage in myelodysplastic syndrome HSCs. Nature Immunology. 2020; 21:535-545.
.Targeting AML-associated FLT3 mutations with a type I kinase inhibitor. The Journal of Clinical Investigation. 2020; 130:2017-2023.
.TIFAB Regulates USP15-Mediated p53 Signaling during Stressed and Malignant Hematopoiesis. Cell Reports. 2020; 30:2776-2790.e6.
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