IRAK1/4/pan-FLT3 Kinase Inhibitors with Reduced hERG Block as Treatments for Acute Myeloid Leukemia. ACS Medicinal Chemistry Letters. 2025; 16:887-895.
.Splicing regulatory dynamics for precision analysis and treatment of heterogeneous leukemias. Science Translational Medicine. 2025; 17:eadr1471.
.Reducing clinical trial eligibility barriers for patients with MDS: an icMDS position statement. Blood. 2025; 145:1369-1381.
.TIFAB modulates metabolic pathways in KMT2A::MLLT3-induced AML through HNF4A. Blood Advances. 2025; 9:844-855.
.Smoking-Associated Carcinogen-Induced Inflammation Promotes Lung Carcinogenesis via IRAK4 Activation. Clinical Cancer Research. 2025; 31:746-755.
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.Chemotherapy resistance in acute myeloid leukemia is mediated by A20 suppression of spontaneous necroptosis. Nature Communications. 2024; 15:9189.
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. Abstract A017: IGF2BP1 is essential for ETO2/GLIS2 leukemogenesis via stabilization of primitive myeloid transcriptional programs. Molecular Cancer Therapeutics.Discovery of IRAK1/4/pan-FLT3 Kinase Inhibitors as Treatments for Acute Myeloid Leukemia. ACS Medicinal Chemistry Letters. 2024; 15:1843-1851.
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. Single-Cell Multi-Omic Analysis of KMT2A-Rearranged Pediatric Acute Leukemia Clonal Evolution. Blood.2024; 144:4572.
. The Zymogen Form of Caspase-1 Is Required to Finetune Excessive Cell-Intrinsic Inflammation in Myelodysplastic Syndromes. Blood.2024; 144:2713.
. Codon-Specific Differences in RAS Mutations in AML and Differential Response to Therapeutic Agents. Blood.DDX41 haploinsufficiency causes inefficient hematopoiesis under stress and cooperates with p53 mutations to cause hematologic malignancy. Leukemia. 2024; 38:1787-1798.
.Dysregulated innate immune signaling cooperates with RUNX1 mutations to transform an MDS-like disease to AML. iScience. 2024; 27:109809.
.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. Frontiers in Hematology.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.
.2023; 4:a46.
. Abstract A46: Heterozygous mutations in DDX41 cause erythroid progenitor cell defects and cooperate with p53 mutations to cause hematologic malignancy. Blood Cancer Discovery.2023; 83:2759.
. Abstract 2759: Real-time cellular target engagement and protein quantification for drug discovery. Cancer Research.2023; 124:s70.
. 3040 – HETEROZYGOUS MUTATIONS IN DDX41 CAUSE ERYTHROID PROGENITOR CELL DEFECTS AND COOPERATE WITH P53 MUTATIONS TO CAUSE HEMATOLOGIC MALIGNANCY. Experimental Hematology.2023; 124:s35.
. 1031 – FROM PRE-LEUKEMIC STATES TO MALIGNANT TRANSFORMATION: UNRAVELING THE ROLE OF DYSREGULATED INNATE IMMUNE SIGNALING AND INFLAMMATION IN MYELOID MALIGNANCIES. Experimental Hematology.Innate immune mediator, Interleukin-1 receptor accessory protein (IL1RAP), is expressed and pro-tumorigenic in pancreatic cancer. Journal of Hematology and Oncology. 2022; 15:70.
.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:e78136.
.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:e20201544.
.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:e66190.
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. 81030 Utilizing a synergistic drug combination to target relapsed/refractory FLT3 mutant AML. Journal of Clinical and Translational Science.