Area of research
Hematology · Molecular Biology
Research interest
Research interests include Acute Myeloid Leukemia Research, Epigenetics and DNA Methylation, Myeloproliferative Neoplasms: Diagnosis and Treatment, and Hemoglobinopathies and Related Disorders.
Pyrimethamine overcomes resistance to hypomethylating agents by reducing de novo pyrimidine synthesis
Epigenetic drug remedies for SCD root cause pathophysiology.
Combining drugs that bypass p53 to treat TP53-mutated leukemias.
Data from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Table 3 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Table 4 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Table 7 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Table 6 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Table 2 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Data from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Supplementary Table 1 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Table 5 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Supplementary Figures S1-S7 from Cytokine-Regulated Phosphorylation and Activation of TET2 by JAK2 in Hematopoiesis
Table S1 from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
A weekly low-dose regimen of decitabine and venetoclax is efficacious and less myelotoxic in a racially diverse cohort.
Oncotherapy resistance explained by Darwinian and Lamarckian models.
A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML.
Combinatorial targeting of epigenome-modifying enzymes with decitabine and RN-1 synergistically increases HbF
Pharmacokinetics and pharmacodynamics of an oral formulation of decitabine and tetrahydrouridine.
Neuroendocrine lineage commitment of small cell lung cancers can be leveraged into p53-independent non-cytotoxic therapy
Combinatorial targeting of epigenome-modifying enzymes with decitabine and RN-1 synergistically increases HbF.
Table S1 from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Data from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Table S1 from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Table S1 from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Table S1 from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Data from A Metabolically Optimized, Noncytotoxic Low-Dose Weekly Decitabine/Venetoclax in MDS and AML
Eltrombopag inhibits TET dioxygenase to contribute to hematopoietic stem cell expansion in aplastic anemia
Changing paradigms in oncology: Toward noncytotoxic treatments for advanced gliomas
Changing paradigms in oncology: Toward noncytotoxic treatments for advanced gliomas.