Yana Pikman, MD
Co-Director, Hematologic Malignancy Program; Attending Physician, Dana-Farber/Boston Children's Cancer and Blood Disorders Center; Investigator, Hematological Malignancy Disease Center
Assistant Professor of Pediatrics, Harvard Medical School
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Yana Pikman, MD
Co-Director, Hematologic Malignancy Program; Attending Physician, Dana-Farber/Boston Children's Cancer and Blood Disorders Center; Investigator, Hematological Malignancy Disease Center
Assistant Professor of Pediatrics, Harvard Medical School
Medical Services
Languages
English
Russian
Education
Medical School
Harvard Medical School
2007
Boston
MA
Internship
Boston Combined Residency Program (BCRP)
2008
Boston
MA
Residency
Pediatrics
Boston Combined Residency Program (BCRP)
2010
Boston
MA
Fellowship
Pediatric Hematology/Oncology
Boston Children's Hospital/Dana-Farber Cancer Institute
2013
Boston
MA
Certifications
American Board of Pediatrics (Hematology-Oncology)
Publications
CEBPA repression by MECOM blocks differentiation to drive aggressive leukemias. View Abstract
Nucleotide depletion promotes cell fate transitions by inducing DNA replication stress. View Abstract
Mezigdomide is effective alone and in combination with menin inhibition in preclinical models of KMT2A-r and NPM1c AML. View Abstract
Pathophysiology of Acute Myeloid Leukemia. View Abstract
Inherent genome instability underlies trisomy 21-associated myeloid malignancies. View Abstract
Splicing modulators impair DNA damage response and induce killing of cohesin-mutant MDS and AML. View Abstract
IKZF1 Alterations and Therapeutic Targeting in B-Cell Acute Lymphoblastic Leukemia. View Abstract
ETV6 fusions from insertions of exons 3-5 in pediatric hematologic malignancies. View Abstract
Treatment of recurrent pediatric myelodysplastic syndrome post hematopoietic stem cell transplantation. View Abstract
Integration of Genomic Sequencing Drives Therapeutic Targeting of PDGFRA in T-Cell Acute Lymphoblastic Leukemia/Lymphoblastic Lymphoma. View Abstract
DHODH: a promising target in the treatment of T-cell acute lymphoblastic leukemia. View Abstract
Outlier Expression of Isoforms by Targeted or Total RNA Sequencing Identifies Clinically Significant Genomic Variants in Hematolymphoid Tumors. View Abstract
Impact of cytoreduction and remission status on hematopoietic cell transplantation outcomes in pediatric myelodysplastic syndrome and related disorders. View Abstract
A single-institution pediatric and young adult interventional oncology collaborative: Novel therapeutic options for relapsed/refractory solid tumors. View Abstract
Unleashing Cell-Intrinsic Inflammation as a Strategy to Kill AML Blasts. View Abstract
Rapid next-generation sequencing aids in diagnosis of transient abnormal myelopoiesis in a phenotypically normal newborn. View Abstract
IKAROS and MENIN coordinate therapeutically actionable leukemogenic gene expression in MLL-r acute myeloid leukemia. View Abstract
Hypoxic, glycolytic metabolism is a vulnerability of B-acute lymphoblastic leukemia-initiating cells. View Abstract
The menin-MLL1 interaction is a molecular dependency in NUP98-rearranged AML. View Abstract
SHMT2 inhibition disrupts the TCF3 transcriptional survival program in Burkitt lymphoma. View Abstract
Targeting serine hydroxymethyltransferases 1 and 2 for T-cell acute lymphoblastic leukemia therapy. View Abstract
Targeting acute myeloid leukemia dependency on VCP-mediated DNA repair through a selective second-generation small-molecule inhibitor. View Abstract
Matched Targeted Therapy for Pediatric Patients with Relapsed, Refractory, or High-Risk Leukemias: A Report from the LEAP Consortium. View Abstract
Corrigendum. View Abstract
Targeting the Ras pathway in pediatric hematologic malignancies. View Abstract
Targeting the Ras pathway in pediatric hematologic malignancies. View Abstract
Identification of prognostic factors in childhood T-cell acute lymphoblastic leukemia: Results from DFCI ALL Consortium Protocols 05-001 and 11-001. View Abstract
The Folate Cycle Enzyme MTHFR Is a Critical Regulator of Cell Response to MYC-Targeting Therapies. View Abstract
Targeting EZH2 for the treatment of hepatosplenic T-cell lymphoma. View Abstract
Resistance Mechanisms to SYK Inhibition in Acute Myeloid Leukemia. View Abstract
Targeted therapy for fusion-driven high-risk acute leukemia. View Abstract
Phase I trial of the mTOR inhibitor everolimus in combination with multi-agent chemotherapy in relapsed childhood acute lymphoblastic leukemia. View Abstract
Exploiting an Asp-Glu "switch" in glycogen synthase kinase 3 to design paralog-selective inhibitors for use in acute myeloid leukemia. View Abstract
The creatine kinase pathway is a metabolic vulnerability in EVI1-positive acute myeloid leukemia. View Abstract
Synergistic Drug Combinations with a CDK4/6 Inhibitor in T-cell Acute Lymphoblastic Leukemia. View Abstract
Targeting MTHFD2 in acute myeloid leukemia. View Abstract
A Prospective Cohort Quality Improvement Study to Reduce the Time to Antibiotics for New Fever in Neutropenic Pediatric Oncology Inpatients. View Abstract
SYK is a critical regulator of FLT3 in acute myeloid leukemia. View Abstract
Pulmonary hypertension associated with scurvy and vitamin deficiencies in an autistic child. View Abstract
The OTT-MAL fusion oncogene activates RBPJ-mediated transcription and induces acute megakaryoblastic leukemia in a knockin mouse model. View Abstract
Genetic profiling of myeloproliferative disorders by single-nucleotide polymorphism oligonucleotide microarray. View Abstract
The CDK-activating kinase (CAK) Csk1 is required for normal levels of homologous recombination and resistance to DNA damage in fission yeast. View Abstract
Advances in the molecular characterization of Philadelphia-negative chronic myeloproliferative disorders. View Abstract
MPL515 mutations in myeloproliferative and other myeloid disorders: a study of 1182 patients. View Abstract
MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. View Abstract
Peters anomaly in association with multiple midline anomalies and a familial chromosome 4 inversion. View Abstract
Expression of a homodimeric type I cytokine receptor is required for JAK2V617F-mediated transformation. View Abstract