A5016322483- Acute Myeloid Leukemia Research
- Protein Degradation and Inhibitors
- Epigenetics and DNA Methylation
- Cancer-related gene regulation
- Histone Deacetylase Inhibitors Research
- Acute Lymphoblastic Leukemia research
- Genomics and Chromatin Dynamics
- Multiple Myeloma Research and Treatments
- RNA Research and Splicing
- Advanced biosensing and bioanalysis techniques
- Chronic Myeloid Leukemia Treatments
- Galectins and Cancer Biology
- Cancer Genomics and Diagnostics
- RNA modifications and cancer
- Chronic Lymphocytic Leukemia Research
- RNA Interference and Gene Delivery
- Hematopoietic Stem Cell Transplantation
- HIV/AIDS drug development and treatment
- CAR-T cell therapy research
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- RNA and protein synthesis mechanisms
- Lymphoma Diagnosis and Treatment
- Gene expression and cancer classification
- T-cell and Retrovirus Studies
- Ubiquitin and proteasome pathways
Harvard University
2011-2023
Boston Children's Hospital
2011-2023
Dana-Farber Cancer Institute
2012-2023
Memorial Sloan Kettering Cancer Center
2012-2018
Kettering University
2017-2018
Cancer Genetics (United States)
2015
Harvard University Press
2011
Brigham and Women's Hospital
2010
Medical University of Silesia
2010
Medical University of Lublin
2010
Leukemia stem cells (LSCs) are capable of limitless self-renewal and responsible for the maintenance leukemia. Because selective eradication LSCs could offer substantial therapeutic benefit, there is interest in identifying signaling pathways that control their development. We studied mouse models acute myelogenous leukemia (AML) induced either by coexpression Hoxa9 Meis1a oncogenes or fusion oncoprotein MLL-AF9. show Wnt/beta-catenin pathway required derived from hematopoietic (HSC) more...
TP53, which encodes the tumor suppressor p53, is most frequently mutated gene in human cancer. The selective pressures shaping its mutational spectrum, dominated by missense mutations, are enigmatic, and neomorphic gain-of-function (GOF) activities have been implicated. We used CRISPR-Cas9 to generate isogenic leukemia cell lines of common TP53 mutations. Functional, DNA-binding, transcriptional analyses revealed loss function but no GOF effects. Comprehensive scanning p53 single-amino acid...
Taking preventive measures Recent technological advances have made it possible to detect, in healthy individuals, premalignant blood cells that are likely progress hematologic cancer. These early detection fueled interest “cancer interception,” the idea drugs designed treat advanced cancer might also be useful for prevention. Uckelmann et al. now provide support this concept a study of mice genetically predisposed develop acute myeloid leukemia. Early administration an epigenetic therapy had...
Abstract Aberrant gene expression is a hallmark of acute leukemias. MYB-driven transcriptional coactivation with CREB-binding protein (CBP)/P300 required for lymphoblastic and myeloid leukemias, including refractory MLL-rearranged Using structure-guided molecular design, we developed peptidomimetic inhibitor MYBMIM that interferes the assembly MYB:CBP/P300 complex rapidly accumulates in nuclei AML cells. Treatment cells led to dissociation cells, its displacement from oncogenic enhancers...
Abstract Menin interacts with oncogenic MLL1-fusion proteins, and small molecules that disrupt these associations are in clinical trials for leukemia treatment. By integrating chromatin-focused genome-wide CRISPR screens genetic, pharmacologic, biochemical approaches, we discovered a conserved molecular switch between the MLL1–Menin MLL3/4–UTX chromatin-modifying complexes dictates response to Menin–MLL inhibitors. safeguards survival by impeding binding of complex at subset target gene...