Leah Billington
A5041199089- Chronic Lymphocytic Leukemia Research
- Acute Lymphoblastic Leukemia research
- Acute Myeloid Leukemia Research
- Renal Diseases and Glomerulopathies
- Calcium signaling and nucleotide metabolism
- Carbohydrate Chemistry and Synthesis
- Immunodeficiency and Autoimmune Disorders
- Pancreatic function and diabetes
- PI3K/AKT/mTOR signaling in cancer
- Epigenetics and DNA Methylation
- Advanced Breast Cancer Therapies
- Chronic Myeloid Leukemia Treatments
- Glycosylation and Glycoproteins Research
- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Genetic Syndromes and Imprinting
- Single-cell and spatial transcriptomics
- Monoclonal and Polyclonal Antibodies Research
Dana-Farber Cancer Institute
2019-2023
Transformation to aggressive disease histologies generates formidable clinical challenges across cancers, but biological insights remain few. We modeled the genetic heterogeneity of chronic lymphocytic leukemia (CLL) through multiplexed in vivo CRISPR-Cas9 B-cell editing recurrent CLL loss-of-function drivers mice and recapitulated process transformation from indolent into large cell lymphoma [i.e., Richter syndrome (RS)]. Evolutionary trajectories 64 carrying diverse combinatorial gene...
Abstract Chronic lymphocytic leukemia (CLL) is characterized by disordered DNA methylation, suggesting these epigenetic changes might play a critical role in disease onset and progression. The methyltransferase DNMT3A key regulator of methylation. Although somatic mutations CLL are rare, we found that low expression associated with more aggressive disease. A conditional knockout mouse model showed homozygous depletion Dnmt3a from B cells results the development 100% penetrance at median age...
<div>Abstract<p>Chronic lymphocytic leukemia (CLL) is characterized by disordered DNA methylation, suggesting these epigenetic changes might play a critical role in disease onset and progression. The methyltransferase <i>DNMT3A</i> key regulator of methylation. Although somatic mutations CLL are rare, we found that low expression associated with more aggressive disease. A conditional knockout mouse model showed homozygous depletion <i>Dnmt3a</i> from B...
<p>Supplementary Materials and Methods Supplementary Figures S1-4</p>
<p>Supplementary Tables contain Supplementary S1-17</p>
<p>Supplementary Materials and Methods Supplementary Figures S1-4</p>
<p>Supplementary Tables contain Supplementary S1-17</p>
<div>Abstract<p>Chronic lymphocytic leukemia (CLL) is characterized by disordered DNA methylation, suggesting these epigenetic changes might play a critical role in disease onset and progression. The methyltransferase <i>DNMT3A</i> key regulator of methylation. Although somatic mutations CLL are rare, we found that low expression associated with more aggressive disease. A conditional knockout mouse model showed homozygous depletion <i>Dnmt3a</i> from B...
<div>Abstract<p>Transformation to aggressive disease histologies generates formidable clinical challenges across cancers, but biological insights remain few. We modeled the genetic heterogeneity of chronic lymphocytic leukemia (CLL) through multiplexed <i>in vivo</i> CRISPR-Cas9 B-cell editing recurrent CLL loss-of-function drivers in mice and recapitulated process transformation from indolent into large cell lymphoma [i.e., Richter syndrome (RS)]. Evolutionary...
<p>Supplementary file contains a PDF version of supplementary figures S1-S7 and associated figure legends.</p>
<div>Abstract<p>Transformation to aggressive disease histologies generates formidable clinical challenges across cancers, but biological insights remain few. We modeled the genetic heterogeneity of chronic lymphocytic leukemia (CLL) through multiplexed <i>in vivo</i> CRISPR-Cas9 B-cell editing recurrent CLL loss-of-function drivers in mice and recapitulated process transformation from indolent into large cell lymphoma [i.e., Richter syndrome (RS)]. Evolutionary...
<p>Supplementary file contains a PDF version of supplementary figures S1-S7 and associated figure legends.</p>