Washington University

Washington University

660 South Euclid Avenue, Campus Box 8018

St. Louis, MO 63110

United States

Investigating the non-canonical role of JARID2 in hematopoietic stem cell self-renewal

Leukemia

Mentor: Dr. Grant Challen

RNA-ECS to Quantify Rare Clonal RNA Species at Diagnosis, Remission and Relapse from the COG AAML1031 Study

Acute Myeloid Leukemia (AML)

Targeting KDM6B in Pediatric Leukemia

Leukemia, Acute Lymphoblastic Leukemia (ALL)

The Role of Inherited MLL3 Single Nucleotide Variants and Fetal Epigenetic Programming in Infant Leukemogenesis

Leukemia

Background

My goal is to improve treatments for infant leukemia patients and genetic counseling efforts for their families. To realize this goal, we will develop mouse models to study the interactions between MLL translocations (the most common mutation in infant leukemia) and inherited genetic variants that potentially predispose to infant leukemia – in this case variants in the MLL3 gene. Mice are the optimal model for these studies because they are genetically tractable and mouse blood development closely approximates human blood development.

A Cell-type Specific Checkpoint Limits Proliferation in Early B Cells

Acute Lymphoblastic Leukemia (ALL)

Background

Pre-B acute lymphoblastic leukemia (pre-B ALL) is the most common malignancy in children. However, remarkably little is known about the molecular basis of the initiation and maintenance of this leukemia. In pre-B ALL, B cell development is arrested at an early developmental stage and the leukemic blasts hijack normal developmental signaling to support their survival and proliferation.

A Computational Analysis of Altered Chromatin Structure and Hematopoietic Development in Infant Leukemia

Acute Myeloid Leukemia (AML)

Background

Infantile leukemia (IL) is the most fatal form of childhood leukemia, which arises in utero due to mechanisms that are incompletely defined. The MLL gene is rearranged in about 70% of IL cases. However, in a lab setting, introducing MLL mutations into model organisms does not recreate IL, suggesting there are other genetic factors at work.

Epigenetic Reprogramming for Cancer Therapy

Leukemia

Background

Epigenetics refer to heritable changes in gene expression that are not associated with changes in the DNA sequence. DNA methylation is a key epigenetic mark responsible for regulating gene expression. When present in high levels, functions to repress gene expression. The aberrant distribution of DNA methylation is associated with the development of many forms of cancer. Thus the ability to modulate oncogenic epigenetic marks would prove advantageous in developing novel prevention and treatment options.

Epigenetic Modifiers as Therapeutic Targets in Pediatric T-cell Acute Lymphoblastic Leukemia - John Nikitas (2015)

Acute Lymphoblastic Leukemia (ALL)

Background

Acute lymphoblastic leukemia (ALL) is the most common cancer in children. Approximately 15% of newly diagnosed ALL cases in children arise from dysfunctional T-cells. T-cell ALL (T-ALL) patients are historically linked with a poor prognosis. We have shown in a mouse model that T-cells lacking Dnmt3a, an enzyme that establishes the DNA methylation epigenetic mark, show reduced differentiation capacity and are more susceptible to cancer development in a NOTCH1-driven model of T-ALL.

Function of IKZF1 in DNA Damage Responses in Normal and Malignant Pre-B Cells

Leukemia, Lymphoma

Developing Personalized (precision) Medicine Strategies to Optimize Pediatric Brain Tumor Management

Astrocytoma, Brain Tumors, Glioma

Alex's Lemonade Stand Foundation for Childhood Cancer