Baylor College of Medicine

Cell metabolism is a key aspect of cell biology. Tumors frequently have significant alterations in the specific types of nutrients they require and the way in which they use these nutrients. Certain genes are often associated with driving these critical changes in tumor cell metabolism, which in turn define their aggressive nature. In particular, MYCN, a potent gene that is altered in several pediatric cancers, such as neuroblastoma, is capable of driving defined changes in tumor metabolism.

Interrogating the Enhancer Landscapes of Ependymoma to Inform Novel Therapies

Ependymoma

This project originated at The Cleveland Clinic in Cleveland, OH. Effective July 2017, Dr. Mack has accepted a new position will be completing his Young Investigator project at Baylor.

Genetically Engineered T Cells as Therapy for Pediatric Glioma

Brain Tumors, Glioma

Background

Optimizing a CD5 CAR Approach to Treat Children with T cell Leukemia and Lymphoma

Non-Hodgkin Lymphoma

Background

T cells transduced with CD19 chimeric antigen receptors (CARs) have had dramatic therapeutic effects in children with B cell acute lymphoblastic leukemia (ALL). This strategy has now progressed to licensing trials. However, utilizing CARs to target T cell malignancies is challenging due to shared expression of most targetable antigens between malignant and normal T cells. This potentially leads to killing CAR expressing T cells.

RECQL4 Expression in RTS Patient Cells

Osteosarcoma

Background

Our laboratory is interested in finding better treatments for osteosarcoma (OS), the most common malignant primary bone tumor in children and adolescents. Survival rates for patients with OS have not changed for more than 30 years. We have been studying a rare genetic disorder called Rothmund-Thomson syndrome (RTS) as a model for OS development, where 2/3 of patients have germline mutations in a gene called RECQL4 (Type II RTS). These patients have an extremely high and specific risk for developing OS.

Investigating the Role of Nucleophosmin as a Novel Caspase-2 Target in Pediatric Leukemia

Leukemia

Background

The tumor suppressor caspase-2’s levels are decreased in the childhood forms of acute leukemia, including T-lineage acute lymphoblastic leukemia (T-ALL) and acute myeloid leukemia (AML). The main role of caspase-2 is to induce a form of cell death called apoptosis but it has also been shown to prevent cell division. Therefore, caspase-2 may protect against leukemia by apoptosis or by stopping cell division.

Alex's Lemonade Stand Foundation for Childhood Cancer