Background

In 30-percent of neuroblastoma cases aberrant activity of the MYCN-gene is present. Current therapies for high-risk MYCN-driven neuroblastoma are ineffective, and only 40% of children with disease can achieve long-term event-free survival. These realities underscore the urgent need to discover novel therapeutic strategies that are more effective in combating neuroblastoma.

Background

Background

While most types of childhood leukemia are routinely cured with therapy, juvenile myelomonocytic leukemia (JMML), a type of blood cancer that affects young children remains exceedingly difficult to treat. Even when cured, the infants and toddlers affected by this disorder have difficulty tolerating the required treatment, which can be very intense. Equally frustrating, it is challenging to predict who will respond to the treatments we currently have versus those that will require experimental therapy in order to cure them of their cancer.

Background

Sarcomas are cancers that derive from soft tissue including skeletal muscle, fat, and connective tissue. The Amatruda lab uses zebrafish that express human cancer genes as a model to study sarcoma origins and their underlying biology. Zebrafish share over 70% of their genes with humans, and approximately 84% of known human disease genes have a zebrafish counterpart.

Project Goal

Background

Following on the completion of the Human Genome Project and using innovative sequencing tools researchers are rapidly annotating the complete repertoire of genetic alterations in cancer. However most of these lesions are located in genomic "dark matter" outside of well-annotated genes.

Project Goal

In this research project we will develop state-of-the-art new tools to analyze the function of critical as yet un-annotated genomic sequences controlling the activity of MYC, a major cancer-driving gene.