T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy of thymocytes. Despite improved therapy, relapsing pediatric patients have less than a 30% survival rate. It is therefore important to identify new drug targets for treatment of relapsed T-ALL. In this project,TOX, which is over-expressed in human T-ALL was studied for modulating T-ALL pathogenesis. Through a zebrafish transgenic screen, Tox was shown to act as a collaborating oncogene that increased T-ALL aggression. Data suggest that Tox over-expression results in a HOX11 signature characteristic of rapid cell division, and likely induces molecular pathways in T-ALL pathogenesis unlike T-ALLs expressing only Myc. Uncovering the TOX-regulated molecular pathways may help identify novel drug targets for T-ALL treatment.

• This report represents the work of one or more WPI undergraduate students submitted to the faculty as evidence of completion of a degree requirement. WPI routinely publishes these reports on its website without editorial or peer review.

Creator

• Abdelfattah, Nouran Saied

Contributors

• Lobbardi, Riadh

Publisher

• Worcester Polytechnic Institute

Identifier

• E-project-011013-112920

Advisor

• Adams, David S.
• Heilman, Destin

Year

• 2013

Sponsor

• Harvard Medical School - David Langenau Lab

Date created

• 2013-01-10

Resource type

• Major Qualifying Project

Major

• Interdisciplinary

Rights statement

• In Copyright