Although great strides have been made in the improvement of outcome for newly diagnosed pediatric acute lymphoblastic leukemia because of refinements in risk stratification and selective intensification of therapy, the prognosis for relapsed leukemia has lagged behind significantly. Understanding the underlying biological pathways responsible for drug resistance is essential to develop novel approaches for the prevention of recurrence and treatment of relapsed disease. High throughput genomic technologies have the potential to revolutionize cancer care in this era of personalized medicine. Using such advanced technologies, we and others have shown that a diverse assortment of cooperative genetic and epigenetic events drive the resistant phenotype. Herein, we summarize results using a variety of genomic technologies to highlight the power of this methodology in providing insight into the biological mechanisms that impart resistant disease.
Division of Pediatric Hematology-Oncology, New York University Cancer Institute, New York University Langone Medical Center, New York, NY
Supported by the National Institute of Health (NIH) 5 R01 CA 140729-04 (WLC), the Ira Sohn Conference Foundation grant (T.B.), NIH Training in Pharmacological Sciences T32 GM066704 (C.L.J.), the American Society of Hematology Research Training Awards for fellows (N.A.V.), the Silber Pediatric Leukemia Fund, and “Jackson Takes Action” Fund.
The authors declare no conflict of interest.
Reprints: Teena Bhatla, MD, Division of Pediatric Hematology-Oncology, New York University Cancer Institute, New York University Langone Medical Center, Smilow 1206, 522 First Avenue New York NY 10016 (e-mail: email@example.com).
Received December 31, 2013
Accepted April 25, 2014