AALL0622: Intensified Tyrosine Kinase Inhibitor Therapy (Dasatinib: IND# 73969, NSC# 732517) in Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia/ Therapy for New Diagnosis Very High Risk Disease

Why are we doing this research?

This study builds on the experience of AALL0031 which safely incorporated imatinib into an intensive chemotherapy backbone for pediatric patients with Ph+ ALL. The proposed treatment plan intensifies AALL0031 TKI therapy and includes substitution of dasatinib for imatinib. AALL0622 patients will receive dasatinib during Induction and during each post-Induction treatment block prior to Maintenance therapy. Concomitant use of filgrastim with dasatinib will be included in AALL0622 as was done in AALL0031 for imatinib.

Who can participate?

Newly diagnosed acute lymphoblastic leukemia (ALL)

  • Definitive evidence of BCR-ABL fusion (Philadelphia chromosome positive [PH+]) from an approved Children's Oncology Group (COG) cytogenetics laboratory
  • Concurrent enrollment on COG-AALL03B1 (or a successor trial) AND a front-line COG ALL clinical trial (e.g., COG-AALL0232, COG-AALL0331, COG-AALL0434 or other front-line COG ALL clinical trial) required
  • Received the first 2 weeks of induction therapy (days 1-14) as specified in the front-line COG ALL clinical trial
  • Patients may NOT have received day 15 of induction therapy on the front-line COG ALL clinical trial prior to enrollment on this study
  • No Down syndrome

Conditions

  • Adult Studies

Gender

  • Female
  • Male

What will happen in the study?

A total number of 195 patients will be enrolled on this study.

An orally bioavailable synthetic small molecule-inhibitor of SRC-family protein-tyrosine kinases. Dasatinib binds to and inhibits the growth-promoting activities of these kinases. Apparently because of its less stringent binding affinity for the BCR-ABL kinase, dasatinib has been shown to overcome the resistance to imatinib of chronic myeloid leukemia (CML) cells harboring BCR-ABL kinase domain point mutations. SRC-family protein-tyrosine kinases interact with variety of cell-surface receptors and participate in intracellular signal transduction pathways; tumorigenic forms can occur through altered regulation or expression of the endogenous protein and by way of virally-encoded kinase genes.

Contact

Rebecca Turner, MS, CCRP
Cincinnati Children's Hospital Medical Center
Division of Hematology / Oncology
3333 Burnet Ave. Cincinnati, OH 45229-3039
Phone: 513-636-2799
cancer@cchmc.org