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 Blood, 15 November 2005, Vol. 106, No. 10, pp. 3532-3537.
Prepublished online as a Blood First Edition Paper on July 28, 2005; DOI 10.1182/blood-2005-04-1640.

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NEOPLASIA

In vitro profiling of the sensitivity of pediatric leukemia cells to tipifarnib: identification of T-cell ALL and FAB M5 AML as the most sensitive subsets

Bianca F. Goemans, Christian M. Zwaan, Amy Harlow, Anne H. Loonen, Brenda E. S. Gibson, Karel Hählen, Dirk Reinhardt, Ursula Creutzig, Michael C. Heinrich, and Gertjan J. L. Kaspers

From the Department of Pediatric Oncology/Hematology, VU university medical center, Amsterdam, The Netherlands; Department of Pediatric Hematology/Oncology, Erasmus MC Sophia Children's Hospital, Rotterdam, The Netherlands; Division of Hematology and Medical Oncology, Department of Medicine, Oregon Health Sciences University Cancer Institute and Portland VA Medical Center, Portland, OR; MRC Childhood Leukaemia Working Party, Glasgow, United Kingdom; Dutch Childhood Oncology Group, The Hague, The Netherlands; and the AML-BFM Study Group, Münster, Germany.

Although the prognosis of pediatric leukemias has improved considerably, many patients still have relapses. Tipifarnib, a farnesyl transferase inhibitor (FTI), was developed to target malignancies with activated RAS, including leukemia. We tested 52 pediatric acute myeloid leukemia (AML) and 36 pediatric acute lymphoblastic leukemia (ALL) samples for in vitro sensitivity to tipifarnib using a total cell-kill assay and compared these results to those obtained with normal bone marrow (N BM) samples (n = 25). AML samples were significantly more sensitive to tipifarnib compared to B-cell precursor ALL (BCP ALL) or N BM samples. Within AML, French-American-British (FAB) M5 samples were most sensitive to tipifarnib. T-cell ALL samples were significantly more sensitive than BCP ALL and N BM samples. In AML there was a marked correlation between tipifarnib resistance and daunorubicin or etoposide resistance, but not to cytarabine or 6-thioguanine. RAS mutations were present in 32% of AML and 18% of ALL samples, but there was no correlation between RAS mutational status and sensitivity to tipifarnib. Future studies are needed to identify biomarkers predictive of tipifarnib sensitivity. In addition, clinical studies, especially in T-cell ALL, seem warranted.


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