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Blood, Vol. 113, Issue 1, 117-126, January 1, 2009 This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef Stratification of pediatric ALL by in vitro cellular responses to DNA double-strand breaks provides insight into the molecular mechanisms underlying clinical response Blood Marston et al. 113: 117 Supplemental materials for: Marston et al Files in this Data Supplement: Table S1. Response to treatment of paediatric B-precursor ALLs with two types of in vitro response to DNA DSBs (PDF, 12.4 KB) Figure S1. Event-free survival of 74 ALL patients according to the apoptosis status in vitro (JPG, 22.7 KB) - Patients with IR apoptosis resistant phenotype in vitro show no significant difference in event-free survival compared to the apoptosis sensitive patients. Figure S2. Differential increased phosphorylation of tyrosine receptor kinases (RTKs) in apoptosis resistant tumours before and after IR (JPG, 70.4 KB) - (A) Before IR apoptosis resistant tumour 106 exhibits comparatively increased phosphorylation of RTK Flt-3 and ALL 102 reveals increased phosphorylation of Erb B4. (B) One hour after IR resistant ALL 102 exhibits comparatively induced phosphorylation of multiple RTKs (Erb B3, FGF R4, HGF R, SCF R, VEGF R1 and VEGF R2); (C) whereas resistant ALL141 displays IR-induced phosphorylation of FGF R3, Insulin R and IGF-IR, resistant ALL111 induced phosphorylation of FGF R3 and ALL106 moderate induction of Mer phosphorylation. This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef

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