Ina Radtke

TL;DR: It is suggested that direct disruption of pathways controlling B-cell development and differentiation contributes to B-progenitor ALL pathogenesis and the power of high-resolution, genome-wide approaches to identify new molecular lesions in cancer.

TL;DR: Using hematopoietic progenitors, a signaling-based measure of cellular phenotype was defined, which led to isolation of a gene expression signature that was predictive of survival in independent cohorts, yielding insights into AML pathophysiology.

TL;DR: In this paper, a cohort of 221 children with high-risk B-cell-progenitor ALL with the use of single-nucleotide-polymorphism microarrays, transcriptional profiling, and resequencing of samples obtained at diagnosis were studied.

TL;DR: Genetic lesions resulting in the loss of Ikaros function are an important event in the development of BCR–ABL1 ALL, according to genome-wide analysis of diagnostic leukaemia samples.

TL;DR: It is seen that murine AMLs harboring two common human AML genotypes show remarkably diverse responses to conventional therapy that mirror clinical experience, and the p53 network is functionally established as a central determinant of chemotherapy response in AML.