The cryptic chromosomal deletion del(11)(p12p13) as a new activation mechanism of LMO2 in pediatric T-cell acute lymphoblastic leukemia.

TL;DR: Insulated neighborhoods in T cell acute lymphoblastic leukemia (T-ALL) are mapped and it is found that tumor cell genomes contain recurrent microdeletions that eliminate the boundary sites of insulated neighborhoods containing prominent T-ALL proto-oncogenes.

TL;DR: Genome-wide profiling of germline and leukaemic cell DNA has identified novel submicroscopic structural genetic changes and sequence mutations that contribute to leukaemogenesis, define new disease subtypes, affect responsiveness to treatment, and might provide novel prognostic markers and therapeutic targets for personalised medicine.

TL;DR: Wala et al. as discussed by the authors investigated whether proto-oncogenes occur within these structures and whether oncogene activation can occur via disruption of insulated neighborhood boundaries in cancer cells.

TL;DR: This review summarizes recent advances in the understanding of the molecular genetics of T-ALL and defines distinct molecular groups ofT-ALL with specific gene expression signatures and clinicobiological features.

TL;DR: Retrovirus vector insertion can trigger deregulated premalignant cell proliferation with unexpected frequency, most likely driven by retrovirus enhancer activity on the LMO2 gene promoter.

TL;DR: This article identified 255 loci across the human genome that contain genomic imbalances among unrelated individuals, and revealed that half of these regions overlap with genes, and many coincide with segmental duplications or gaps in human genome assembly.

TL;DR: These findings greatly expand the role of activated NOTCH1 in the molecular pathogenesis of human T-ALL and provide a strong rationale for targeted therapies that interfere with NOTCH signaling.

TL;DR: It is shown that five different T cell oncogenes are often aberrantly expressed in the absence of chromosomal abnormalities, and HOX11L2 activation is identified as a novel event in T cell leukemogenesis.