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Article
Signalling input from divergent pathways subverts B cell transformation
Malignant transformation of cells typically involves several genetic lesions, whose combined activity gives rise to cancer1. Here we analyse 1,148 patient-derived B-cell leukaemia (B-ALL) samples, and find that i...
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Article
Author Correction: Metabolic gatekeeper function of B-lymphoid transcription factors
In Fig. 3c of this Letter, the the effects of CRISPR–Cas9-mediated deletion of NR3C1, TXNIP and CNR2 in patient-derived B-lineage leukaemia cells were shown. For curves depicting NR3C1 (left graph), data s for TX...
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Article
Metabolic gatekeeper function of B-lymphoid transcription factors
The B-lymphoid transcription factors PAX5 and IKZF1 restrict the supply of glucose and energy to B cells to levels that are not enough to fuel a driver-oncogene, thereby acting as tumour suppressors and sensit...
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Article
Correction: Corrigendum: Signalling thresholds and negative B-cell selection in acute lymphoblastic leukaemia
Nature 521, 357–361 (2015); doi:10.1038/nature14231 In Extended Data Fig. 3b of this Letter, 52 flow cytometry dot plots with double stainings for CD19 and ITIM-bearing receptors (PECAM1, LAIR1, CD300A and BTL...
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Article
PTEN opposes negative selection and enables oncogenic transformation of pre-B cells
As opposed to its tumor suppressor role in other cancers, PTEN inhibition in pre-B ALL is therapeutically effective and triggers cell death.
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Article
Signalling thresholds and negative B-cell selection in acute lymphoblastic leukaemia
This study shows that, despite malignant transformation, autoimmune checkpoints are still functional in B-cell leukaemia, with targeted activation of these checkpoints effectively killing patient-derived B-cel...
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Article
BCL6 enables Ph+ acute lymphoblastic leukaemia cells to survive BCR–ABL1 kinase inhibition
Targeted cancer therapies are often associated with drug resistance, a phenomenon that has been observed with tyrosine kinase inhibitors (TKIs), widely used to treat leukaemia driven by BCR–ABL1 mutations. Markus...