ArticleOncotarget2015
LCK over-expression drives STAT5 oncogenic signaling in PAX5 translocated BCP-ALL patients.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Dasatinib Produces Lengthy Remissions of Extramedullary Leukemia: A Retrospective Observational Study.European journal of haematology · 2026Observational
- Genetics of B-Cell Acute Lymphoblastic Leukemia (B-ALL): Recent Updates and Indian Perspective.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2025Review
- PAX Family, Master Regulator in Cancer.Diagnostics (Basel, Switzerland) · 2025Review
- A Self-Activating IL-15 Chimeric Cytokine Receptor to Empower Cancer Immunotherapy.ImmunoTargets and therapy · 2024Article
- Review
- Review
- New horizons in drug discovery of lymphocyte-specific protein tyrosine kinase (Lck) inhibitors: a decade review (2011-2021) focussing on structure-activity relationship (SAR) and docking insights.Journal of enzyme inhibition and medicinal chemistry · 2021Review
- Beyond TCR Signaling: Emerging Functions of Lck in Cancer and Immunotherapy.International journal of molecular sciences · 2019Review
- Biophysical basis underlying dynamic Lck activation visualized by ZapLck FRET biosensor.Science advances · 2019Article
- Akt and STAT5 mediate naïve human CD4+ T-cell early metabolic response to TCR stimulation.Nature communications · 2019Article
- The Src family kinase LCK cooperates with oncogenic FLT3/ITD in cellular transformation.Scientific reports · 2017Article
- Molecular role of the PAX5-ETV6 oncoprotein in promoting B-cell acute lymphoblastic leukemia.The EMBO journal · 2017Article
- A genome wide transcriptional model of the complex response to pre-TCR signalling during thymocyte differentiation.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PAX5 gene is altered in 30% of BCP-ALL patients and PAX5 chromosomal translocations account for 2-3% of cases. Although PAX5 fusion genes significantly affect the transcription of PAX5 target genes, their role in sustaining leukemia cell survival is poorly understood. In an in vitro model of PAX5/ETV6 leukemia, we demonstrated that Lck hyper-activation, and down-regulation of its negative regulator Csk, lead to STAT5 hyper-activation and consequently to the up-regulation of the downstream effectors, cMyc and Ccnd2. More important, cells from PAX5 translocated patients show LCK up-regulation and over-activation, as well as STAT5 hyper-phosphorylation, compared to PAX5 wt and PAX5 deleted cases. As in BCR/ABL1 positive ALL, the hyper-activation of STAT5 pathway can represent a survival signal in PAX5 translocated cells, alternative to the pre-BCR, which is down-regulated. The LCK inhibitor BIBF1120 selectively reverts this phenomenon both in the murine model and in leukemic primary cells. LCK inhibitor could therefore represent a suitable candidate drug to target this subgroup of ALL patients.
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Registered trials
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