ArticleLeukemia2019
SH2B3 inactivation through CN-LOH 12q is uniquely associated with B-cell precursor ALL with iAMP21 or other chromosome 21 gain.
Article in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Loss of Heterozygosity in Pediatric Acute Lymphoblastic Leukemia and Its Prognostic Impact: A Retrospective Study.Cancers · 2025Article
- LNK/SH2B3 Loss Exacerbates the Development of Myeloproliferative Neoplasms in CBL-deficient Mice.Stem cell reviews and reports · 2025Article
- Secondary lesions and sensitivity to signaling inhibitors in iAMP21 acute lymphoblastic leukemia.HemaSphere · 2025Article
- Article
- Review
- The Gene Expression Classifier ALLCatchR Identifies B-cell Precursor ALL Subtypes and Underlying Developmental Trajectories Across Age.HemaSphere · 2023Article
- The genomic landscape of acute lymphoblastic leukemia with intrachromosomal amplification of chromosome 21.Blood · 2023Article
- Disruption to the FOXO-PRDM1 axis resulting from deletions of chromosome 6 in acute lymphoblastic leukaemia.Leukemia · 2023Article
- Whole genome sequencing provides comprehensive genetic testing in childhood B-cell acute lymphoblastic leukaemia.Leukemia · 2023Article
- Integrating copy number data of 64 iAMP21 BCP-ALL patients narrows the common region of amplification to 1.57 Mb.Frontiers in oncology · 2023Article
- Characterization of unusual iAMP21 B-lymphoblastic leukemia (iAMP21-ALL) from the Mayo Clinic and Children's Oncology Group.Genes, chromosomes & cancer · 2022Article
- Identification of epigenetic dysregulation gene markers and immune landscape in kidney renal clear cell carcinoma by comprehensive genomic analysis.Frontiers in immunology · 2022Article
- The Role of LNK (SH2B3) in the Regulation of JAK-STAT Signalling in Haematopoiesis.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Advances in the Diagnosis and Treatment of Pediatric Acute Lymphoblastic Leukemia.Journal of clinical medicine · 2021Review
- SH2B3, Transcribed by STAT1, Promotes Glioblastoma Progression Through Transducing IL-6/gp130 Signaling to Activate STAT3 Signaling.Frontiers in cell and developmental biology · 2021Article
- POLQ suppresses interhomolog recombination and loss of heterozygosity at targeted DNA breaks.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Gain of chromosome 21 in hematological malignancies: lessons from studying leukemia in children with Down syndrome.Leukemia · 2020Review
- Constitutive Activation of RAS/MAPK Pathway Cooperates with Trisomy 21 and Is Therapeutically Exploitable in Down Syndrome B-cell Leukemia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Chromosome Abnormalities: New Insights into Their Clinical Significance in Cancer.Molecular therapy oncolytics · 2020Review
- Article
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In more than 30% of B-cell precursor acute lymphoblastic leukaemia (B-ALL), chromosome 21 sequence is overrepresented through aneuploidy or structural rearrangements, exemplified by intrachromosomal amplification of chromosome 21 (iAMP21). Although frequent, the mechanisms by which these abnormalities promote B-ALL remain obscure. Intriguingly, we found copy number neutral loss of heterozygosity (CN-LOH) of 12q was recurrent in iAMP21-ALL, but never observed in B-ALL without some form of chromosome 21 gain. As a consequence of CN-LOH 12q, mutations or deletions of the adaptor protein, SH2B3, were converted to homozygosity. In patients without CN-LOH 12q, bi-allelic abnormalities of SH2B3 occurred, but only in iAMP21-ALL, giving an overall incidence of 18% in this sub-type. Review of published data confirmed a tight association between overrepresentation of chromosome 21 and both CN-LOH 12q and SH2B3 abnormalities in B-ALL. Despite relatively small patient numbers, preliminary analysis linked 12q abnormalities to poor outcome in iAMP21-ALL (p = 0.03). Homology modelling of a leukaemia-associated SH2 domain mutation and in vitro analysis of patient-derived xenograft cells implicated the JAK/STAT pathway as one likely target for SH2B3 tumour suppressor activity in iAMP21-ALL.
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