ArticleLeukemia2001
A new recurrent and specific cryptic translocation, t(5;14)(q35;q32), is associated with expression of the Hox11L2 gene in T acute lymphoblastic leukemia.
Article in Leukemia, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 255 citations in OpenAlex.
- The effect of TLX3 expression on the prognosis of pediatric T cell acute lymphocytic leukemia--a systematic review.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- TCRα rearrangements identify a subgroup of NKL-deregulated adult T-ALLs associated with favorable outcome.Leukemia · 2018Trial
- Trial
- TLX3 regulates CGN progenitor proliferation during cerebellum development and its dysfunction can lead to autism.iScience · 2024Article
- Dual role ofBlood science (Baltimore, Md.) · 2024Review
- Acute lymphoblastic leukaemia.Nature reviews. Disease primers · 2024Review
- Molecular subgroups of T-cell acute lymphoblastic leukemia in adults treated according to pediatric-based GMALL protocols.Leukemia · 2024Article
- Developmental origins shape the paediatric cancer genome.Nature reviews. Cancer · 2024Review
- Cytogenomic characterization of pediatric T-cell acute lymphoblastic leukemia reveals TCR rearrangements as predictive factors for exceptional prognosis.Molecular cytogenetics · 2024Article
- The oncogenetic landscape and clinical impact ofHaematologica · 2023Article
- Article
- TAL1 activation in T-cell acute lymphoblastic leukemia: a novel oncogenic 3' neo-enhancer.Haematologica · 2023Article
- Elevated enhancer-oncogene contacts and higher oncogene expression levels by recurrent CTCF inactivating mutations in acute T cell leukemia.Cell reports · 2023Article
- Review
- Genomes for Kids: The Scope of Pathogenic Mutations in Pediatric Cancer Revealed by Comprehensive DNA and RNA Sequencing.Cancer discovery · 2021Article
- The Role of NKL Homeobox Genes in T-Cell Malignancies.Biomedicines · 2021Review
- Enhancer Hijacking Drives OncogenicCancer discovery · 2021Article
- NKL-Code in Normal and Aberrant Hematopoiesis.Cancers · 2021Review
- An updated account on molecular heterogeneity of acute leukemia.American journal of blood research · 2021Review
- The Genetics and Mechanisms of T-Cell Acute Lymphoblastic Leukemia.Cold Spring Harbor perspectives in medicine · 2020Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
FISH identified a cryptic t(5;14)(q35;q32) in T acute lymphoblastic leukemia (ALL), whereas it was not observed in B ALL samples. This translocation is present in five out of 23 (22%) children and adolescents with T ALL tested. RanBP17, a gene coding for a member of the importin beta protein family, and Hox11Like2, an orphan homeobox gene were mapped close to the chromosome 5 breakpoints and CTIP2, which is highly expressed during normal T cell differentiation, was localized in the vicinity of the chromosome 14 breakpoints. The Hox11L2 gene was found to be transcriptionally activated as a result of the translocation, probably under the influence of CTIP2 transcriptional regulation elements. These data establish the t(5;14)(q35;q32) as a major abnormality, and Hox11 family member activation as an important pathway in T ALL leukemogenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.