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Page 1
Emerging molecular subtypes and therapies in acute lymphoblastic leukemia.
Davis K, Sheikh T, Aggarwal N. Davis K, et al. Semin Diagn Pathol. 2023 May;40(3):202-215. doi: 10.1053/j.semdp.2023.04.003. Epub 2023 Apr 9. Semin Diagn Pathol. 2023. PMID: 37120350 Review.
The established B-ALL entities include B-ALL with BCR::ABL1 fusion, BCR::ABL1-like features, KMT2A rearrangement, ETV6::RUNX1 rearrangement, high hyperdiploidy, hypodiploidy (focusing on near haploid and low hypodiploid), IGH::IL3 rearrangement, TCF3::PBX1 rearrange …
The established B-ALL entities include B-ALL with BCR::ABL1 fusion, BCR::ABL1-like features, KMT2A rearrangement, ETV6::RUNX1
Precision medicine in acute lymphoblastic leukemia.
Pui CH. Pui CH. Front Med. 2020 Dec;14(6):689-700. doi: 10.1007/s11684-020-0759-8. Epub 2020 Oct 19. Front Med. 2020. PMID: 33074527 Free PMC article. Review.
Further improvement in outcome will need to rely more heavily on molecular therapeutic as well as immuno-and cellular-therapy approaches together with precise risk stratification. Children with ETV6-RUNX1 or hyperdiploid > 50 ALL who achieve negative minimal resi …
Further improvement in outcome will need to rely more heavily on molecular therapeutic as well as immuno-and cellular-therapy approaches tog …
Comparative features and outcomes between paediatric T-cell and B-cell acute lymphoblastic leukaemia.
Teachey DT, Pui CH. Teachey DT, et al. Lancet Oncol. 2019 Mar;20(3):e142-e154. doi: 10.1016/S1470-2045(19)30031-2. Lancet Oncol. 2019. PMID: 30842058 Free PMC article. Review.
Second, a higher proportion of patients with B-cell ALL have favourable genetic subtypes (eg, ETV6-RUNX1 and high hyperdiploidy), which confer a superior outcome compared with favourable subtypes of T-cell ALL. ...
Second, a higher proportion of patients with B-cell ALL have favourable genetic subtypes (eg, ETV6-RUNX1 and high hyperdiploid …
Siblings with ETV6/RUNX1-positive B-lymphoblastic leukemia: A single site experience and review of the literature.
Martig DS, Williamson CM, Xu X, Sukov WR, Greipp PT, Hoppman NL, Baughn LB, Ketterling RP, Peterson JF. Martig DS, et al. Ann Diagn Pathol. 2020 Oct;48:151588. doi: 10.1016/j.anndiagpath.2020.151588. Epub 2020 Aug 14. Ann Diagn Pathol. 2020. PMID: 32836179 Review.
Herein, we report three pairs of siblings (one non-identical pair, one maternal half-sibling pair, and one identical pair) all diagnosed with ETV6/RUNX1-positive B-ALL. Considering that ETV6/RUNX1 fusion is thought to represent a prenatal event and nec …
Herein, we report three pairs of siblings (one non-identical pair, one maternal half-sibling pair, and one identical pair) all diagnosed wit …
ETV6::RUNX1-like Acute Lymphoblastic Leukemia.
Murthy A, Lee B, Zavala A, Tirado CA. Murthy A, et al. J Assoc Genet Technol. 2024;50(2):61-63. J Assoc Genet Technol. 2024. PMID: 38824653
ETV6::RUNX1-like acute lymphoblastic leukemia (ALL) is a novel B-cell precursor leukemia subtype with similarities to ETV6::RUNX1 ALL without the presence of the ETV6-RUNX1 fusion gene. In this review, we survey the body of literat
ETV6::RUNX1-like acute lymphoblastic leukemia (ALL) is a novel B-cell precursor leukemia subtype with similarities to ETV6
Mechanism of ETV6-RUNX1 Leukemia.
Sundaresh A, Williams O. Sundaresh A, et al. Adv Exp Med Biol. 2017;962:201-216. doi: 10.1007/978-981-10-3233-2_13. Adv Exp Med Biol. 2017. PMID: 28299659 Review.
Since its discovery in the 1990s, the function of the ETV6-RUNX1 fusion gene has attracted intense interest. In this chapter, we will summarize current knowledge on the clinical significance of ETV6-RUNX1, the experimental models used to unravel its fu …
Since its discovery in the 1990s, the function of the ETV6-RUNX1 fusion gene has attracted intense interest. In this chapter, …
Pathogenesis of ETV6/RUNX1-positive childhood acute lymphoblastic leukemia and mechanisms underlying its relapse.
Sun C, Chang L, Zhu X. Sun C, et al. Oncotarget. 2017 May 23;8(21):35445-35459. doi: 10.18632/oncotarget.16367. Oncotarget. 2017. PMID: 28418909 Free PMC article. Review.
ETV6/RUNX1 (E/R) is the most common fusion gene in childhood acute lymphoblastic leukemia (ALL). ...Accordingly, a variety of studies have focused on the relationship between the clones giving rise to the primary and recurrent E/R-positive ALL. We review here
ETV6/RUNX1 (E/R) is the most common fusion gene in childhood acute lymphoblastic leukemia (ALL). ...Accordingly, a variety of
Neoantigens in Hematologic Malignancies.
Biernacki MA, Bleakley M. Biernacki MA, et al. Front Immunol. 2020 Feb 14;11:121. doi: 10.3389/fimmu.2020.00121. eCollection 2020. Front Immunol. 2020. PMID: 32117272 Free PMC article. Review.
These include mutated nucleophosmin1 and PML-RARA in acute myeloid leukemia, ETV6-RUNX1 fusions and other mutated proteins in acute lymphoblastic leukemia, BCR-ABL1 fusions in chronic myeloid leukemia, driver mutations in myeloproliferative neoplasms, immunoglobulin …
These include mutated nucleophosmin1 and PML-RARA in acute myeloid leukemia, ETV6-RUNX1 fusions and other mutated proteins in …
Prognostification of ALL by Cytogenetics.
Hakeem A, Shiekh AA, Bhat GM, Lone AR. Hakeem A, et al. Indian J Hematol Blood Transfus. 2015 Sep;31(3):322-31. doi: 10.1007/s12288-014-0483-0. Epub 2014 Dec 11. Indian J Hematol Blood Transfus. 2015. PMID: 26085716 Free PMC article. Review.
Some chromosomal abnormalities are associated with more favorable outcomes, such as high hyperdiploidy (51-65 chromosomes) and the ETV6-RUNX1 fusion. Others are associated with a poorer prognosis, including the Philadelphia chromosome [t(9;22)], rearrangements of th …
Some chromosomal abnormalities are associated with more favorable outcomes, such as high hyperdiploidy (51-65 chromosomes) and the ETV6
Germline predisposition to myeloid neoplasms: Characteristics and management of high versus variable penetrance disorders.
Trottier AM, Feurstein S, Godley LA. Trottier AM, et al. Best Pract Res Clin Haematol. 2024 Mar;37(1):101537. doi: 10.1016/j.beha.2024.101537. Epub 2024 Feb 1. Best Pract Res Clin Haematol. 2024. PMID: 38490765 Review.
Penetrance, age of onset, phenotypic heterogeneity, and somatic driver events differ widely among these conditions and sometimes even within family members with the same variant, making risk assessment and counseling of these individuals inherently difficult. In this review
Penetrance, age of onset, phenotypic heterogeneity, and somatic driver events differ widely among these conditions and sometimes even within …
60 results