ArticleBlood2014
Acute lymphoblastic leukemia in children with Down syndrome: a retrospective analysis from the Ponte di Legno study group.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers, 4 of them syntheses that pooled it.
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Who cites it
116 citing papers in PubMed, 4 syntheses or guidelines pooled it.
- PEG-asparaginase treatment regimens for acute lymphoblastic leukaemia in children: a network meta-analysis.The Cochrane database of systematic reviews · 2023Pooled it
- The Clinical Spectrum of Inflammatory Bowel Disease Associated With Specific Genetic Syndromes: Two Novel Pediatric Cases and a Systematic Review.Frontiers in pediatrics · 2021Pooled it
- Pooled it
- Pooled it
- Tandem CD19/CD22 CAR T-cells as potential therapy for children and young adults with high-risk r/r B-ALL.EBioMedicine · 2025Trial
- Excellent long-term survival of children with Down syndrome and standard-risk ALL: a report from the Children's Oncology Group.Blood advances · 2019Trial
- Relapsed childhood acute lymphoblastic leukemia in the Nordic countries: prognostic factors, treatment and outcome.Haematologica · 2016Trial
- Transplantation outcomes in patients with Down syndrome-associated acute lymphoblastic leukaemia: Implications for treatment intensity and the use of novel therapies.British journal of haematology · 2026Article
- Inotuzumab ozogamicin in individuals with Down syndrome and acute lymphoblastic leukemia.Leukemia · 2026Article
- Biological and clinical characteristics ofHemaSphere · 2026Article
- A cancer-predisposing syndrome is always there: a sequential occurrence of acute lymphoblastic leukemia after acute myeloid leukemia in a child with down syndrome.Frontiers in oncology · 2026Article
- The very rare association between T-cell acute lymphoblastic leukemia and down syndrome: a case report and review of the literature.Frontiers in pediatrics · 2026Article
- B-cell lymphoblastic leukemia/lymphoma with mutatedHaematologica · 2025Article
- Complex genotype-phenotype relationships shape the response to treatment of down syndrome childhood acute lymphoblastic leukaemia.Scientific reports · 2025Article
- Real-world data for tisagenlecleucel in patients with R/R B-ALL: subgroup analyses from the CIBMTR registry.Blood advances · 2025Article
- Perspectives on the origin and therapeutic opportunities in Down syndrome-associated leukemia.Cancer metastasis reviews · 2025Review
- Mortality after cancer diagnosis among children with congenital heart disease in Denmark and Sweden.Journal of the National Cancer Institute · 2025Article
- All genetic subtypes of B-cell acute lymphoblastic leukemia exhibit increased incidence rates in children with Down syndrome.Leukemia · 2025Article
- Inotuzumab ozogamicin for relapse prevention in a boy with Down syndrome and relapsed acute lymphoblastic leukemia.International journal of hematology · 2025Article
- Inherited Predispositions to Myeloid Neoplasms: Pathogenesis and Clinical Implications.Annual review of pathology · 2025Review
56 more citing papers are in PubMed but not listed here.
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36 authors.
Funding
Abstract
Children with Down syndrome (DS) have an increased risk of B-cell precursor (BCP) acute lymphoblastic leukemia (ALL). The prognostic factors and outcome of DS-ALL patients treated in contemporary protocols are uncertain. We studied 653 DS-ALL patients enrolled in 16 international trials from 1995 to 2004. Non-DS BCP-ALL patients from the Dutch Child Oncology Group and Berlin-Frankfurt-Münster were reference cohorts. DS-ALL patients had a higher 8-year cumulative incidence of relapse (26% ± 2% vs 15% ± 1%, P < .001) and 2-year treatment-related mortality (TRM) (7% ± 1% vs 2.0% ± <1%, P < .0001) than non-DS patients, resulting in lower 8-year event-free survival (EFS) (64% ± 2% vs 81% ± 2%, P < .0001) and overall survival (74% ± 2% vs 89% ± 1%, P < .0001). Independent favorable prognostic factors include age <6 years (hazard ratio [HR] = 0.58, P = .002), white blood cell (WBC) count <10 × 10(9)/L (HR = 0.60, P = .005), and ETV6-RUNX1 (HR = 0.14, P = .006) for EFS and age (HR = 0.48, P < .001), ETV6-RUNX1 (HR = 0.1, P = .016) and high hyperdiploidy (HeH) (HR = 0.29, P = .04) for relapse-free survival. TRM was the major cause of death in ETV6-RUNX1 and HeH DS-ALLs. Thus, while relapse is the main contributor to poorer survival in DS-ALL, infection-associated TRM was increased in all protocol elements, unrelated to treatment phase or regimen. Future strategies to improve outcome in DS-ALL should include improved supportive care throughout therapy and reduction of therapy in newly identified good-prognosis subgroups.
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