ArticleBlood advances2021
Secondary cytogenetic abnormalities in core-binding factor AML harboring inv(16) vs t(8;21).
Article in Blood advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 47 citations in OpenAlex.
- Integrated Analysis of Genomics, Molecular Responses, and Outcomes of CBF-AML with FLAG-Based Therapy on a Phase II Trial.Blood cancer discovery · 2026Trial
- RUNX1 upregulation and RUNX1-ETO depletion inhibits survival of t(8;21)-positive leukemia cells.Global medical genetics · 2026Article
- Newly diagnosed acute myeloid leukemia in Fit patients: 2026 treatment algorithms.Blood cancer journal · 2026Review
- CBFB::MYH11 MRD after the second chemotherapy cycle: a guide for allogeneic transplantation in favorable-risk AML.Bone marrow transplantation · 2026Article
- High-risk cytogenetic abnormalities impact the cytological and clinical behavior of core binding factor acute myeloid leukemia: a case-control study.BMC cancer · 2026Article
- Is sex chromosome loss a predictive marker for outcome after sex-mismatched allogeneic hematopoietic stem cell transplantation?Bone marrow transplantation · 2026Article
- Characterization of Acute Myeloid Leukemia With t(16;21) Translocation: Cytogenetic, Molecular, and Immunophenotypic Findings.World journal of oncology · 2026Article
- Whole Genome Sequencing Informed Patient Personalized Measurable Residual Disease Assays for Acute Myeloid Leukemia.medRxiv : the preprint server for health sciences · 2026Article
- AML Disparities Across Racial Ancestry Groups: A Spotlight on the NPM1 Mutations.International journal of molecular sciences · 2026Review
- PredictingiScience · 2025Article
- WTAP-mediated mOncogene · 2025Article
- Cytogenetic Abnormalities and Their Impact on Acute Myeloid Leukemia Outcomes Following Allogeneic Hematopoietic Stem Cell Transplantation: A Single-Center Retrospective Study.Health science reports · 2025Article
- Genetic abnormalities predict outcomes in patients with core binding factor acute myeloid leukemia.Annals of hematology · 2025Article
- NK cell-based immunotherapy strategies for myeloid leukemia.Frontiers in immunology · 2025Review
- Molecular genetics profiling of core-binding factor acute myeloid leukemia in pediatrics.Therapeutic advances in hematology · 2025Review
- Article
- Genomic profiles and outcomes in de novo versus therapy-related core binding factor AML.Blood cancer journal · 2024Article
- Prevalence and Prognosis of Secondary Genetic Aberrations Among Patients With Core Binding Factor Acute Myeloid Leukemia: A Mitelman Database Analysis.World journal of oncology · 2023Article
- Clinical characteristics and prognostic factors analysis of core binding factor acute myeloid leukemia in real world.Cancer medicine · 2023Article
- What Influences the Decision to Proceed to Transplant for Patients With AML in First Remission?Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Review
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Authors and funding
47 authors at 19 institutions in 5 countries.
Funding
Abstract
Patients with core-binding factor (CBF) acute myeloid leukemia (AML), caused by either t(8;21)(q22;q22) or inv(16)(p13q22)/t(16;16)(p13;q22), have higher complete remission rates and longer survival than patients with other subtypes of AML. However, ∼40% of patients relapse, and the literature suggests that patients with inv(16) fare differently from those with t(8;21). We retrospectively analyzed 537 patients with CBF-AML, focusing on additional cytogenetic aberrations to examine their impact on clinical outcomes. Trisomies of chromosomes 8, 21, or 22 were significantly more common in patients with inv(16)/t(16;16): 16% vs 7%, 6% vs 0%, and 17% vs 0%, respectively. In contrast, del(9q) and loss of a sex chromosome were more frequent in patients with t(8;21): 15% vs 0.4% for del(9q), 37% vs 0% for loss of X in females, and 44% vs 5% for loss of Y in males. Hyperdiploidy was more frequent in patients with inv(16) (25% vs 9%, whereas hypodiploidy was more frequent in patients with t(8;21) (37% vs 3%. In multivariable analyses (adjusted for age, white blood counts at diagnosis, and KIT mutation status), trisomy 8 was associated with improved overall survival (OS) in inv(16), whereas the presence of other chromosomal abnormalities (not trisomy 8) was associated with decreased OS. In patients with t(8;21), hypodiploidy was associated with improved disease-free survival; hyperdiploidy and del(9q) were associated with improved OS. KIT mutation (either positive or not tested, compared with negative) conferred poor prognoses in univariate analysis only in patients with t(8;21).
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