ArticleBlood advances2022
TP53 mutation defines a unique subgroup within complex karyotype de novo and therapy-related MDS/AML.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
107 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The role of clonal progression leading to the development of therapy-related myeloid neoplasms.Annals of hematology · 2024Pooled it
- Treatment ofHaematologica · 2026Trial
- Influence of Cytogenetics on the Outcome of Patients With High-Risk Myelodysplastic Syndrome Including Deletion 5q Treated With Azacitidine With or Without Lenalidomide.Genes, chromosomes & cancer · 2025Trial
- Germ line landscape stratification defines distinct molecular and prognostic groups in therapy-related myeloid neoplasms.Blood advances · 2026Article
- Article
- Therapy-related myeloid neoplasms following treatment for high-risk gestational trophoblastic neoplasia: a case series and retrospective analysis.International journal of clinical oncology · 2026Article
- Complex Genomic Alterations in TP53-Mutated Myelodysplastic Syndrome and Acute Myeloid Leukemia Involving EPOR/JAK2 Amplification, ERG Copy Gains, and TCF3 Deletion.Genes, chromosomes & cancer · 2026Article
- Clinical significance of TP53 mutations in patients with acute myeloid leukemia: the HM-SCREEN-JAPAN 01/02 study.International journal of hematology · 2026Article
- TP53 Amplification, a Rare but Recurrent Alteration in Myeloid Neoplasms.Genes, chromosomes & cancer · 2026Article
- The Impact of Post-Transplant Interventions and Chronic GVHD on Survival in Myeloid Malignancies Harboring TP53 Alterations.Transplantation and cellular therapy · 2026Article
- Identification of two novel TP53 mutations in secondary acute myeloid leukemia following multiple myeloma: a case report.Blood science (Baltimore, Md.) · 2026Article
- HDAC8 inhibition targets STAT3-MYC axis and synergizes with Venetoclax in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- Genetic and Clinical Features in TP53-Mutated Patients With Myelodysplastic Neoplasms: A Retrospective Study Based on Next-Generation Sequencing Data.Cancer reports (Hoboken, N.J.) · 2026Article
- Integrated proteogenomic and metabolomic profiling of acute myeloid leukemias to identify molecular subtypes and associated therapy targets.Nature cancer · 2026Article
- Validation of ICC hierarchical classification in secondary AML.Blood advances · 2026Article
- Comparative effectiveness of HMA with venetoclax vs intensive chemotherapy in AML with very high-risk cytogenetics.Blood neoplasia · 2026Article
- Frequency and impact of somatic co-occurring mutations on post-transplant outcomes in acute myeloid leukemia: a multicenter registry analysis on behalf of the EBMT ALWP.Bone marrow transplantation · 2026Article
- Biomarkers and advances in AML-MRC: from bench to bedside.Annals of hematology · 2026Review
- Myelodysplastic neoplasms with unbalanced whole-arm translocation der(5;19)(p10;q10): association with double-hit TP53 mutations.International journal of hematology · 2026Article
- Genocopy of EVI1-AML with paraneoplastic diabetes insipidus: PRDM16 overexpression by t(1;2)(p36;p21) and enhancer hijacking.British journal of haematology · 2026Article
47 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A subset of myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML) show complex karyotype (CK), and these cases include a relatively high proportion of cases of therapy-related myeloid neoplasms and TP53 mutations. We aimed to evaluate the clinicopathologic features of outcome of 299 AML and MDS patients with CK collected from multiple academic institutions. Mutations were present in 287 patients (96%), and the most common mutation detected was in TP53 gene (247, 83%). A higher frequency of TP53 mutations was present in therapy-related cases (P = .008), with a trend for worse overall survival (OS) in therapy-related patients as compared with de novo disease (P = .08) and within the therapy-related group; the presence of TP53 mutation strongly predicted for worse outcome (P = .0017). However, there was no difference in survival between CK patients based on categorization of AML vs MDS (P = .96) or presence of absence of circulating blasts ≥1% (P = .52). TP53-mutated patients presented with older age (P = .06) and lower hemoglobin levels (P = .004) and marrow blast counts (P = .02) compared with those with CK lacking TP53 mutation. Multivariable analysis identified presence of multihit TP53 mutation as strongest predictor of worse outcome, whereas neither a diagnosis of AML vs MDS nor therapy-relatedness independently influenced OS. Our findings suggest that among patients with MDS and AML, the presence of TP53 mutation (in particular multihit TP53 mutation) in the context of CK identifies a homogeneously aggressive disease, irrespective of the blast count at presentation or therapy-relatedness. The current classification of these cases into different disease categories artificially separates a single biologic disease entity.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.