SynthesisJournal of hematopathology2025
Acute myeloid leukemia with bipotential erythroid and megakaryocytic differentiation: a case series and literature review.
Synthesis in Journal of hematopathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Global bibliometric analysis of TP53-mutated acute myeloid leukemia: research hotspots and evolution.Translational cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
backgroundAcute myeloid leukemia with erythroid and megakaryocytic differentiation (AML-EMD) is a rare and aggressive presentation of AML characterized by overlapping morphologic, immunophenotypic, and genetic features of erythroid and megakaryocytic lineages. The classification, pathogenesis, and clinical behavior of this entity remain poorly defined.
methodsWe report a series of three patients in conjunction with a systematic review of reported cases in published literature with AML-EMD.
resultsCytogenetic and molecular studies revealed frequent abnormalities including complex karyotypes, TP53 mutations, and JAK1/2 mutations. Clinically, patients demonstrated a poor-risk profile.
conclusionsCollective phenotypic and genetic features suggest that AML-EMD represents a high-risk subgroup of either TP53-mutated AML or AML with myelodysplasia-related genetics, likely reflecting leukemic transformation from multipotent progenitors retaining erythro-megakaryocytic potential. Despite shared biologic features, current classification systems for AML-EMD are diagnostically incongruent. Recognition of this entity will allow for consistent subclassification, prognostication, and future studies aimed at defining its molecular underpinnings and therapeutic vulnerabilities.
Indexed as
Identifiers
What Socratic 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 Socratic graph.