Evidence map›Paper›PMID 41721060›Full record

ArticleJournal of hematopathology2026

Morphologic findings and mutational profiles of myelodysplastic neoplasms with normal versus abnormal karyotype.

Jyoti Kumar, Alexandria Jensen, Rong Lu, Vishesh Khanna, Henning Stehr, Michael Spinner, Sebastian Fernandez-Pol, Peter L Greenberg, Brent Tan

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Article in Journal of hematopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Jyoti KumarDepartment of Diagnostic Medicine, Division of Pathology, The University of Texas at Austin, Austin, TX, USA.
Alexandria JensenDepartment of Medicine, Quantitative Sciences Unit, Stanford University School of Medicine, Stanford, CA, USA.
Rong LuDepartment of Medicine, Quantitative Sciences Unit, Stanford University School of Medicine, Stanford, CA, USA.
Vishesh KhannaDepartment of Medicine, Division of Hematology and Medical Oncology, Oregon Health and Science University, Portland, OR, USA.
Henning StehrDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Lane Building, L235, Stanford, CA 94305, USA.
Michael SpinnerDepartment of Medicine, Division of Hematology, Stanford University School of Medicine, Stanford, CA, USA.
Sebastian Fernandez-PolDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Lane Building, L235, Stanford, CA 94305, USA.
Peter L GreenbergDivision of Hematology/Oncology, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
Brent TanDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Lane Building, L235, Stanford, CA 94305, USA. btan@stanford.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyelodysplastic syndromes are clonal bone marrow failure disorders demonstrating variable degrees of cytopenias, morphologic dysplasia, and risk of progression to acute myeloid leukemia. PURPOSE: We hypothesized that MDS with a normal karyotype (NK) would exhibit a unique mutational or morphologic signature.

methodsWe investigated the morphologic features and genetic profiles of 89 patients with myelodysplastic syndrome (MDS), including 42 with a NK and 47 with an abnormal karyotype (non-NK). We used next-generation sequencing (NGS) to detect pathogenic variants and performed morphologic review by two independent hematopathologists in a blinded manner with a nested set of 43 control cases.

resultsNK and non-NK cases showed similar levels of dysplasia in granulocytes and erythroids, but non-NK cases showed significantly more dysplasia in megakaryocytes (P = 0.037). The mutational burden was similar between NK and non-NK cases. TET2 and SF3B1 mutations were more frequent in NK cases (P = 0.029 and P = 0.013, respectively), and TP53 mutations were more frequent in non-NK cases (P = 0.007). Overall, higher mutational burden was associated with higher levels of megakaryocyte dysplasia (P = 0.003), but there was no association with granulocytic or erythroid dysplasia. Cases with STAG2 mutations were associated with higher overall megakaryocyte dysplasia (P = 0.0016) and proportion of megakaryocytes with separate nuclear lobes (P < 0.0001).

conclusionsThe megakaryocyte lineage is the most expressive in terms of reflecting morphologic dysplasia due to cytogenetic or molecular abnormalities. MDS with NK shows similar morphologic features to non-NK cases, but our findings suggest that non-NK cases exhibit higher levels of megakaryocytic dysplasia.

Indexed as

Abnormal KaryotypeMutationMyelodysplastic SyndromesAdultAgedAged, 80 and overFemaleHigh-Throughput Nucleotide SequencingHumansKaryotypeKaryotypingMaleMegakaryocytesMiddle AgedCytogeneticsMarrowMorphologyMyelodysplasiaSequencing

Identifiers

PMID41721060

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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.