Cited by 463Acute Myeloid Leukemia ResearchCancer-related Molecular PathwaysRetinoids in leukemia and cellular processes

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TP53 Mutations in Low-Risk Myelodysplastic Syndromes With del(5q) Predict Disease Progression

Jädersten, Martin, Saft, Leonie, Smith, Alexander, Kulasekararaj, Austin, Pomplun, Sabine, Göhring, Gudrun, Hedlund, Anette, Hast, Robert, Schlegelberger, Brigitte, Porwit, Anna, Hellström-Lindberg, Eva, Mufti, Ghulam J.·2011·Journal of Clinical Oncology

DOI 10.1200/jco.2010.31.8576

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Abstract

Purpose: To determine the frequency of TP53 mutations and the level of p53 protein expression by immunohistochemistry (IHC) in low-risk myelodysplastic syndromes (MDS) with del(5q) and to assess their impact on disease progression. Patients and Methods: Pre- and postprogression bone marrow (BM) samples from 55 consecutive patients with International Prognostic Scoring System low risk (n = 32) or intermediate-1 risk (n = 23) were studied by next-generation sequencing of TP53. IHC for p53 was performed on 148 sequential BM samples. Results: TP53 mutations with a median clone size of 11% (range, 1% to 54%) were detected in 10 patients (18%) already at an early phase of the disease. Mutations were equally common in low-risk and intermediate-1–risk patients and were associated with evolution to acute myeloid leukemia (5 of 10 v 7 of 45; P = .045). Nine of 10 patients carrying mutations showed more than 2% BM progenitors with strong p53 staining. The probability of a complete cytogenetic response to lenalidomide was lower in mutated patients (0 of 7 v 12 of 24; P = .024). Conclusion: By using sensitive deep-sequencing technology, we demonstrated that TP53 mutated populations may occur at an early disease stage in almost a fifth of low-risk MDS patients with del(5q). Importantly, mutations were present years before disease progression and were associated with an increased risk of leukemic evolution. TP53 mutations could not be predicted by common clinical features but were associated with p53 overexpression. Our findings indicate a previously unrecognized heterogeneity of the disease which may significantly affect clinical decision making.

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Self-citation

Authors: Jädersten, M., Saft, L., Smith, A., Kulasekararaj, A., Pomplun, S., Göhring, G., Hedlund, A., Hast, R., Schlegelberger, B., Porwit, A., Hellström-Lindberg, E., & Mufti, G. J.
Affiliations: King's College London (GB)
From the Department of Medicine, Center for Experimental Hematology, and Department of Pathology and Oncology, Karolinska Institutet, Stockholm, Sweden; King's College London School of Medicine, London, United Kingdom; and Institute of Cell and Molecular Pathology, Hannover Medical School, Hannover, Germany.
ORCID: Jädersten, Martin
Saft, Leonie
Smith, Alexander
Kulasekararaj, Austin
Göhring, Gudrun
Schlegelberger, Brigitte
Mufti, Ghulam J.
Venue: Journal of Clinical Oncology
Publisher: American Society of Clinical Oncology (ASCO)
Published: 2011-05-20
Volume: 29
Issue: 15
Pages: 1971-1979
ISSN: 0732-183X (ISSN-L)
1527-7755
DOI: 10.1200/jco.2010.31.8576
OpenAlex: W2131256397
Cited by: 463
References: 33
Citations by year: 2026: 10 · 2025: 12 · 2024: 26 · 2023: 23 · 2022: 27 · 2021: 31 · 2020: 27 · 2019: 33 · 2018: 28 · 2017: 37 · 2016: 34 · 2015: 44 · 2014: 38 · 2013: 47 · 2012: 26
FWCI: 28.44
Type: journal article
Language: en
Open access: closed
Locations: Journal of Clinical Oncology (publishedVersion)
PubMed (publishedVersion)
Research Portal (King's College London) (submittedVersion)
Topics: Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Keywords: TP53 mutation, myelodysplastic syndrome, del(5q), p53 expression, disease progression, cytogenetic response, clone size, disease heterogeneity
MeSH terms: Adult, Aged, Aged, 80 and over, Chromosome Deletion, Chromosomes, Human, Pair 5, Female, Humans, Male, Middle Aged, Myelodysplastic Syndromes, Peptide Fragments, Prognosis, Risk, Leukemia, Myeloid, Acute, Genes, p53, Tumor Suppressor Protein p53, Disease Progression

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TP53 Mutations in Low-Risk Myelodysplastic Syndromes With del(5q) Predict Disease Progression

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