Impact of TP53 mutation variant allele frequency on phenotype and outcomes in myelodysplastic syndromes

Sallman, D A; Komrokji, R; Vaupel, C; Cluzeau, T; Geyer, S M; McGraw, K L; Al Ali, N H; Lancet, J; McGinniss, M J; Nahas, S; Smith, A E; Kulasekararaj, A; Mufti, G; List, A; Hall, J; Padron, E

doi:10.1038/leu.2015.304

Cited by 231Acute Myeloid Leukemia ResearchCancer Genomics and DiagnosticsRetinoids in leukemia and cellular processes

Impact of TP53 mutation variant allele frequency on phenotype and outcomes in myelodysplastic syndromes

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Sallman, D A, Komrokji, R, Vaupel, C, Cluzeau, T, Geyer, S M, McGraw, K L, Al Ali, N H, Lancet, J +8 more·2016·Leukemia

DOI 10.1038/leu.2015.304PMC PMC7864381

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Abstract

Although next-generation sequencing has allowed for the detection of somatic mutations in myelodysplastic syndromes (MDS), the clinical relevance of variant allele frequency (VAF) for the majority of mutations is unknown. We profiled TP53 and 20 additional genes in our training set of 219 patients with MDS or secondary acute myeloid leukemia with findings confirmed in a validation cohort. When parsed by VAF, TP53 VAF predicted for complex cytogenetics in both the training (P=0.001) and validation set (P<0.0001). MDS patients with a TP53 VAF > 40% had a median overall survival (OS) of 124 days versus an OS that was not reached in patients with VAF <20% (hazard ratio (HR), 3.52; P=0.01) with validation in an independent cohort (HR, 4.94, P=0.01). TP53 VAF further stratified distinct prognostic groups independent of clinical prognostic scoring systems (P=0.0005). In multivariate analysis, only a TP53 VAF >40% was an independent covariate (HR, 1.61; P<0.0001). In addition, SRSF2 VAF predicted for monocytosis (P=0.003), RUNX1 VAF with thrombocytopenia (P=0.01) and SF3B1 with ringed sideroblasts (P=0.001). Together, our study indicates that VAF should be incorporated in patient management and risk stratification in MDS.

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TP53 mutation burden (high variant allele frequency, concurrent complex karyotype, and/or multihit state) is linked to inferior survival with median overall survival of 6-8 months.
“The TP53 mutation burden (ie, high variant allele frequency [VAF], concurrent complex karyotype, and/or multihit state) is integrally linked to inferior survival with median OS of 6-8 months.8-10,12”
From Eprenetapopt (APR-246) and Azacitidine in TP53 -Mutant Myelodysplastic Syndromes (2021) · cites this paper as [8]
The Results sections on TP53 VAF and survival and on complex cytogenetics (page not provided) link higher VAF to shorter survival and to complex karyotype. They report median OS of 183 days for VAF ≥20%, but 124 days for VAF >40% in the training cohort and 272 days in the validation cohort—not a consistent 6–8 months. The paper does not establish the claimed survival figure for a multihit state. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Remissions in TP53-mutant patients are brief, with a median overall survival ranging from 5 to 12 months.
“However, remissions in TP53-mutant patients are brief with a median overall survival (OS) ranging from 5 to 12 months,8,9,12,13,15-17”
From Eprenetapopt (APR-246) and Azacitidine in TP53 -Mutant Myelodysplastic Syndromes (2021) · cites this paper as [8]
The Results section (“TP53 VAF and survival”; page unavailable) reports a median overall survival of 162 days—about 5 months—for TP53-mutant patients, supporting the claim of poor survival. It does not report remission duration, and its survival estimates vary by variant allele frequency, including a median above 12 months for patients with low-frequency mutations. Thus it does not support brief remissions or a 5–12-month range for all TP53-mutant patients. (LLM, conf=0.88)
Experimental — accuracy not yet measured
mTP53 patients with high VAF (>20-23%), biallelic state, and/or complex karyotype have particularly poor risk.
“Specifically, mTP53 patients with a high variant allele frequency (VAF; i.e., >20%–23%), biallelic state, and/or complex karyotype (CK) have particularly poor risk.”
From Long‐term follow‐up and combined Phase 2 results of eprenetapopt and azacitidine in patients with TP53 mutant MDS/AML (2025) · cites this paper as [4]
The Results (TP53 VAF and survival; page unavailable) identify 20% as an optimal survival-stratification cutoff and report poorer survival with higher TP53 VAF. The Results (TP53 VAF and complex cytogenetics; page unavailable) link higher VAF to complex karyotype, while the Discussion notes inferior survival with greater chromosomal complexity. Our copy does not establish a 23% cutoff or assess biallelic TP53 state as a separate risk factor. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Treatment outcomes for patients with TP53 mutations are poor with available therapies.
“Treatment outcomes for patients with TP53 mutations are poor with available therapies.8-12”
From Eprenetapopt (APR-246) and Azacitidine in TP53 -Mutant Myelodysplastic Syndromes (2021) · cites this paper as [8]

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High flow cytometric scores identify adverse prognostic subgroups within the revised international prognostic scoring system for myelodysplastic syndromes
Alhan, C., Westers, T. M., Cremers, E. M. P., et al. (2014) · British Journal of Haematology · doi:10.1111/bjh.12994 · Cited by 34 · see citing works

Authors: Sallman, D. A., Komrokji, R., Vaupel, C., Cluzeau, T., Geyer, S. M., McGraw, K. L., Al Ali, N. H., Lancet, J., McGinniss, M. J., Nahas, S., Smith, A. E., Kulasekararaj, A., Mufti, G., List, A., Hall, J., & Padron, E.
Affiliations: Moffitt Cancer Center (US)
Inserm (FR)
University of South Florida (US)
King's College London (GB)
Corresponding author: Padron, E
ORCID: Sallman, D A
Komrokji, R
Cluzeau, T
McGraw, K L
Lancet, J
Nahas, S
Smith, A E
Kulasekararaj, A
Mufti, G
List, A
Hall, J
Padron, E
Venue: Leukemia
Publisher: Springer Science and Business Media LLC
Published: 2015-10-30
Volume: 30
Issue: 3
Pages: 666-673
ISSN: 0887-6924 (ISSN-L)
1476-5551
DOI: 10.1038/leu.2015.304
PMC: PMC7864381
OpenAlex: W2191233876
Cited by: 231
References: 32
Citations by year: 2026: 9 · 2025: 21 · 2024: 22 · 2023: 28 · 2022: 24 · 2021: 25 · 2020: 33 · 2019: 26 · 2018: 12 · 2017: 14 · 2016: 14 · 2014: 1
FWCI: 10.46
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: Leukemia (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Cancer Institute (P30CA076292)
Topics: Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
Keywords: myelodysplastic syndrome, TP53 mutation, variant allele frequency, secondary acute myeloid leukemia, prognostic stratification, overall survival, complex cytogenetics, SRSF2, RUNX1, SF3B1, monocytosis, thrombocytopenia, ring sideroblasts, risk stratification
MeSH terms: Serine-Arginine Splicing Factors, RNA Splicing Factors, Aged, Aged, 80 and over, Alleles, Female, Follow-Up Studies, Gene Frequency, Humans, Male, Middle Aged, Mutation, Myelodysplastic Syndromes, Nuclear Proteins, Phenotype, Phosphoproteins, Prognosis, Ribonucleoproteins, Leukemia, Myeloid, Acute, Gene Expression, Multivariate Analysis, Survival Analysis, Tumor Suppressor Protein p53, Ribonucleoprotein, U2 Small Nuclear, Cytogenetic Analysis, Core Binding Factor Alpha 2 Subunit, High-Throughput Nucleotide Sequencing

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Impact of TP53 mutation variant allele frequency on phenotype and outcomes in myelodysplastic syndromes

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