Evidence map›Paper›PMID 36485102›Full record

ArticleHematology. American Society of Hematology. Education Program2022

Transplant for TP53-mutated MDS and AML: because we can or because we should?

Jurjen Versluis, R Coleman Lindsley

Open access · bronzeAbstract read
In one paragraph

Article in Hematology. American Society of Hematology. Education Program, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.8field-weighted citation impact, top 5% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 26 citations in OpenAlex.

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  13. Outcome heterogeneity ofHaematologica · 2024
    Article
  14. Article
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  16. Article
  17. TP53-Mutated Myelodysplasia and Acute Myeloid Leukemia.Mediterranean journal of hematology and infectious diseases · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Jurjen VersluisErasmus University Medical Center Cancer Institute, Rotterdam, the Netherlands.
R Coleman LindsleyDana-Farber Cancer Institute, Harvard Medical School, Boston, MA.
Dana-Farber Cancer Institute · USErasmus MC Cancer Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TP53 mutations impair the cellular response to genotoxic stress and drive intrinsic resistance to conventional cytotoxic therapies. Clinical outcomes in patients with TP53-mutated myeloid malignancies are poor and marked by high-risk clinical features, such as complex karyotype and prior exposure to leukemogenic therapies, and short survival due to a high risk of relapse after allogeneic transplantation. TP53 mutations are thus included as adverse markers in clinical prognostic models, including European LeukemiaNet recommendations and the Molecular International Prognostic Scoring System for myelodysplastic syndromes (MDS). Recent data indicate that the TP53 allelic state, co-occurring somatic mutations, and the position of the TP53 mutation within the clonal hierarchy define genetic heterogeneity among TP53-mutated MDS and acute myeloid leukemia that may influence clinical outcomes, thereby informing the selection of patients most suitable for transplantation. Further, novel therapeutic methods such as antibody-based agents (monoclonals or dual-affinity retargeting antibodies), cellular therapies (natural killer cells, chimeric antigen receptor T cells), or targeted agents (eprenetapopt) may offer opportunities to modify the approach to pretransplant conditioning or posttransplant maintenance and improve clinical outcomes.

Indexed as

Hematopoietic Stem Cell TransplantationLeukemia, Myeloid, AcuteMyelodysplastic SyndromesHumansMutationPrognosisTransplantation, HomologousTumor Suppressor Protein p53TP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID36485102
PMCPMC9820679
OpenAlexW4311671021

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.