Evidence map›Paper›PMID 34017087›Full record

ArticleBritish journal of cancer2021

TP53 mutations increase radioresistance in rhabdomyosarcoma and Ewing sarcoma.

Dana L Casey, Kenneth L Pitter, Leonard H Wexler, Emily K Slotkin, Gaorav P Gupta, Suzanne L Wolden

Open access · bronzeAbstract read
In one paragraph

Article in British journal of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  4. Variable cellular and radiobiological effects of [Journal of experimental & clinical cancer research : CR · 2026
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  18. Heterogeneity in precision oncology.Cambridge prisms. Precision medicine · 2024
    Review
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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

6 authors at 2 institutions in 1 country.

Dana L CaseyDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA. dana_casey@med.unc.edu.ORCID http://orcid.org/0000-0001-6851-7653
Kenneth L PitterDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Leonard H WexlerDepartment of Pediatric Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Emily K SlotkinDepartment of Pediatric Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Gaorav P GuptaDepartment of Radiation Oncology, University of North Carolina School of Medicine, Chapel Hill, NC, USA.ORCID http://orcid.org/0000-0001-9177-552X
Suzanne L WoldenDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Memorial Sloan Kettering Cancer Center · USUniversity of North Carolina at Chapel Hill · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) P30CA008748
6 · The paper itself

Abstract

backgroundp53 plays a key role in the DNA repair process and response to ionising radiation. We sought to determine the clinical phenotype of TP53 mutations and p53 pathway alterations in patients with rhabdomyosarcoma (RMS) and Ewing sarcoma (ES) treated with radiation.

methodsOf patients with available genomic sequencing, we identified 109 patients with RMS and ES treated to a total of 286 radiation sites. We compared irradiated tumour control among tumours with TP53 mutations (n = 40) to those that were TP53 wild-type (n = 246). We additionally compared irradiated tumour control among tumours with any p53 pathway alteration (defined as tumours with TP53 mutations or TP53 wild-type tumours identified to have MDM2/4 amplification and/or CDKN2A/B deletion, n = 78) to those without such alterations (n = 208).

resultsThe median follow-up was 26 months from radiation. TP53 mutations were associated with worse irradiated tumour control among the entire cohort (hazard ratio, HR = 2.8, P < 0.0001). Tumours with any p53 pathway alteration also had inferior irradiated tumour control (HR = 2.0, P = 0.003). On multivariable analysis, after controlling for tumour histology, intent of radiation, presence of gross disease, and biologically effective dose, TP53 mutations continued to be associated with a radioresistant phenotype (HR = 7.1, P < 0.0001).

conclusionsOur results show that TP53 mutations are associated with increased radioresistance in RMS and ES. Novel strategies to overcome this radioresistance are important for improved outcomes in p53 disruptive RMS and ES.

Indexed as

MutationRadiation ToleranceAdolescentAdultAgedChildChild, PreschoolHumansInfantMiddle AgedPrognosisRhabdomyosarcomaSarcoma, EwingSequence Analysis, DNATumor Suppressor Protein p53Young AdultTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID34017087
PMCPMC8368014
OpenAlexW3162151317

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.