Evidence map›Paper›PMID 37730754›Full record

ArticleNPJ precision oncology2023

Sequential genomic analysis using a multisample/multiplatform approach to better define rhabdomyosarcoma progression and relapse.

Henry de Traux de Wardin, Josephine K Dermawan, Marie-Sophie Merlin, Leonard H Wexler, Daniel Orbach, Fabio Vanoli, Gudrun Schleiermacher, Birgit Geoerger, Stelly Ballet, Delphine Guillemot and 5 more

Open access · goldAbstract read
In one paragraph

Article in NPJ precision oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 13 citations in OpenAlex.

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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

15 authors at 5 institutions in 2 countries.

Henry de Traux de Wardin *Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0009-0000-0615-8982
Josephine K Dermawan *Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Marie-Sophie MerlinUniversity of Lorraine, Centre Hospitalier Régional Universitaire (CHRU), Childrens' Hospital, Department of Pediatric Oncology, Vandoeuvre-lès-Nancy, France.ORCID http://orcid.org/0009-0001-0891-2931
Leonard H WexlerDepartment of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0003-0724-8263
Daniel OrbachSIREDO Oncology Center (Care, Innovation and Research for Children, Adolescents and Young Adults with Cancer), PSL University, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0002-2520-139X
Fabio VanoliDepartment of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.ORCID http://orcid.org/0000-0002-1260-8078
Gudrun SchleiermacherSIREDO Oncology Center (Care, Innovation and Research for Children, Adolescents and Young Adults with Cancer), PSL University, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0002-0133-5879
Birgit GeoergerGustave Roussy Cancer Center, Department of Pediatric and Adolescent Oncology, Institut National de la Santé Et de la Recherche Médicale (INSERM) U1015, Université Paris-Saclay, Villejuif, 94805, France.
Stelly BalletUnit of Somatic Genetics, Institut Curie, Paris, France.ORCID http://orcid.org/0009-0009-2027-0351
Delphine GuillemotUnit of Somatic Genetics, Institut Curie, Paris, France.
Eléonore FrouinUnit of Somatic Genetics, Institut Curie, Paris, France.ORCID http://orcid.org/0000-0002-7631-188X
Stacy CyrilleDepartment of Biometrics, Institut Curie, Paris, France.
Olivier DelattreSIREDO Oncology Center (Care, Innovation and Research for Children, Adolescents and Young Adults with Cancer), PSL University, Institut Curie, Paris, France.
Gaelle Pierron *Unit of Somatic Genetics, Institut Curie, Paris, France. Gaelle.pierron@curie.fr.ORCID http://orcid.org/0000-0002-2536-7680
Cristina R Antonescu *Department of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA. antonesc@mskcc.org.ORCID http://orcid.org/0000-0002-9717-8205
Institut Curie · FRMemorial Sloan Kettering Cancer Center · USInserm · FRCentre Hospitalier Régional et Universitaire de Nancy · FRUniversité Paris Sciences et Lettres · FR

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Targeting Oncogenic Pathways in Genetically Complex SarcomasP50CA217694 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Marc Ladanyi · 2018 to 2026
$21.5M
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA217694
6 · The paper itself

Abstract

The genomic spectrum of rhabdomyosarcoma (RMS) progression from primary to relapse is not fully understood. In this pilot study, we explore the sensitivity of various targeted and whole-genome NGS platforms in order to assess the best genomic approach of using liquid biopsy in future prospective clinical trials. Moreover, we investigate 35 paired primary/relapsed RMS from two contributing institutions, 18 fusion-positive (FP-RMS) and 17 fusion-negative RMS (FN-RMS) by either targeted DNA or whole exome sequencing (WES). In 10 cases, circulating tumor DNA (ctDNA) from multiple timepoints through clinical care and progression was analyzed for feasibility of liquid biopsy in monitoring treatment response/relapse. ctDNA alterations were evaluated using a targeted 36-gene custom RMS panel at high coverage for single-nucleotide variation and fusion detection, and a shallow whole-genome sequencing for copy number variation. FP-RMS have a stable genome with relapse, with common secondary alterations CDKN2A/B, MYCN, and CDK4 present at diagnosis and impacting survival. FP-RMS lacking major secondary events at baseline acquire recurrent MYCN and AKT1 alterations. FN-RMS acquire a higher number of new alterations, most commonly SMARCA2 missense mutations. ctDNA analyses detect pathognomonic variants in all RMS patients within our collection at diagnosis, regardless of type of alterations, and confirmed at relapse in 86% of FP-RMS and 100% FN-RMS. Moreover, a higher number of fusion reads is detected with increased disease burden and at relapse in patients following a fatal outcome. These results underscore patterns of tumor progression and provide rationale for using liquid biopsy to monitor treatment response.

Identifiers

PMID37730754
PMCPMC10511463
OpenAlexW4386889646

What OpenQuestion holds

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Registered trials

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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.