Evidence map›Paper›PMID 38722224›Full record

ArticleGenes, chromosomes & cancer2024

Genomic profiling of pleomorphic rhabdomyosarcoma reveals a genomic signature distinct from that of embryonal rhabdomyosarcoma.

Carla Saoud, Josephine K Dermawan, Aarti E Sharma, William Tap, Leonard H Wexler, Cristina R Antonescu

Abstract read
In one paragraph

Article in Genes, chromosomes & cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Review
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  6. Review
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  11. Rhabdomyosarcoma in children and young adults.Virchows Archiv : an international journal of pathology · 2025
    Review
  12. Article
  13. Article
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.

Carla SaoudDepartment of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Josephine K DermawanRobert J. Tomsich Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Aarti E SharmaDepartment of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
William TapDepartment of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Leonard H WexlerDepartment of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Cristina R AntonescuDepartment of Pathology and Laboratory Medicine, Memorial Sloan Kettering Cancer Center, New York, New York, USA.ORCID 0000-0002-9717-8205

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Targeting Oncogenic Pathways in Genetically Complex SarcomasP50CA217694 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI William D. Tap · 2018 to 2026
$21.5M
NCI NIH HHS P30 CA008748NCI NIH HHS P50 CA217694
6 · The paper itself

Abstract

Pleomorphic rhabdomyosarcoma (PRMS) is a rare and highly aggressive sarcoma, occurring mostly in the deep soft tissues of middle-aged adults and showing a variable degree of skeletal muscle differentiation. The diagnosis is challenging as pathologic features overlap with embryonal rhabdomyosarcoma (ERMS), malignant Triton tumor, and other pleomorphic sarcomas. As recurrent genetic alterations underlying PRMS have not been described to date, ancillary molecular diagnostic testing is not useful in subclassification. Herein, we perform genomic profiling of a well-characterized cohort of 14 PRMS, compared to a control group of 23 ERMS and other pleomorphic sarcomas (undifferentiated pleomorphic sarcoma and pleomorphic liposarcoma) using clinically validated DNA-targeted Next generation sequencing (NGS) panels (MSK-IMPACT). The PRMS cohort included eight males and six females, with a median age of 53 years (range 31-76 years). Despite similar tumor mutation burdens, the genomic landscape of PRMS, with a high frequency of TP53 (79%) and RB1 (43%) alterations, stood in stark contrast to ERMS, with 4% and 0%, respectively. CDKN2A deletions were more common in PRMS (43%), compared to ERMS (13%). In contrast, ERMS harbored somatic driver mutations in the RAS pathway and loss of function mutations in BCOR, which were absent in PRMS. Copy number variations in PRMS showed multiple chromosomal arm-level changes, most commonly gains of chr17p and chr22q and loss of chr6q. Notably, gain of chr8, commonly seen in ERMS (61%) was conspicuously absent in PRMS. The genomic profiles of other pleomorphic sarcomas were overall analogous to PRMS, showing shared alterations in TP53, RB1, and CDKN2A. Overall survival and progression-free survival of PRMS were significantly worse (p < 0.0005) than that of ERMS. Our findings revealed that the molecular landscape of PRMS aligns with other adult pleomorphic sarcomas and is distinct from that of ERMS. Thus, NGS assays may be applied in select challenging cases toward a refined classification. Finally, our data corroborate the inclusion of PRMS in the therapeutic bracket of pleomorphic sarcomas, given that their clinical outcomes are comparable.

Indexed as

Rhabdomyosarcoma, EmbryonalAdultAgedBiomarkers, TumorFemaleGenomicsHigh-Throughput Nucleotide SequencingHumansMaleMiddle AgedMutationRetinoblastoma Binding ProteinsRhabdomyosarcomaUbiquitin-Protein LigasesBiomarkers, TumorRB1 protein, humanRetinoblastoma Binding ProteinsUbiquitin-Protein Ligasesembryonalgenomicspleomorphicrhabdomyosarcoma

Identifiers

PMID38722224
PMCPMC11664927

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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.