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Embryonal Rhabdomyosarcoma

Embryonal Rhabdomyosarcoma (ERMS): Disease Characteristics Research Report

2026-05-08
Falcon MONDO:0009993 Model: Edison Scientific Literature 28 citations

Embryonal Rhabdomyosarcoma (ERMS): Disease Characteristics Research Report

Target Disease

  • Disease name: Embryonal rhabdomyosarcoma (ERMS)
  • Category: Malignant pediatric soft-tissue sarcoma (skeletal muscle differentiation)
  • MONDO ID: Not identified in the retrieved evidence (see “Limitations”)

Executive summary (current understanding)

Embryonal rhabdomyosarcoma (ERMS) is the most common pediatric rhabdomyosarcoma subtype and largely overlaps with FOXO1 fusion–negative rhabdomyosarcoma (FN‑RMS) in modern molecular classification, which is increasingly used for risk stratification and treatment selection. Clinically, RMS frequently presents as a mass in the head/neck, genitourinary tract, or extremities. ERMS/FN‑RMS is characterized by recurrent chromosomal gains, 11p15 allelic loss/LOH (IGF2 region), and frequent RAS‑pathway alterations; poor‑prognosis subsets include TP53 and MYOD1 (L122R) altered tumors. Standard-of-care remains multimodal therapy (chemotherapy plus surgery and/or radiotherapy), while contemporary trials incorporate molecular risk markers and emerging biomarkers such as circulating tumor DNA (ctDNA). (vries2023imaginginrhabdomyosarcoma pages 1-3, oberoi2023childrensoncologygroups pages 1-3, oberoi2023childrensoncologygroups pages 3-5)

A compact, evidence-backed fact table is provided below.

Table (click to expand)
Domain Item Summary Quantitative detail Citation-year Primary citation context id
Identifier/classification Disease name Embryonal rhabdomyosarcoma (ERMS) is the embryonal subtype of rhabdomyosarcoma and is a fusion-negative RMS category in most cases ERMS constitutes 70–80% of RMS in one clinicopathologic review; another review lists ERMS as 57% of RMS 2025; 2025 pqac-00000006
Identifier/classification Synonyms ERMS; embryonal RMS; fusion-negative RMS (FN-RMS) often used as molecular proxy because most ERMS are FOXO1 fusion-negative Not quantified 2025; 2025 pqac-00000003
Identifier/classification WHO classification WHO/2020-era classification lists four RMS subtypes: embryonal, alveolar, pleomorphic, spindle cell/sclerosing 4 major subtypes 2025; 2026 pqac-00000008
Identifier/classification MeSH / ICD / MONDO / Orphanet Specific MeSH, ICD-10/11, MONDO, and Orphanet identifiers were not provided in the retrieved evidence; Open Targets lists disease term “embryonal rhabdomyosarcoma” as EFO_0000437 Not available in provided evidence 2023–2025 evidence set pqac-00000000
Epidemiology Pediatric cancer burden RMS is the most common pediatric soft tissue sarcoma and accounts for about 3% of pediatric cancers ~3% of pediatric cancers 2023 pqac-00000010
Epidemiology Annual U.S. cases Approximate number of U.S. pediatric RMS diagnoses per year ~350 cases/year 2023 pqac-00000010
Epidemiology Incidence Pediatric RMS annual incidence 4.6 per million children (COG blueprint); ~4 per million age 0–19 in European registry summary 2023; 2023 pqac-00000010
Epidemiology Age/sex distribution RMS median age at diagnosis is early childhood and males are more often affected Median age 5 years; 72–81% diagnosed before age 10; male:female ratio ~1.4 2023 pqac-00000001
Prognosis Overall localized vs metastatic RMS Outcomes vary strongly by risk group and metastatic status 5-year OS ~80% for localized disease; ~35% for metastatic disease 2023 pqac-00000001
Prognosis COG low/intermediate/high risk Long-term survival ranges by risk group in COG framework ~90% / 50–70% / ~20% 5-year survival for low / intermediate / high risk STS/RMS frameworks 2023 pqac-00000010
Prognosis Favorable fusion-negative groups Excellent survival for selected favorable FN-RMS groups 5-year EFS/OS 92%/99% for FN Stage 1, Clinical Group I; 87%/97% for FN Stage 1 CG II / Stage 2 CG I-II / orbit CG III 2023 pqac-00000010
Prognosis ctDNA prognostic value in FN-RMS Detectable baseline ctDNA identifies worse-outcome intermediate-risk FN-RMS ctDNA detectable in 13/75 FN-RMS sera (17%); EFS 33.3% vs 68.9%, OS 33.3% vs 83.2%, P=.0028 and P<.0001 2023 pqac-00000014
Prognosis Poor-risk biomarkers MYOD1 and TP53 mutations worsen prognosis in FN-RMS MYOD1 L122R associated survival 0–30%; TP53 mutations in ~13% FN-RMS and worse outcomes 2023 pqac-00000012
Molecular feature FOXO1 status Fusion status has replaced histologic subtype in risk stratification; FOXO1 fusion-negative disease has better prognosis than fusion-positive disease Qualitative prognostic effect; no single percentage for ERMS itself 2023 pqac-00000010
Molecular feature 11p15 loss ERMS frequently shows 11p15 loss of heterozygosity involving IGF2 region ~80% have 11p15 LOH 2023 pqac-00000007
Molecular feature RAS-pathway mutations Fusion-negative/embryonal RMS is characterized by recurrent RAS-pathway alterations Frequent, but no single pooled percentage given in retrieved evidence 2023 pqac-00000012
Molecular feature TP53 TP53 is a recurrent poor-risk alteration in FN-RMS/ERMS ~13% of FN-RMS 2023 pqac-00000012
Molecular feature MYOD1 MYOD1 L122R marks biologically aggressive RMS subset and is integrated into modern risk frameworks Survival 0–30% in MYOD1-mutant disease 2023 pqac-00000012
Molecular feature DICER1 in gynecologic ERMS DICER1 alterations are enriched in cervical and uterine ERMS and may aid diagnosis Almost all cervical ERMS and nearly 67% of uterine corpus ERMS carry DICER1 mutations; 4/5 tested gynecologic ERMS in one cohort were DICER1-mutant 2025 pqac-00000006
Molecular feature Chromosomal/copy-number pattern FN-RMS/ERMS shows whole-chromosome gains; one transcriptomic/genomic analysis highlighted chromosome 8 cytoband amplification/gain in FN-RMS chr8-related amplification highlighted; exact ERMS frequency not provided in compact evidence set 2023 pqac-00000012
Diagnostics Histology/IHC ERMS diagnosis relies on morphology plus skeletal muscle markers Common markers: desmin, myogenin, MyoD1; in one gynecologic ERMS series Myogenin 11/13, Desmin 13/13, MyoD1 12/13, Myoglobin 5/9 2025 pqac-00000006

Table: This table condenses the most actionable evidence from the retrieved sources for embryonal rhabdomyosarcoma, covering classification, epidemiology, prognosis, and molecular features. It is useful as a compact reference for knowledge-base population using only facts directly supported by the available context IDs.

1. Disease information

1.1 Definition/overview

Rhabdomyosarcoma (RMS) is described as the most frequent pediatric soft tissue sarcoma, with major subtypes including embryonal and alveolar; ERMS is typically fusion-negative and is described as being driven by oncogenic driver mutations such as RAS and TP53 in the imaging-focused review by de Vries et al. (Pediatric Radiology, 2023‑02, URL: https://doi.org/10.1007/s00247-023-05596-8). (vries2023imaginginrhabdomyosarcoma pages 1-3)

1.2 Key identifiers and classifications

  • WHO classification: Reviews in the retrieved set summarize the WHO approach as including four main RMS subtypes (embryonal, alveolar, pleomorphic, spindle cell/sclerosing). (nakano2026thedevelopmentof pages 1-2)
  • Fusion status classification: COG and other cooperative groups increasingly classify RMS into FOXO1 fusion‑positive vs FOXO1 fusion‑negative, with fusion status replacing histology as a key risk classifier. (oberoi2023childrensoncologygroups pages 1-3)
  • Open Targets disease concept: “Embryonal rhabdomyosarcoma” appears as EFO_0000437 in Open Targets outputs. (OpenTargets Search: embryonal rhabdomyosarcoma)

Not found in the retrieved evidence: ICD‑10/ICD‑11, MeSH identifier, Orphanet (ORPHA) code, MONDO ID.

1.3 Synonyms and alternative names

1.4 Evidence provenance

This report is derived from aggregated disease-level resources (COG blueprint review; imaging guideline review; multi-institutional clinical study; trial registry) and selected clinicopathologic series. (vries2023imaginginrhabdomyosarcoma pages 1-3, oberoi2023childrensoncologygroups pages 1-3, abbou2023circulatingtumordna pages 1-2)

2. Etiology

2.1 Primary causal factors (molecular/genetic)

ERMS/FN‑RMS is characterized by: - Chromosomal alterations: Whole-chromosome gains and 11p15.5 allelic loss are described as characteristic genomic features in the COG blueprint review. (oberoi2023childrensoncologygroups pages 3-5) - 11p15 loss of heterozygosity (LOH): A 2023 review reports that ~80% of ERMS have LOH at 11p15 involving the IGF‑2/IGF2 region. (zarrabi2023rhabdomyosarcomacurrenttherapy pages 3-5) - RAS pathway alterations: The COG blueprint describes frequent RAS‑pathway and point mutations (e.g., NRAS, KRAS, HRAS) in fusion-negative disease. (oberoi2023childrensoncologygroups pages 3-5)

2.2 Risk factors

2.2.1 Genetic predisposition syndromes

Multiple cancer predisposition syndromes are reported as increasing RMS risk in a 2023 imaging guideline review, including: - Neurofibromatosis type 1 (NF1) - Li–Fraumeni syndrome (TP53 germline) - DICER1 syndrome - Noonan syndrome - Beckwith–Wiedemann syndrome - Costello syndrome (vries2023imaginginrhabdomyosarcoma pages 1-3)

2.2.2 Environmental/lifestyle risk factors

No specific environmental or lifestyle risk factors were identified in the retrieved evidence.

2.3 Protective factors

No protective genetic or environmental factors were identified in the retrieved evidence.

2.4 Gene–environment interactions

No ERMS-specific gene–environment interaction evidence was identified in the retrieved set.

3. Phenotypes (clinical presentation)

3.1 Typical phenotypes and presentation

RMS “can present as a mass at nearly any site in the body,” with most common presentations in head and neck, genitourinary tract, and extremities. (vries2023imaginginrhabdomyosarcoma pages 1-3)

3.2 Age of onset and sex ratio

European registry–summarized epidemiology in the imaging review reports: - Median age at diagnosis: ~5 years - Proportion <10 years: ~72–81% - Male:female ratio: ~1.4 (95% CI 1.2–1.6) (vries2023imaginginrhabdomyosarcoma pages 1-3)

3.3 Suggested HPO terms (examples)

Evidence in the retrieved set is not granular enough to assign frequencies per phenotype; the following HPO terms are consistent with common presentations noted (mass lesion by site): - Mass of head and neck (e.g., HP:0000235 Abnormality of head or neck [broad parent]; site-specific “mass” terms may be used in implementation) - Pelvic mass (HP:0002681) / Abdominal mass (HP:0003270) for genitourinary presentations - Soft tissue mass (HP:0030832 [soft-tissue abnormality/mass terms])

Note: HPO IDs above are provided as ontology suggestions; confirm exact term mapping during curation.

4. Genetic / molecular information

4.1 Causal genes and recurrent somatic alterations (ERMS/FN‑RMS)

From the COG blueprint review, fusion‑negative disease is described as having frequent point mutations including NRAS, KRAS, HRAS, TP53, MYOD1, PIK3CA, FGFR4 and characteristic chromosomal events including 11p15.5 allelic loss. (oberoi2023childrensoncologygroups pages 3-5)

4.2 Clinically important poor-risk biomarkers

4.3 DICER1 (site-associated enrichment)

A clinicopathological series of female reproductive system ERMS highlights enrichment for DICER1 alterations, stating: “Almost all cervical ERMS and nearly 67% of uterine corpus ERMS carry DICER1 mutations,” and in their cohort 4/5 tested cases had DICER1 mutations. (Frontiers in Oncology, 2025‑03, URL: https://doi.org/10.3389/fonc.2025.1546607) (bai2025clinicopathologicalanalysisof pages 1-2)

4.4 Epigenetics and omics

The retrieved evidence set did not provide ERMS-specific quantitative epigenetic signatures; however, the COG blueprint emphasizes that molecular profiling (including fusion status and specific mutations) is increasingly incorporated into risk stratification and prospective trials. (oberoi2023childrensoncologygroups pages 1-3)

4.5 Suggested GO and CL terms (mechanism-relevant)

Based on evidence-supported biology (RAS pathway activation; differentiation blockade implied by MYOD1 axis and RMS myogenic markers): - GO (Biological Process) suggestions: - Ras protein signal transduction (e.g., GO:0007265) - Regulation of cell proliferation (GO:0042127) - Myoblast differentiation / skeletal muscle cell differentiation (myogenic program dysregulation; use appropriate child terms during curation) - CL (Cell Ontology) suggestions: - Skeletal muscle cell / myoblast lineages (tumor shows skeletal muscle differentiation markers)

5. Environmental information

No ERMS-specific environmental, lifestyle, or infectious causal contributors were identified in the retrieved evidence.

6. Mechanism / pathophysiology (causal chain)

6.1 Upstream initiating events

In ERMS/FN‑RMS, recurrent genomic alterations include 11p15.5 allelic loss/LOH (IGF2 locus region) and frequent RAS pathway mutations (NRAS/KRAS/HRAS), with subsets harboring TP53 or MYOD1 alterations that confer poor prognosis. (zarrabi2023rhabdomyosarcomacurrenttherapy pages 3-5, oberoi2023childrensoncologygroups pages 3-5)

6.2 Downstream cellular consequences and clinical manifestation

A mechanistic chain supported by the retrieved evidence: 1. Genetic alterations (e.g., 11p15 LOH; RAS-pathway mutations; TP53/MYOD1 in poor-risk subsets) (zarrabi2023rhabdomyosarcomacurrenttherapy pages 3-5, oberoi2023childrensoncologygroups pages 3-5) 2. Promote oncogenic signaling and tumor growth in mesenchymal lineage cells with skeletal muscle differentiation, producing a soft-tissue mass presentation at diverse sites (head/neck, GU tract, extremity) (vries2023imaginginrhabdomyosarcoma pages 1-3) 3. Disease aggressiveness and treatment resistance are increased in molecularly defined high-risk subsets (TP53, MYOD1), reflected in poorer survival outcomes. (oberoi2023childrensoncologygroups pages 3-5)

7. Anatomical structures affected

7.1 Organ/system level (common sites)

Most common presentations: head and neck, genitourinary tract, extremities. (vries2023imaginginrhabdomyosarcoma pages 1-3)

7.2 Suggested UBERON terms (examples)

8. Temporal development

9. Inheritance and population

9.1 Epidemiology

9.2 Sex ratio and age distribution

9.3 Inheritance pattern

Most ERMS appears sporadic; however, multiple germline cancer predisposition syndromes increase risk (NF1, Li–Fraumeni/TP53, DICER1, Noonan, Beckwith–Wiedemann, Costello). (vries2023imaginginrhabdomyosarcoma pages 1-3)

10. Diagnostics

10.1 Pathology and immunohistochemistry (IHC)

A 2023 RMS review notes use of IHC muscle markers including alpha-actin, MyoD1, myogenin, and desmin to distinguish RMS from other small round blue cell tumors. (zarrabi2023rhabdomyosarcomacurrenttherapy pages 3-5)

In a 13‑patient gynecologic ERMS series, IHC positivity rates were: - Desmin: 13/13 - MyoD1: 12/13 - Myogenin: 11/13 - Myoglobin: 5/9 (bai2025clinicopathologicalanalysisof pages 1-2)

10.2 Molecular testing and risk stratification

COG emphasizes fusion status as central: FOXO1 fusion status has replaced histologic subtype in risk stratification, with FOXO1 fusion-positive conferring worse prognosis than fusion-negative. (oberoi2023childrensoncologygroups pages 1-3)

10.3 Imaging and staging (real-world implementation)

The imaging guideline review highlights multidisciplinary management and notes European collaborative imaging guidance (EpSSG/CWS/ESPR collaboration) spanning clinical suspicion, biopsy, staging, response assessment, and follow-up. (vries2023imaginginrhabdomyosarcoma pages 1-3)

10.4 Liquid biopsy / ctDNA (emerging diagnostic/prognostic tool)

In intermediate-risk RMS, baseline ctDNA detection is feasible and prognostic. - Cohort: 124 intermediate-risk RMS patients (75 FN‑RMS; 49 FP‑RMS) - FN‑RMS ctDNA detection at diagnosis: 13/75 (17%) - FN‑RMS outcomes with detectable ctDNA vs not detectable: - EFS: 33.3% vs 68.9% (P = .0028) - OS: 33.3% vs 83.2% (P < .0001) - Similar adverse associations were reported for FP‑RMS. (Journal of Clinical Oncology, 2023‑05, URL: https://doi.org/10.1200/JCO.22.00409) (abbou2023circulatingtumordna pages 1-2)

Additional quantitative details from the same study (alternate excerpt) include: CNAs in tumors 71%, translocations in tumors 93%, and overall ctDNA detection 57% using combined approaches. (abbou2023circulatingtumordna pages 6-7)

11. Outcome / prognosis

11.1 Risk-group outcome ranges

In the imaging-focused review, 5-year overall survival is summarized as: - Localized disease: ~80% - Metastatic disease: ~35% - Broad risk-group range: ~50.6% (very high-risk) to 100% (low-risk) (vries2023imaginginrhabdomyosarcoma pages 1-3)

COG blueprint examples for favorable fusion-negative groups include: - FN Stage 1, Clinical Group I: 5‑year EFS/OS 92% / 99% - Other favorable groups: EFS/OS 87% / 97% (oberoi2023childrensoncologygroups pages 1-3)

11.2 Prognostic biomarkers

Poorer prognosis is associated with FOXO1 fusion positivity, and within FN‑RMS, MYOD1 and TP53 mutations are noted as adverse factors. (oberoi2023childrensoncologygroups pages 1-3, oberoi2023childrensoncologygroups pages 3-5)

12. Treatment

12.1 Standard multimodal therapy

The imaging review describes standard management as multimodal: systemic chemotherapy plus local therapy (surgery and/or radiotherapy). (vries2023imaginginrhabdomyosarcoma pages 1-3)

COG blueprint specifies typical chemotherapy backbones: - VA (vincristine + dactinomycin) ± cyclophosphamide (VAC) - VAC/VI (VAC with irinotecan-containing components) (oberoi2023childrensoncologygroups pages 1-3)

COG-reported comparative outcomes in intermediate-risk trials: - ARST0531: 4-year EFS 63% vs 59% and OS 73% vs 72% for VAC vs VAC/VI strategies (with different cumulative cyclophosphamide exposure). (oberoi2023childrensoncologygroups pages 1-3)

12.2 Current applications: molecularly informed treatment intensification

COG notes that patients meeting very-low/low-risk clinical criteria but with TP53 or MYOD1 mutations are treated with 42 weeks VAC (cumulative cyclophosphamide 16.6 g/m²) and not considered very-low/low risk. (oberoi2023childrensoncologygroups pages 19-20)

12.3 Ongoing / recent clinical trials (selected)

COG ARST2032: very low/low-risk FN-RMS (real-world implementation: enrolling)

  • Trial: NCT05304585 (ClinicalTrials.gov)
  • Title: “Chemotherapy for the Treatment of Patients With Newly Diagnosed Very Low-Risk and Low Risk Fusion Negative Rhabdomyosarcoma”
  • Sponsor/Group: Children’s Oncology Group
  • Status: Recruiting (per retrieved registry snippet)
  • Key regimens: Regimen VA (very low-risk), VAC/VA (low-risk), and a regimen for mutation-positive patients (“Regimen M”) that includes radiotherapy; uses vincristine, dactinomycin, cyclophosphamide (and imaging/staging procedures).
  • Primary endpoint: 3‑year failure‑free survival (Kaplan–Meier)
  • Feasibility endpoint: central molecular risk stratification feasible if ≥80% results returned by 6 weeks. (NCT05304585 chunk 2)

12.4 Suggested MAXO terms (examples)

  • Multiagent chemotherapy (MAXO term for antineoplastic chemotherapy)
  • Tumor resection / surgical excision
  • Radiotherapy
  • Molecular diagnostic procedure (for fusion testing)

13. Prevention

No primary prevention strategies specific to ERMS were identified in the retrieved evidence. Secondary prevention in practice centers on timely recognition, imaging workup, and standardized staging/risk stratification within multidisciplinary pediatric oncology pathways. (vries2023imaginginrhabdomyosarcoma pages 1-3)

14. Other species / natural disease

The retrieved evidence did not provide specific naturally occurring veterinary ERMS epidemiology.

15. Model organisms

A 2023 RMS review notes that in vivo mouse and zebrafish models are used to screen future therapeutic approaches and study mechanisms. (zarrabi2023rhabdomyosarcomacurrenttherapy pages 3-5)

A 2026 review emphasizes that advances in animal models and tissue acquisition have improved understanding of RMS biology, though the provided excerpt does not enumerate specific engineered ERMS models. (hebron2026biologicaladvancesand pages 22-23)

Visual evidence: COG RMS prognostic groups

The COG rhabdomyosarcoma prognostic group table (risk stratification schema with associated long-term EFS ranges) is provided in the retrieved cropped table image. (oberoi2023childrensoncologygroups media 44b370af)

Limitations of the current evidence set

  • Ontology identifiers (MONDO, Orphanet/ORPHA, ICD‑10/11, MeSH) were not present in the retrieved texts; additional targeted retrieval (Orphanet/MONDO/MeSH/ICD sources) would be required for a fully populated identifier section.
  • Several topics requested in the template (environmental modifiers, epigenomic signatures, metabolomics, detailed differential diagnosis lists, and cross-species natural disease frequency) were not covered with ERMS-specific primary data in the retrieved evidence.

Key sources (with publication dates and URLs)

References

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  12. (NCT05304585 chunk 2): Chemotherapy for the Treatment of Patients With Newly Diagnosed Very Low-Risk and Low Risk Fusion Negative Rhabdomyosarcoma. Children's Oncology Group. 2022. ClinicalTrials.gov Identifier: NCT05304585

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