Infantile inflammatory myofibroblastic tumors: clinicopathological and molecular characterization of 12 cases.
Antineoplastic Agents
/ therapeutic use
Biomarkers, Tumor
/ analysis
Crizotinib
/ therapeutic use
Female
Gene Fusion
Gene Rearrangement
Genetic Predisposition to Disease
Humans
Infant
Infant, Newborn
Italy
Kinesins
Male
Myofibroblasts
/ drug effects
Neoplasms, Muscle Tissue
/ drug therapy
Phenotype
Philadelphia
Protein Kinase Inhibitors
/ therapeutic use
Registries
Soft Tissue Neoplasms
/ drug therapy
Journal
Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
ISSN: 1530-0285
Titre abrégé: Mod Pathol
Pays: United States
ID NLM: 8806605
Informations de publication
Date de publication:
04 2020
04 2020
Historique:
received:
16
08
2019
accepted:
07
10
2019
revised:
06
10
2019
pubmed:
7
11
2019
medline:
26
1
2021
entrez:
7
11
2019
Statut:
ppublish
Résumé
Inflammatory myofibroblastic tumors arising in infants are rare, poorly investigated and mostly reported as isolated cases or as a part of larger series thus, their clinicopathological and molecular features are essentially unknown. Archival files from two large pediatric institutions and a tumor registry were queried for pediatric inflammatory myofibroblastic tumors. Available material from patients ≤12 months of age was reviewed. Additional immunostains (ALK-1, D240, WT1) and ALK-FISH studies were performed as needed. Targeted anchored multiplex PCR with next-generation sequencing was done in all cases. A total of 12 of 131 infantile cases (mean 5.5 months) were identified (M:F of 2:1). Anatomic locations included intestinal/mesenteric (n = 6), head/neck (n = 3), and viscera (n = 3). Half of tumors showed a hypocellular myxoid pattern, perivascular condensation, and prominent vasculature with vague glomeruloid structures present in four of them. The remaining cases exhibited a more cellular pattern with minimal myxoid component. ALK-1 immunohistochemistry was positive in most cases (11/12) with cytoplasmic-diffuse (n = 6), cytoplasmic-granular (n = 2), and dot-like (n = 3) staining patterns. ALK fusion partners identified in five cases included EML4, TPM4, RANBP2, and a novel KLC1. Three inflammatory myofibroblastic tumors showed fusions with other kinases including TFG-ROS1 and novel FN1-ROS1 and RBPMS-NTRK3 rearrangements. Favorable outcome was documented in most cases (10/11) with available follow-up (median 17 months) while three patients were successfully treated with crizotinib. In summary, infantile inflammatory myofibroblastic tumors are rare and can exhibit paucicellular, extensively myxoid/vascular morphology with peculiar immunophenotype mimicking other mesenchymal or vascular lesions. All tumors harbored kinase fusions involving ALK, ROS1, and NTRK3 including three novel fusion partners (KLC1, FN1, and RBPMS, respectively). A favorable response to crizotinib seen in three cases supports its potential use in infants as seen in older patients. Awareness of these unusual morphologic, immunophenotypic, and molecular features is critical for appropriate diagnosis and optimized targeted therapy.
Identifiants
pubmed: 31690781
doi: 10.1038/s41379-019-0406-6
pii: S0893-3952(22)00884-5
doi:
Substances chimiques
Antineoplastic Agents
0
Biomarkers, Tumor
0
KLC1 protein, human
0
Protein Kinase Inhibitors
0
Crizotinib
53AH36668S
Kinesins
EC 3.6.4.4
Types de publication
Journal Article
Multicenter Study
Langues
eng
Sous-ensembles de citation
IM
Pagination
576-590Références
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