Comparative molecular analysis of testicular Leydig cell tumors demonstrates distinct subsets of neoplasms with aggressive histopathologic features.


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:
10 2021
Historique:
received: 20 03 2021
accepted: 24 05 2021
revised: 19 05 2021
pubmed: 10 6 2021
medline: 18 3 2022
entrez: 9 6 2021
Statut: ppublish

Résumé

Testicular Leydig cell tumor (LCT), the most common sex-cord stromal tumor in men, represents a small fraction of all testicular tumors (~1 to 3%). Although most testicular LCTs are indolent and cured by radical orchiectomy, 5-10% have aggressive biology and metastatic potential. In primary LCTs, large size, cytologic atypia, necrosis, increased mitotic activity, and vascular invasion have been associated with clinically aggressive tumors. From a molecular perspective, the characteristics of aggressive LCTs and the differences between aggressive and nonaggressive LCTs remain largely unexplored. This study compares the genomic landscape of aggressive and nonaggressive testicular LCTs. Twenty-six cases were analyzed using next-generation DNA sequencing (NGS) and immunohistochemistry. Cases were classified as aggressive LCT if they met published criteria for malignancy in primary (i.e., testicular) tumors or if they had pathology-proven metastatic disease; otherwise, cases were considered nonaggressive. This multi-institutional series included 18 aggressive LCTs (14 primary/testicular, 4 metastatic) and 8 nonaggressive LCTs. Two cases (2/26, 8%; both aggressive LCTs) failed sequencing and had negative (i.e., uninformative) FH immunohistochemistry results. One additional primary aggressive LCT failed sequencing but had informative FH immunohistochemistry results. Combined NGS and immunohistochemical analysis demonstrated FH inactivation in 5/26 cases (19%). In addition, NGS demonstrated CTNNB1 mutations or biallelic APC inactivation in 9/23 cases (39%), copy number changes without recurrent mutations in 6/23 (26%) cases, and no alterations in 4/23 cases (17%). CTNNB1 mutations were present in both aggressive and nonaggressive LCTs. In contrast, FH inactivation and multiple copy number changes were only identified in aggressive LCTs. In conclusion, three distinct subgroups of aggressive LCTs were characterized by FH inactivation, Wnt pathway activation, and copy number changes without recurrent mutations, respectively. Nuclear translocation of β-catenin and Wnt pathway activation appear to be early driver events that provide an environment conducive for progression to aggressive biology in a subset of LCTs.

Identifiants

pubmed: 34103665
doi: 10.1038/s41379-021-00845-3
pii: S0893-3952(22)00538-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1935-1946

Informations de copyright

© 2021. The Author(s), under exclusive licence to United States & Canadian Academy of Pathology.

Références

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Auteurs

Natalie M Rizzo (NM)

Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Lynette M Sholl (LM)

Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Muhammad T Idrees (MT)

Department of Pathology, Indiana University School of Medicine, Indianapolis, IN, USA.

John C Cheville (JC)

Department of Pathology, Mayo Clinic, Mayo Clinic Alix School of Medicine, Rochester, MN, USA.

Sounak Gupta (S)

Department of Pathology, Mayo Clinic, Mayo Clinic Alix School of Medicine, Rochester, MN, USA.

Kristine M Cornejo (KM)

Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.

Hiroshi Miyamoto (H)

Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, University of Rochester School of Medicine and Dentistry, Rochester, NY, USA.

Michelle S Hirsch (MS)

Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

Katrina Collins (K)

Department of Pathology, Indiana University School of Medicine, Indianapolis, IN, USA.

Andrés M Acosta (AM)

Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. aacosta4@bwh.harvard.edu.

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