KMT2A-rearranged sarcoma with unusual fusion gene CBX6::KMT2A::PYGO1.


Journal

Virchows Archiv : an international journal of pathology
ISSN: 1432-2307
Titre abrégé: Virchows Arch
Pays: Germany
ID NLM: 9423843

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 15 06 2023
accepted: 24 08 2023
revised: 22 08 2023
medline: 7 12 2023
pubmed: 15 9 2023
entrez: 15 9 2023
Statut: ppublish

Résumé

Recently, rare sarcomas harboring KMT2A rearrangements have been reported. They occur in relatively young individuals, exhibit a sclerosing epithelioid fibrosarcoma-like morphology, and often have an aggressive prognosis. YAP1::KMT2A::YAP1 is the most common fusion gene, followed by VIM::KMT2A. We report the case of a 47-year-old man with a spindle cell tumor arising from the subcutaneous tissue of the right anterior chest. The tumor harbored an unusual novel fusion gene, CBX6::KMT2A::PYGO1. Histologically, the tumor consisted of proliferating spindle-shaped cells with uniform nuclei, which varied in cell density and the amount of intervening collagen fibers. After 2 years and 8 months without postoperative treatment, the patient showed no recurrence or metastasis. Although highly likely irreproducible, tumors with the CBX6::KMT2A::PYGO1 fusion gene were morphologically somewhat different from those containing the YAP1::KMT2A::YAP1. This suggests that KMT2A rearrangements with fusion gene partners different from YAP1 result in purely spindle-shaped cell tumors that produce collagen fibers.

Identifiants

pubmed: 37713130
doi: 10.1007/s00428-023-03639-x
pii: 10.1007/s00428-023-03639-x
doi:

Substances chimiques

Collagen 9007-34-5
Oncogene Proteins, Fusion 0
Biomarkers, Tumor 0
PYGO1 protein, human 0
Adaptor Proteins, Signal Transducing 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

891-897

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.

Références

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Auteurs

Harumi Nakamura (H)

Laboratory of Genomic Pathology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan. harumi.nakamura@oici.jp.
Department of Diagnostic Pathology and Cytology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan. harumi.nakamura@oici.jp.

Yoji Kukita (Y)

Laboratory of Genomic Pathology, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan.

Toru Wakamatsu (T)

Department of Orthopedic Surgery, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan.

Satoshi Takenaka (S)

Department of Orthopedic Surgery, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan.

Keiichi Yoshida (K)

Next-generation Precision Medicine Research Center, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan.

Toshinari Yagi (T)

Department of Outpatient Chemotherapy, Osaka International Cancer Institute, 3-1-69 Otemae, Chuo-ku, Osaka, Osaka, 5418567, Japan.

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