Identification of fusions with potential clinical significance in melanoma.


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:
12 2022
Historique:
received: 23 09 2021
accepted: 04 07 2022
revised: 01 07 2022
pubmed: 24 7 2022
medline: 2 12 2022
entrez: 23 7 2022
Statut: ppublish

Résumé

Though uncommon in melanoma, gene fusions may have therapeutic implications. Next generation sequencing-based clinical assays, designed to detect relevant gene fusions, mutations, and copy number changes, were performed on 750 melanomas (375 primary and 375 metastases) at our institution from 2014-2021. These included 599 (80%) cutaneous, 38 (5%) acral, 11 (1.5%) anorectal, 23 (3%) sinonasal, 27 (3.6%) eye (uveal/ conjunctiva), 11 (1.5%) genital (vulva/penile), and 41 (5.5%) melanomas of unknown primary. Sixteen fusions (2%) were detected in samples from 16 patients: 12/599 (2%) cutaneous, 2/38 (5%) acral, 1/9 (11%) vulva, 1/23(4.3%) sinonasal; and 12/16 (75%) fusions were potentially targetable. We identified two novel rearrangements: NAGS::MAST2 and NOTCH1::GNB1; and two fusions that have been reported in other malignancies but not in melanoma: CANT1::ETV4 (prostate cancer) and CCDC6::RET (thyroid cancer). Additional fusions, previously reported in melanoma, included: EML4::ALK, MLPH::ALK, AGAP3::BRAF, AGK::BRAF, CDH3::BRAF, CCT8::BRAF, DIP2B::BRAF, EFNB1::RAF1, LRCH3::RAF1, MAP4::RAF1, RUFY1::RAF1, and ADCY2::TERT. Fusion positive melanomas harbored recurrent alterations in TERT and CDKN2A, among others. Gene fusions were exceedingly rare (0.2%) in BRAF/RAS/NF1-mutant tumors and were detected in 5.6% of triple wild-type melanomas. Interestingly, gene rearrangements were significantly enriched within the subset of triple wild-type melanomas that harbor TERT promoter mutations (18% versus 2%, p < 0.0001). Thirteen (81%) patients were treated with immunotherapy for metastatic disease or in the adjuvant setting. Six of 12 (50%) patients with potentially actionable fusions progressed on immunotherapy, and 3/6 (50%) were treated with targeted agents (ALK and MEK inhibitors), 2 off-label and 1 as part of a clinical trial. One patient with an AGAP3::BRAF fusion positive melanoma experienced a 30-month long response to trametinib. We show that, detecting fusions, especially in triple wild-type melanomas with TERT promoter mutations, may have a clinically significant impact in patients with advanced disease who have failed front-line immunotherapy.

Identifiants

pubmed: 35871080
doi: 10.1038/s41379-022-01138-z
pii: S0893-3952(22)05496-5
doi:

Substances chimiques

Proto-Oncogene Proteins B-raf EC 2.7.11.1
Receptor Protein-Tyrosine Kinases EC 2.7.10.1
DIP2B protein, human 0
Nerve Tissue Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1837-1847

Informations de copyright

© 2022. The Author(s), under exclusive licence to United States & Canadian Academy of Pathology.

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Auteurs

Jakob M T Moran (JMT)

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

Long P Le (LP)

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

Valentina Nardi (V)

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

Josephine Golas (J)

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

Alexander A Farahani (AA)

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

Sylvia Signorelli (S)

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

Maristela L Onozato (ML)

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

Ruth K Foreman (RK)

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

Lyn M Duncan (LM)

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

Donald P Lawrence (DP)

Division of Medical Oncology, Department of Medicine, Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA.

Jochen K Lennerz (JK)

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

Dora Dias-Santagata (D)

Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. ddiassantagata@mgh.harvard.edu.

Mai P Hoang (MP)

Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. mhoang@mgh.harvard.edu.

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