Endometrial carcinomas with ambiguous histology often harbor TP53 mutations.

Ambiguous endometrial carcinoma Survival TP53 Whole-exome sequencing

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:
05 Sep 2024
Historique:
received: 06 07 2024
accepted: 25 08 2024
revised: 01 08 2024
medline: 5 9 2024
pubmed: 5 9 2024
entrez: 5 9 2024
Statut: aheadofprint

Résumé

The objective of the present study was to characterize the molecular features of endometrial carcinomas with ambiguous histology. Eighteen carcinomas that could not be conclusively typed based on morphology and immunohistochemistry underwent analysis of mismatch repair (MMR) status, microsatellite status, and whole-exome sequencing. None of the tumors had pathogenic POLE mutation. Twelve tumors (67%) were microsatellite stable, and 6 (33%) had microsatellite instability. Fourteen tumors (78%) harbored TP53 mutations, and 2 (11%) had mutations in MMR genes. Eleven carcinomas (61%) were classified as copy number high and 7 (39%) as MSI-hypermutated, the latter including 3 tumors with TP53 mutation who concomitantly had MSI or mutation in a MMR gene. Other mutations that were found in > 1 tumor affected MUC16 (7 tumors), PIK3CA (6 tumors), PPP2R1A (6 tumors), ARID1A (5 tumors), PTEN (5 tumors), FAT1 (4 tumors), FAT4 (3 tumors), BRCA2 (2 tumors), ERBB2 (2 tumors), FBXW7 (2 tumors), MET (2 tumors), MTOR (2 tumors), JAK1 (2 tumors), and CSMD3 (2 tumors). At the last follow-up (median = 68.6 months), 8 patients had no evidence of disease, 1 patient was alive with disease, 8 patients were dead of disease, and 1 patient died of other cause. In conclusion, based on this series, the molecular landscape of endometrial carcinomas with ambiguous histology is dominated by TP53 mutations and the absence of POLE mutations, with heterogeneous molecular profile with respect to other genes. A high proportion of these tumors is clinically aggressive.

Identifiants

pubmed: 39235515
doi: 10.1007/s00428-024-03912-7
pii: 10.1007/s00428-024-03912-7
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s).

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Auteurs

Ben Davidson (B)

Department of Pathology, Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310, Oslo, Norway. bend@medisin.uio.no.
Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, N-0316, Oslo, Norway. bend@medisin.uio.no.

Karin Teien Lande (K)

Department of Cancer Genetics, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310, Oslo, Norway.

Daniel Nebdal (D)

Department of Cancer Genetics, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310, Oslo, Norway.

Anne Jorunn Nesbakken (AJ)

Department of Pathology, Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310, Oslo, Norway.

Arild Holth (A)

Department of Pathology, Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310, Oslo, Norway.

Kristina Lindemann (K)

Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, N-0316, Oslo, Norway.
Section for Gynecologic Oncology, Division of Surgical Oncology, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.

Ane Gerda Zahl Eriksson (AG)

Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, N-0316, Oslo, Norway.
Section for Gynecologic Oncology, Division of Surgical Oncology, Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway.

Therese Sørlie (T)

Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, N-0316, Oslo, Norway. tsorlie@rr-research.no.
Department of Cancer Genetics, Institute for Cancer Research, Norwegian Radium Hospital, Oslo University Hospital, Montebello, N-0310, Oslo, Norway. tsorlie@rr-research.no.

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