Transcriptomes of Prostate Cancer with TMPRSS2:ERG and Other ETS Fusions.


Journal

Molecular cancer research : MCR
ISSN: 1557-3125
Titre abrégé: Mol Cancer Res
Pays: United States
ID NLM: 101150042

Informations de publication

Date de publication:
03 01 2023
Historique:
received: 06 06 2022
revised: 30 07 2022
accepted: 15 09 2022
pubmed: 21 9 2022
medline: 5 1 2023
entrez: 20 9 2022
Statut: ppublish

Résumé

The most common somatic event in primary prostate cancer is a fusion between the androgen-related TMPRSS2 gene and the ERG oncogene. Tumors with these fusions, which occur early in carcinogenesis, have a distinctive etiology. A smaller subset of other tumors harbor fusions between TMPRSS2 and members of the ETS transcription factor family other than ERG. To assess the genomic similarity of tumors with non-ERG ETS fusions and those with fusions involving ERG, this study derived a transcriptomic signature of non-ERG ETS fusions and assessed this signature and ERG-related gene expression in 1,050 men with primary prostate cancer from three independent population-based and hospital-based studies. Although non-ERG ETS fusions involving ETV1, ETV4, ETV5, or FLI1 were individually rare, they jointly accounted for one in seven prostate tumors. Genes differentially regulated between non-ERG ETS tumors and tumors without ETS fusions showed similar differential expression when ERG tumors and tumors without ETS fusions were compared (differences explained: R2 = 69-77%), including ETS-related androgen receptor (AR) target genes. Differences appeared to result from similarities among ETS tumors rather than similarities among non-ETS tumors. Gene sets associated with ERG fusions were consistent with gene sets associated with non-ERG ETS fusions, including fatty acid and amino acid metabolism, an observation that was robust across cohorts. Considering ETS fusions jointly may be useful for etiologic studies on prostate cancer, given that the transcriptome is profoundly impacted by ERG and non-ERG ETS fusions in a largely similar fashion, most notably genes regulating metabolic pathways.

Identifiants

pubmed: 36125519
pii: 709264
doi: 10.1158/1541-7786.MCR-22-0446
pmc: PMC9812892
mid: NIHMS1838547
doi:

Substances chimiques

Oncogene Proteins, Fusion 0
Proto-Oncogene Proteins c-ets 0
Transcriptional Regulator ERG 0
ERG protein, human 0
TMPRSS2 protein, human EC 3.4.21.-
Serine Endopeptidases EC 3.4.21.-

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

14-23

Subventions

Organisme : NCI NIH HHS
ID : P50 CA090381
Pays : United States
Organisme : NCI NIH HHS
ID : U01 CA167552
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA136578
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA141298
Pays : United States

Informations de copyright

©2022 American Association for Cancer Research.

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Auteurs

Konrad H Stopsack (KH)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Xiaofeng A Su (XA)

David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, Massachusetts.

J Bailey Vaselkiv (JB)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Rebecca E Graff (RE)

Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California.
Division of Research, Kaiser Permanente Northern California, Oakland, California.
Helen Diller Family Comprehensive Cancer Center, University of California San Francisco, San Francisco, California.

Ericka M Ebot (EM)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

Andreas Pettersson (A)

Clinical Epidemiology Division, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden.

Rosina T Lis (RT)

Department of Pathology and Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute, Boston, Massachusetts.

Michelangelo Fiorentino (M)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Pathology Unit, Addarii Institute, S. Orsola-Malpighi Hospital, Bologna, Italy.

Massimo Loda (M)

Department of Pathology, Weill Cornell Medical College, New York, New York.

Kathryn L Penney (KL)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Maryland.

Tamara L Lotan (TL)

Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland.

Lorelei A Mucci (LA)

Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.

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