Assessment of Androgen Receptor Splice Variant-7 as a Biomarker of Clinical Response in Castration-Sensitive Prostate Cancer.


Journal

Clinical cancer research : an official journal of the American Association for Cancer Research
ISSN: 1557-3265
Titre abrégé: Clin Cancer Res
Pays: United States
ID NLM: 9502500

Informations de publication

Date de publication:
15 08 2022
Historique:
received: 16 03 2022
revised: 17 05 2022
accepted: 08 06 2022
pubmed: 14 6 2022
medline: 17 8 2022
entrez: 13 6 2022
Statut: ppublish

Résumé

Therapies targeting the androgen receptor (AR) have improved the outcome for patients with castration-sensitive prostate cancer (CSPC). Expression of the constitutively active AR splice variant-7 (AR-V7) has shown clinical utility as a predictive biomarker of AR-targeted therapy resistance in castration-resistant prostate cancer (CRPC), but its importance in CSPC remains understudied. We assessed different approaches to quantify AR-V7 mRNA and protein in prostate cancer cell lines, patient-derived xenograft (PDX) models, publicly available cohorts, and independent institutional clinical cohorts, to identify reliable approaches for detecting AR-V7 mRNA and protein and its association with clinical outcome. In CSPC and CRPC cohorts, AR-V7 mRNA was much less abundant when detected using reads across splice boundaries than when considering isoform-specific exonic reads. The RM7 AR-V7 antibody had increased sensitivity and specificity for AR-V7 protein detection by immunohistochemistry (IHC) in CRPC cohorts but rarely identified AR-V7 protein reactivity in CSPC cohorts, when compared with the EPR15656 AR-V7 antibody. Using multiple CRPC PDX models, we demonstrated that AR-V7 expression was exquisitely sensitive to hormonal manipulation. In CSPC institutional cohorts, AR-V7 protein quantification by either assay was associated neither with time to development of castration resistance nor with overall survival, and intense neoadjuvant androgen-deprivation therapy did not lead to significant AR-V7 mRNA or staining following treatment. Neither pre- nor posttreatment AR-V7 levels were associated with volumes of residual disease after therapy. This study demonstrates that further analytical validation and clinical qualification are required before AR-V7 can be considered for clinical use in CSPC as a predictive biomarker.

Identifiants

pubmed: 35695870
pii: 707390
doi: 10.1158/1078-0432.CCR-22-0851
pmc: PMC9378683
mid: NIHMS1817508
doi:

Substances chimiques

Androgen Antagonists 0
Biomarkers 0
Protein Isoforms 0
RNA, Messenger 0
Receptors, Androgen 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

3509-3525

Subventions

Organisme : Medical Research Council
ID : MR/M018318/1
Pays : United Kingdom
Organisme : NCI NIH HHS
ID : P50 CA090381
Pays : United States
Organisme : NCI NIH HHS
ID : P50 CA097186
Pays : United States
Organisme : NCI NIH HHS
ID : R01 CA234715
Pays : United States
Organisme : Medical Research Council
ID : MR/W018217/1
Pays : United Kingdom
Organisme : NCI NIH HHS
ID : P01 CA163227
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA BC011679
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA BC011838
Pays : United States
Organisme : Intramural NIH HHS
ID : Z99 CA999999
Pays : United States

Informations de copyright

©2022 The Authors; Published by the American Association for Cancer Research.

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Auteurs

Adam G Sowalsky (AG)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Ines Figueiredo (I)

Institute of Cancer Research, London, UK.

Rosina T Lis (RT)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Ilsa Coleman (I)

Fred Hutchinson Cancer Research Center, Seattle, Washington.

Bora Gurel (B)

Institute of Cancer Research, London, UK.

Denisa Bogdan (D)

Institute of Cancer Research, London, UK.

Wei Yuan (W)

Institute of Cancer Research, London, UK.

Joshua W Russo (JW)

Beth Israel Deaconess Medical Center, Boston, Massachusetts.

John R Bright (JR)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Nichelle C Whitlock (NC)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Shana Y Trostel (SY)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Anson T Ku (AT)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Radhika A Patel (RA)

Fred Hutchinson Cancer Research Center, Seattle, Washington.

Lawrence D True (LD)

University of Washington, Seattle, Washington.

Jonathan Welti (J)

Institute of Cancer Research, London, UK.

Juan M Jimenez-Vacas (JM)

Institute of Cancer Research, London, UK.

Daniel Nava Rodrigues (DN)

Institute of Cancer Research, London, UK.

Ruth Riisnaes (R)

Institute of Cancer Research, London, UK.

Antje Neeb (A)

Institute of Cancer Research, London, UK.

Cynthia T Sprenger (CT)

University of Washington, Seattle, Washington.

Amanda Swain (A)

Institute of Cancer Research, London, UK.

Scott Wilkinson (S)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Fatima Karzai (F)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

William L Dahut (WL)

Center for Cancer Research, NCI, NIH, Bethesda, Maryland.

Steven P Balk (SP)

Beth Israel Deaconess Medical Center, Boston, Massachusetts.

Eva Corey (E)

University of Washington, Seattle, Washington.

Peter S Nelson (PS)

Fred Hutchinson Cancer Research Center, Seattle, Washington.
University of Washington, Seattle, Washington.

Michael C Haffner (MC)

Fred Hutchinson Cancer Research Center, Seattle, Washington.
University of Washington, Seattle, Washington.

Stephen R Plymate (SR)

University of Washington, Seattle, Washington.
Geriatrics Research, Education and Clinical Center, VAPSHCS, Seattle, Washington.

Johann S de Bono (JS)

Institute of Cancer Research, London, UK.
Royal Marsden NHS Foundation Trust, London, UK.

Adam Sharp (A)

Institute of Cancer Research, London, UK.
Royal Marsden NHS Foundation Trust, London, UK.

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