PARP inhibition with rucaparib alone followed by combination with atezolizumab: Phase Ib COUPLET clinical study in advanced gynaecological and triple-negative breast cancers.


Journal

British journal of cancer
ISSN: 1532-1827
Titre abrégé: Br J Cancer
Pays: England
ID NLM: 0370635

Informations de publication

Date de publication:
06 Jul 2024
Historique:
received: 30 01 2024
accepted: 18 06 2024
revised: 03 06 2024
medline: 7 7 2024
pubmed: 7 7 2024
entrez: 6 7 2024
Statut: aheadofprint

Résumé

Combining PARP inhibitors (PARPis) with immune checkpoint inhibitors may improve clinical outcomes in selected cancers. We evaluated rucaparib and atezolizumab in advanced gynaecological or triple-negative breast cancer (TNBC). After identifying the recommended dose, patients with PARPi-naive BRCA-mutated or homologous recombination-deficient/loss-of-heterozygosity-high platinum-sensitive ovarian cancer or TNBC received rucaparib plus atezolizumab. Tumour biopsies were collected pre-treatment, during single-agent rucaparib run-in, and after starting combination therapy. The most common adverse events with rucaparib 600 mg twice daily and atezolizumab 1200 mg on Day 1 every 3 weeks were gastrointestinal effects, fatigue, liver enzyme elevations, and anaemia. Responding patients typically had BRCA-mutated tumours and higher pre-treatment tumour levels of PD-L1 and CD8 + T cells. Markers of DNA damage repair decreased during rucaparib run-in and combination treatment in responders, but typically increased in non-responders. Apoptosis signature expression showed the reverse. CD8 + T-cell activity and STING pathway activation increased during rucaparib run-in, increasing further with atezolizumab. In this small study, rucaparib plus atezolizumab demonstrated acceptable safety and activity in BRCA-mutated tumours. Increasing anti-tumour immunity and inflammation might be a key mechanism of action for clinical benefit from the combination, potentially guiding more targeted development of such regimens. ClinicalTrials.gov (NCT03101280).

Sections du résumé

BACKGROUND BACKGROUND
Combining PARP inhibitors (PARPis) with immune checkpoint inhibitors may improve clinical outcomes in selected cancers. We evaluated rucaparib and atezolizumab in advanced gynaecological or triple-negative breast cancer (TNBC).
METHODS METHODS
After identifying the recommended dose, patients with PARPi-naive BRCA-mutated or homologous recombination-deficient/loss-of-heterozygosity-high platinum-sensitive ovarian cancer or TNBC received rucaparib plus atezolizumab. Tumour biopsies were collected pre-treatment, during single-agent rucaparib run-in, and after starting combination therapy.
RESULTS RESULTS
The most common adverse events with rucaparib 600 mg twice daily and atezolizumab 1200 mg on Day 1 every 3 weeks were gastrointestinal effects, fatigue, liver enzyme elevations, and anaemia. Responding patients typically had BRCA-mutated tumours and higher pre-treatment tumour levels of PD-L1 and CD8 + T cells. Markers of DNA damage repair decreased during rucaparib run-in and combination treatment in responders, but typically increased in non-responders. Apoptosis signature expression showed the reverse. CD8 + T-cell activity and STING pathway activation increased during rucaparib run-in, increasing further with atezolizumab.
CONCLUSIONS CONCLUSIONS
In this small study, rucaparib plus atezolizumab demonstrated acceptable safety and activity in BRCA-mutated tumours. Increasing anti-tumour immunity and inflammation might be a key mechanism of action for clinical benefit from the combination, potentially guiding more targeted development of such regimens.
CLINICAL TRIAL REGISTRATION BACKGROUND
ClinicalTrials.gov (NCT03101280).

Identifiants

pubmed: 38971950
doi: 10.1038/s41416-024-02776-7
pii: 10.1038/s41416-024-02776-7
doi:

Banques de données

ClinicalTrials.gov
['NCT03101280']

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024. The Author(s).

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Auteurs

Rebecca Kristeleit (R)

University College London Cancer Institute, London, UK. rebecca.kristeleit@gstt.nhs.uk.
School of Cancer and Pharmaceutical Sciences, King's College London, London, UK. rebecca.kristeleit@gstt.nhs.uk.
Guy's and St Thomas' NHS Foundation Trust and King's College London, London, UK. rebecca.kristeleit@gstt.nhs.uk.

Alexandra Leary (A)

Gustave Roussy, Villejuif, France.

Ana Oaknin (A)

Gynaecologic Cancer Programme, Vall d'Hebron Institute of Oncology (VHIO), Hospital Universitario Vall d'Hebron, Vall d'Hebron Barcelona Hospital Campus, Barcelona, Spain.

Andres Redondo (A)

Medical Oncology Department, La Paz University Hospital-IdiPAZ, Madrid, Spain.

Angela George (A)

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

Stephen Chui (S)

Product Development Oncology, Genentech Inc., South San Francisco, CA, USA.

Aicha Seiller (A)

F. Hoffmann-La Roche Ltd, Basel, Switzerland.

Mario Liste-Hermoso (M)

F. Hoffmann-La Roche Ltd, Basel, Switzerland.

Jenna Willis (J)

Product Development Safety, Roche Products Ltd, Welwyn Garden City, UK.

Colby S Shemesh (CS)

Clinical Pharmacology Oncology, Genentech Inc, South San Francisco, CA, USA.

Jim Xiao (J)

Clovis Oncology, San Francisco, CA, USA.

Kevin K Lin (KK)

Clovis Oncology, San Francisco, CA, USA.

Luciana Molinero (L)

Translational Medicine, Genentech Inc., South San Francisco, CA, USA.

Yinghui Guan (Y)

Translational Medicine, Genentech Inc., South San Francisco, CA, USA.

Isabelle Ray-Coquard (I)

Centre Leon Bérard, HESPER laboratory EA 7425, Université Claude Bernard Lyon Est, Lyon, France.

Linda Mileshkin (L)

Department of Medical Oncology, Peter MacCallum Cancer Centre and University of Melbourne, Melbourne, VIC, Australia.

Classifications MeSH