Targeted therapy for advanced salivary gland carcinoma based on molecular profiling: results from MyPathway, a phase IIa multiple basket study.


Journal

Annals of oncology : official journal of the European Society for Medical Oncology
ISSN: 1569-8041
Titre abrégé: Ann Oncol
Pays: England
ID NLM: 9007735

Informations de publication

Date de publication:
03 2020
Historique:
received: 28 08 2019
revised: 08 11 2019
accepted: 28 11 2019
entrez: 19 2 2020
pubmed: 19 2 2020
medline: 7 1 2021
Statut: ppublish

Résumé

Systemic therapy options for salivary cancers are limited. MyPathway (NCT02091141), a phase IIa study, evaluates targeted therapies in non-indicated tumor types with actionable molecular alterations. Here, we present the efficacy and safety results for a subgroup of MyPathway patients with advanced salivary gland cancer (SGC) matched to targeted therapies based on tumor molecular characteristics. MyPathway is an ongoing, multiple basket, open-label, non-randomized, multi-center study. Patients with advanced SGC received pertuzumab + trastuzumab (HER2 alteration), vismodegib (PTCH-1/SMO mutation), vemurafenib (BRAF V600 mutation), or atezolizumab [high tumor mutational burden (TMB)]. The primary endpoint is the objective response rate (ORR). As of January 15, 2018, 19 patients with SGC were enrolled and treated in MyPathway (15 with HER2 amplification and/or overexpression and one each with a HER2 mutation without amplification or overexpression, PTCH-1 mutation, BRAF mutation, and high TMB). In the 15 patients with HER2 amplification/overexpression (with or without mutations) who were treated with pertuzumab + trastuzumab, 9 had an objective response (1 complete response, 8 partial responses) for an ORR of 60% (9.2 months median response duration). The clinical benefit rate (defined by patients with objective responses or stable disease >4 months) was 67% (10/15), median progression-free survival (PFS) was 8.6 months, and median overall survival was 20.4 months. Stable disease was observed in the patient with a HER2 mutation (pertuzumab + trastuzumab, n = 1/1, PFS 11.0 months), and partial responses in patients with the PTCH-1 mutation (vismodegib, n = 1/1, PFS 14.3 months), BRAF mutation (vemurafenib, n = 1/1, PFS 18.5 months), and high TMB (atezolizumab, n = 1/1, PFS 5.5+ months). No unexpected toxicity occurred. Overall, 12 of 19 patients (63%) with advanced SGC, treated with chemotherapy-free regimens matched to specific molecular alterations, experienced an objective response. Data from MyPathway suggest that matched targeted therapy for SGC has promising efficacy, supporting molecular profiling in treatment determination.

Sections du résumé

BACKGROUND
Systemic therapy options for salivary cancers are limited. MyPathway (NCT02091141), a phase IIa study, evaluates targeted therapies in non-indicated tumor types with actionable molecular alterations. Here, we present the efficacy and safety results for a subgroup of MyPathway patients with advanced salivary gland cancer (SGC) matched to targeted therapies based on tumor molecular characteristics.
PATIENTS AND METHODS
MyPathway is an ongoing, multiple basket, open-label, non-randomized, multi-center study. Patients with advanced SGC received pertuzumab + trastuzumab (HER2 alteration), vismodegib (PTCH-1/SMO mutation), vemurafenib (BRAF V600 mutation), or atezolizumab [high tumor mutational burden (TMB)]. The primary endpoint is the objective response rate (ORR).
RESULTS
As of January 15, 2018, 19 patients with SGC were enrolled and treated in MyPathway (15 with HER2 amplification and/or overexpression and one each with a HER2 mutation without amplification or overexpression, PTCH-1 mutation, BRAF mutation, and high TMB). In the 15 patients with HER2 amplification/overexpression (with or without mutations) who were treated with pertuzumab + trastuzumab, 9 had an objective response (1 complete response, 8 partial responses) for an ORR of 60% (9.2 months median response duration). The clinical benefit rate (defined by patients with objective responses or stable disease >4 months) was 67% (10/15), median progression-free survival (PFS) was 8.6 months, and median overall survival was 20.4 months. Stable disease was observed in the patient with a HER2 mutation (pertuzumab + trastuzumab, n = 1/1, PFS 11.0 months), and partial responses in patients with the PTCH-1 mutation (vismodegib, n = 1/1, PFS 14.3 months), BRAF mutation (vemurafenib, n = 1/1, PFS 18.5 months), and high TMB (atezolizumab, n = 1/1, PFS 5.5+ months). No unexpected toxicity occurred.
CONCLUSIONS
Overall, 12 of 19 patients (63%) with advanced SGC, treated with chemotherapy-free regimens matched to specific molecular alterations, experienced an objective response. Data from MyPathway suggest that matched targeted therapy for SGC has promising efficacy, supporting molecular profiling in treatment determination.

Identifiants

pubmed: 32067683
pii: S0923-7534(19)41724-9
doi: 10.1016/j.annonc.2019.11.018
pmc: PMC9743163
mid: NIHMS1849778
pii:
doi:

Substances chimiques

Receptor, ErbB-2 EC 2.7.10.1
Trastuzumab P188ANX8CK

Types de publication

Clinical Trial, Phase II Journal Article Multicenter Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

412-421

Subventions

Organisme : NCI NIH HHS
ID : P30 CA016672
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 The Author(s). Published by Elsevier Ltd.. All rights reserved.

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Auteurs

R Kurzrock (R)

Moores Cancer Center, UC San Diego, San Diego, USA. Electronic address: rkurzrock@ucsd.edu.

D W Bowles (DW)

Department of Medicine, University of Colorado Denver, Aurora, USA.

H Kang (H)

Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, USA.

F Meric-Bernstam (F)

Department of Investigational Cancer Therapeutics, University of Texas MD Anderson Cancer Center, Houston, USA.

J Hainsworth (J)

Oncology Department, Sarah Cannon Research Institute, Nashville, USA; Tennessee Oncology, PLLC, Nashville, USA.

D R Spigel (DR)

Oncology Department, Sarah Cannon Research Institute, Nashville, USA; Tennessee Oncology, PLLC, Nashville, USA.

R Bose (R)

Division of Oncology, Department of Medicine, Washington University School of Medicine, St. Louis, USA.

H Burris (H)

Oncology Department, Sarah Cannon Research Institute, Nashville, USA; Tennessee Oncology, PLLC, Nashville, USA.

C J Sweeney (CJ)

Dana-Farber Cancer Institute, Harvard Medical School, Boston, USA.

M S Beattie (MS)

Department of Product Development, Medical Affairs, Genentech, Inc., South San Francisco, USA.

S Blotner (S)

Department of Biostatistics, Genentech, Inc., South San Francisco, USA.

K Schulze (K)

Department of Oncology Biomarker Development, Genentech, Inc., South San Francisco, USA.

V Cuchelkar (V)

Department of BioOncology, Genentech, Inc., South San Francisco, USA.

C Swanton (C)

Department of Tumour Biology, Francis Crick Institute, London, UK.

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Classifications MeSH