Title
Tumor-specific major histocompatibility-II expression predicts benefit to anti⇓PD-1/L1 therapy in patients with HER2-negative primary breast cancer
Date Issued
01 October 2021
Access level
open access
Resource Type
journal article
Author(s)
Gonzalez-Ericsson P.I.
Wulfkhule J.D.
Gallagher R.I.
Sun X.
Axelrod M.L.
Sheng Q.
Luo N.
Sanchez V.
Sanders M.
Pusztai L.
Petricoin E.
Blenman K.R.M.
Balko J.M.
Publisher(s)
American Association for Cancer Research Inc.
Abstract
Purpose: Immunotherapies targeting PD-1/L1 enhance pathologic complete response (pCR) rates when added to standard neoadjuvant chemotherapy (NAC) regimens in early-stage triple-negative, and possibly high-risk estrogen receptor–positive breast cancer. However, immunotherapy has been associated with significant toxicity, and most patients treated with NAC do not require immunotherapy to achieve pCR. Biomarkers discerning patients benefitting from the addition of immunotherapy from those who would achieve pCR to NAC alone are clearly needed. In this study, we tested the ability of MHC-II expression on tumor cells, to predict immunotherapy-specific benefit in the neoadjuvant breast cancer setting. Patients and Methods: This was a retrospective tissue-based analysis of 3 cohorts of patients with breast cancer: (i) primary nonimmunotherapy-treated breast cancers (n ¼ 381), (ii) triple-negative breast cancers (TNBC) treated with durvalumab and standard NAC (n ¼ 48), and (iii) HER2-negative patients treated with standard NAC (n ¼ 87) or NAC and pembrolizumab (n ¼ 66). Results: HLA-DR positivity on ≥5% of tumor cells, defined a priori, was observed in 10% and 15% of primary non-immunotherapy–treated hormone receptor–positive and triple-negative breast cancers, respectively. Quantitative assessment of MHC-II on tumor cells was predictive of durvalumab þ NAC and pembrolizumab þ NAC (ROC AUC, 0.71; P ¼ 0.01 and AUC, 0.73; P ¼ 0.001, respectively), but not NAC alone (AUC, 0.5; P ¼ 0.99). Conclusions: Tumor-specific MHC-II has a strong candidacy as a specific biomarker of anti–PD-1/L1 immunotherapy benefit when added to standard NAC in HER2-negative breast cancer. Combined with previous studies in melanoma, MHC-II has the potential to be a pan-cancer biomarker. Validation is warranted in existing and future phase II/III clinical trials in this setting.
Start page
5299
End page
5306
Volume
27
Issue
19
Language
English
OCDE Knowledge area
Patología
Oncología
Scopus EID
2-s2.0-85117788750
PubMed ID
Source
Clinical Cancer Research
ISSN of the container
10780432
Sponsor(s)
J.D. Wulfkhule reports grants from Gateway for Cancer Research during the conduct of the study, as well as other support from Theralink Technologies and personal fees and non-financial support from Baylor College of Medicine outside the submitted work; in addition, J.D. Wulfkhule has numerous patents pending, issued, licensed, and with royalties paid from George Mason University. R.I. Gallagher reports grants from Gateway Foundation for Cancer Research during the conduct of the study. M.L. Axelrod reports a patent for “Detection of immune signatures in a breast cancer subject” pending to Vanderbilt University. L. Pusztai reports grants and personal fees from Merck, Pfizer, Bristol Myers Squibb, and AstraZeneca and grants from Seagen outside the submitted work. E. Petricoin reports grants from Gateway for Cancer Research during the conduct of the study, as well as personal fees from Perthera, Inc. and Theralink Technologies, Inc. outside the submitted work. K.R.M. Blenman is on the scientific advisory board of CDI Labs (Puerto Rico). J.M. Balko reports grants from NIH during the conduct of the study, as well as grants from Genentech/Roche and Incyte outside the submitted work; in addition, J.M. Balko has a patent for “Immunotherapy biomarkers/HLA-DR” issued. No disclosures were reported by the other authors.
This work was supported by Susan G. Komen Career Catalyst Grant CCRCR18552647 (to J.M. Balko), NIH/NCI SPORE 2P50CA098131–17 (to J.M. Balko), Department of Defense Era of Hope Award BC170037 (to J.M. Balko), and the Vanderbilt-Ingram Cancer Center Support Grant P30 CA68485. Additional funding was provided by NIH T32GM007347 (to M.L. Axelrod) and F30CA236157 (to M.L. Axelrod). The I-SPY 2 Trial and RPPA work was supported by the Gateway for Cancer Research (grant no. G-16–900), QuantumLeap Healthcare Collaborative, Foundation for the NIH, NCI Center for Biomedical Informatics and Information Technology (grant no. 28XS197), a Sta Op Tegen Kanker International Translational Cancer Research Grant, Safeway Foundation, the Bill Bowes Foundation, Quintiles Transnational, Johnson & Johnson, Genentech, Amgen, the San Francisco Foundation, Give Breast Cancer the Boot, Eli Lilly, Pfizer, Eisai, the Harlan family, the Avon Foundation for Women, and Alexandria Real Estate Equities. The Medimmune Durvalumab trial was partly supported by AstraZeneca and grants from the NCI (R01CA219647), the Breast Cancer Research Foundation, a Susan Komen Foundation Leadership Grant (SAC 160076), and an annual Investigator Award from the Breast Cancer Research Foundation (to L. Pusztai).
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