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Cited by 233Cancer Immunotherapy and BiomarkersImmunotherapy and Immune ResponsesBreast Cancer Treatment Studies

Immunotherapy for Breast Cancer: What Are We Missing?

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Vonderheide, Robert H., Domchek, Susan M., Clark, Amy S.·2017·Clinical Cancer Research
DOI 10.1158/1078-0432.ccr-16-2569PMC PMC5480967
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Abstract

The recent demonstration of modest single-agent activity of programmed death-ligand 1 (PD-L1) and programmed death receptor-1 (PD-1) antibodies in patients with breast cancer has generated hope that breast cancer can be made amenable to immunotherapy. Depending on the subtype of breast cancer, it is now clear in both primary and metastatic disease that the extent of tumor-infiltrating T cells is not only prognostic for survival but predictive of response to nonimmune, standard therapies. Despite these findings, immune cytolytic activity in spontaneous breast tumors, the burden of nonsynonymous tumor mutations, and the predicted load of neoepitopes—factors linked to response to checkpoint blockade in other malignancies—are all relatively modest in breast cancer compared with melanoma or lung cancer. Thus, in breast cancer, combinations of immune agents with nonredundant mechanisms of action are high-priority strategies. For most breast cancers that exhibit relatively modest T-cell infiltration, major challenges include immune suppression in the tumor microenvironment as well as failed or suboptimal T-cell priming. Agents that trigger de novo T-cell responses may be critical for the successful development of cancer immunotherapy and immune prevention in breast cancer. Success may also require reaching beyond nonsynonymous mutations as the T-cell epitopes to target, especially as numerous unmutated proteins were validated as breast cancer–associated antigens in the pre-checkpoint era. A deeper understanding of the immunobiology of breast cancer will be critical for immunotherapy to become broadly relevant in this disease. Clin Cancer Res; 23(11); 2640–6. ©2017 AACR. See all articles in this CCR Focus section, “Breast Cancer Research: From Base Pairs to Populations.”

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  • Highly immune suppressive myeloid cells such as macrophages are one factor driving resistance to immune therapy.

    “One factor driving resistance is highly immune suppressive myeloid cells (MCs) such as macrophages.”

    From Cholesterol efflux protein, ABCA1, supports anticancer functions of myeloid immune cells (2026) · cites this paper as [13]

    In “Turning cold tumors hot” (page unavailable), the paper says suppressive myeloid cells can contribute to T-cell exclusion and that checkpoint blockade may be insufficient when other suppressive pathways remain active. The “Therapeutic vaccines in breast cancer” section also discusses targeting myeloid inflammation, but the paper does not specifically identify macrophages as the cells driving resistance. (LLM, conf=0.84)

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Cited by

Sorted by citations

Authors
Vonderheide, R. H., Domchek, S. M., & Clark, A. S.
Affiliations
Abramson Cancer Center (US)
Corresponding author
Vonderheide, Robert H.
ORCID
Venue
Clinical Cancer Research
Publisher
American Association for Cancer Research (AACR)
Published
2017-05-31
Volume
23
Issue
11
Pages
2640-2646
ISSN
  • 1078-0432 (ISSN-L)
  • 1557-3265
DOI
10.1158/1078-0432.ccr-16-2569
PMC
PMC5480967
OpenAlex
W2621295461
Cited by
233
References
5
Citations by year
2026: 10 · 2025: 23 · 2024: 19 · 2023: 22 · 2022: 25 · 2021: 47 · 2020: 30 · 2019: 31 · 2018: 21 · 2017: 5
FWCI
10.49
Type
journal article
Language
en
Open access
Locations
  • Clinical Cancer Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Cancer Institute (R01CA111377)
Topics
  • Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
Keywords
breast cancer immunotherapy, PD-1/PD-L1 blockade, tumor-infiltrating T cells, T cell priming, neoantigens, non-synonymous mutations, tumor-associated antigens, combination immunotherapy, metastatic breast cancer, immune checkpoint inhibitors
MeSH terms
Breast Neoplasms, Female, Humans, Immunotherapy, Lymphocytes, Tumor-Infiltrating, Epitopes, T-Lymphocyte, Tumor Microenvironment, B7-H1 Antigen, Programmed Cell Death 1 Receptor

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