MHC Class I Loss in Triple-negative Breast Cancer

三阴性乳腺癌 MHC I级 主要组织相容性复合体 癌症研究 乳腺癌 免疫系统 免疫检查点 组织微阵列 医学 免疫学 癌症 生物 内科学 免疫疗法
作者
Anna C. Dusenbery,Joseph L. Maniaci,Natalie D. Hillerson,Erik Dill,Timothy N. J. Bullock,Anne M. Mills
出处
期刊:The American Journal of Surgical Pathology [Ovid Technologies (Wolters Kluwer)]
卷期号:45 (5): 701-707 被引量:29
标识
DOI:10.1097/pas.0000000000001653
摘要

Suppression of the immune system is intimately linked to the development and progression of malignancy, and immune modulating treatment options have shown promise in a variety of tumor types, including some triple-negative breast cancers (TNBC). The most dramatic therapeutic success has been seen with immune checkpoint inhibitors targeting programmed cell death protein 1 (PD-1) and its ligand, PD-L1. Difficulty remains, however, in appropriate patient selection for treatment, as many PD-L1-positive cancers fail to show durable responses to PD-1/PD-L1 inhibition. Checkpoint inhibitor targeting of the adaptive immune response relies on the presence of major histocompatibility complex (MHC) class I molecules on the tumor cell surface for tumor antigen presentation. MHC class I loss has been previously described in breast cancer and represents a putative mechanism of immunotherapeutic resistance in this tumor type. One hundred seventeen invasive primary breast carcinomas with a range of histologic subtypes were evaluated on tissue microarrays containing formalin-fixed paraffin-embedded tissue. Loss of MHC class I expression was common among breast cancers, with greater than half of cases demonstrating either subclonal or diffuse loss. Fifty-nine percent of TNBC demonstrated loss of MHC class I, including 46% of those meeting the Food and Drug Administration-approved threshold of 1% for tumor-associated immune cell PD-L1 expression. MHC class I loss was particularly common in the apocrine subtype of TNBC (78%). MHC class I’s employment as a predictive biomarker should be considered, as its loss may represent a barrier to successful enhancement of the antitumor adaptive immune response by PD-1/PD-L1 inhibition.
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