Strategies for Increasing Pancreatic Tumor Immunogenicity

被引：137

作者：

Johnson, Burles A., III ^{[1
]}

Yarchoan, Mark ^{[1
]}

Lee, Valerie ^{[1
]}

Laheru, Daniel A. ^{[1
]}

Jaffee, Elizabeth M. ^{[1
,2
]}

机构：

[1] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Bloomberg Kimmel Inst Canc Immunotherapy, Dept Oncol, Baltimore, MD USA

[2] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Dept Pathol, Baltimore, MD USA

来源：

CLINICAL CANCER RESEARCH | 2017年 / 23卷 / 07期

关键词：

REGULATORY T-CELLS; FOCAL ADHESION KINASE; COLONY-STIMULATING FACTOR; PLASMACYTOID DENDRITIC CELLS; CANCER STEM-CELLS; PHASE-I; DUCTAL ADENOCARCINOMA; INDOLEAMINE 2,3-DIOXYGENASE; MONOCLONAL-ANTIBODY; PERIODONTAL-DISEASE;

D O I：

10.1158/1078-0432.CCR-16-2318

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Immunotherapy has changed the standard of care for multiple deadly cancers, including lung, head and neck, gastric, and some colorectal cancers. However, single-agent immunotherapy has had little effect in pancreatic ductal adenocarcinoma (PDAC). Increasing evidence suggests that the PDAC microenvironment is comprised of an intricate network of signals between immune cells, PDAC cells, and stroma, resulting in an immunosuppressive environment resistant to single-agent immunotherapies. In this review, we discuss differences between immunotherapy-sensitive cancers and PDAC, the complex interactions between PDAC stroma and suppressive tumor-infiltrating cells that facilitate PDAC development and progression, the immunologic targets within these complex networks that are druggable, and data supporting combination drug approaches that modulate multiple PDAC signals, which should lead to improved clinical outcomes.

引用

页码：1656 / 1669

页数：14

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