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Journal Archive

Cancer Immunology Research (2013-Present)

(ISSN 2326-6066) Published monthly since 2013.

Cancer Immunity (2001-2013; volumes 1-13)

(EISSN 1424-9634) Published periodically from 2001-2013.

Table of Contents

What We're Reading

In the Spotlight

Cancer Immunology at the Crossroads

Research Articles

Carcinogen-induced rat mammary tumors are shown to recapitulate many aspects of human breast cancer, including the immune environment. Tumor growth is associated with immune escape, which can be reversed by immunotherapy, highlighting the potential utility of this model.

Maximizing bispecific T-cell engager (BiTE) efficacy in solid tumors is challenging. Here, key requirements for BiTE efficacy are identified, including tumor diffusion, target expression level, lymphoid tissue involvement, and DC-driven responses, highlighting possible strategies to improve this therapy.

Local anti–PD-L1 nanobody delivery by tumor-specific T cells increases therapeutic efficacy and reduces systemic exposure compared to systemic injection of PD-L1–specific antibody. Poor intratumoral penetration of PD-L1–specific antibody is a factor limiting efficacy in vivo.

In the first ten patients treated with a combination immunotherapy comprising a neoantigen-loaded dendritic cell vaccine and neoantigen-activated T cells, those who had a neoantigen-specific immune response had improved disease-free survival, supporting continuation of the phase II trial.

This study demonstrates the efficacy of an engineered oncolytic Vaccinia virus (Pexa-Vec) in patients with metastatic cancers. A single intravenous infusion associates with tumor necrosis, IFNα secretion and chemokine expression, and transient innate and long-lived adaptive antitumor responses.

Treatment of immune checkpoint blockade (ICB)-resistant preclinical melanoma models with WEE1 and AKT inhibitors promotes tumor immune infiltration and induces ICB responses. The data suggest that similar approaches in humans could enhance the clinical utility of ICB drugs.

The minimal responsiveness of glioblastoma to immunotherapy is partly due to robust infiltration of immune-suppressive microglia. Inhibition of the CLOCK–OLFML3–HIF1α–LGMN axis reduces microglial infiltration and immune-suppressive polarization, increases antitumor immunity, and enhances immunotherapy efficiency.

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