Skip to Main Content


Skip Nav Destination


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


Priority Brief

The data suggest the metabolic demand of adoptively transferred CAR T cells may drive a hypophosphatemia state that is associated with commonly observed neurological symptoms. This study may provide clinicians with a way to monitor for ICANS development.

Research Articles

This first in-human study demonstrates proof-of-mechanism of an immune-stimulator antibody conjugate consisting of a tumor-targeting antibody and a TLR agonist. The study identifies critical challenges and provides important biological insights for novel immunotherapies.

Extracellular adenosine in the tumor microenvironment can impair antitumor immunity by suppressing CTL responses. Inhibition of adenosine signaling stabilizes CTL–target cell conjugation and increases sublethal hit frequency, and thereby restores CTL-mediated cytotoxicity against antigenic melanoma tumors.

The subcellular compartmentalization of Ras is regulated by interacting with intracellular CD59. CD59 deficiency results in reduced trafficking of Ras to the plasma membrane in T cells, thus inducing increased T-cell signal transduction and antitumor activity.

Regulatory T cells suppress antitumor immunity and promote tumor growth. This study reports mechanisms that protect regulatory T cells from inactivation in the tumor microenvironment. Targeting these mechanisms can reactivate antitumor immunity and suppress tumor growth.

DKK1 is demonstrated to induce immunosuppressive polarization of macrophages, promoting tumor immune evasion in gastric cancer. The data showcase the potential of targeting DKK1, alone and in combination with anti–PD-1, to enhance antitumor responses in gastric cancer.

The authors show that subcapsular sinus macrophages promote aggressiveness of metastatic melanoma cells by releasing IL1α, which upregulates STAT3 signaling in the tumor. Blocking IL1α could synergize with STAT3 inhibitors in treating metastatic melanoma.

The authors show that neutrophil extracellular traps can trigger oxaliplatin-induced peripheral neuropathy (OIPN) in a preclinical model. This can be blocked by targeting NLRP3 or IL18 or with an omega-3 fatty acid, suggesting new ways to alleviate OIPN.

High cancer-intrinsic expression of MHC-II is associated with better immunotherapy responses and clinical outcomes. Multiomic analyses and gene editing experiments demonstrate that MHC-II expression is regulated by the Hippo signaling pathway in melanoma.

Close Modal

or Create an Account

Close Modal
Close Modal