Masters of Immunology
Cancer Immunol Res December 1 2013 1 (6) 351-356; DOI:10.1158/2326-6066.CIR-13-0151
The combination of local radiotherapy to a liver metastasis and systemic anti-CTLA-4 antibody resulted in a sustained complete clinical and radiologic remission in a patient with chemotherapy-refractory metastatic non–small cell lung cancer.
Severe systemic toxicities developed in two patients during vemurafenib therapy following disease progression after treatment with anti-PD-1 agents; these results have important implications for the management of melanoma patients and future clinical trials involving anti-PD-1 and BRAF inhibitors.
In a retrospective, nested, case–control study of 98 primary clear cell renal cell carcinoma tumors, Joseph and colleagues demonstrate an inverse correlation between genes in the VEGF pathway and PD-L1 expression, providing further support of the immunosuppressive role of VEGF on the tumor microenvironment.
Diken, Kreiter, and colleagues report that treatment of mice in the B16 melanoma model with rapamycin at the effector-to-memory transition phase skews the vaccine-induced immune response toward the memory pool, with alterations of the tumor microenvironment, and prolongs survival.
Bak, Barnkob, and colleagues show that treatment with antigen-specific CD8+ T cells effectively eliminated antigen-expressing prostate cells within the tumor bed, but the antigen-negative tumor cells with downregulated MHC class I continued to grow.
Combining the analyses of samples from melanoma patients and from melanoma-bearing humanized mice, the authors delineated the mechanism by which plasmacytoid dendritic cells mediate tumor progression and early relapse and identified potential therapeutic options for patients with metastatic melanoma.
Using overlapping peptides spanning oncofetal antigen 5T4 as targets, Scurr and colleagues identify an inverse correlation between the anti-5T4 CD4+ T-cell responses in peripheral blood and colorectal cancer disease progression and show this selective loss is driven in part by regulatory T cells.
Using two different murine models of pre–B-cell leukemia, Sandoval and colleagues delineate the mechanism of tumor suppression by the PDZ domain polarity gene DLG1, which interacts with and stabilizes the PTEN protein in early-stage B cells.