What We're Reading
Cancer Immunol Res May 1 2020 8 (5) 579-579;
Determining links to tumor formation is critical for combating cancer. A 7-year study of over 50,000 patients indicates that certain previous infections are linked to the formation of various cancers.
Altering protein translation in T cells can affect their antitumor function. IL15-conditioned T cells have diminished protein translation in vitro but reinvigorate translation in tumors, a property that is attributed to T cells that produce superior tumor control.
A CD3 bispecific antibody that targets a prostate tumor antigen elicits effective antitumor responses against smaller, but not larger, solid tumors. Addition of 4-1BB controls tumors through enhanced T-cell responses, T-cell memory formation, and response persistence.
Circulating immune subsets that associate with survival in pancreatic cancer patients treated with GVAX pancreas and/or CRS-207 immunotherapy are identified. These immune subsets can potentially be used as biomarkers to stratify patients most likely to respond to treatment.
Genomic alterations of oncolytic viruses can improve their antitumor efficacy. Various genomic alterations of VACV are tested “head-to-head” in order to determine their impact on antitumor efficacy and immunity in murine tumor models.
Oncolytic virus activity is often limited by an immunosuppressive tumor microenvironment. The antitumor efficacy of oncolytic herpes simplex virus is improved by delivering a single-chain variable fragment specific for PD-1. Pairing this with TIGIT blockade enhances antitumor responses.
Merkel cell carcinoma is frequently associated with Merkel cell polyomavirus infection. Most patients' tumors contain virus-specific CD8+ T cells restricted by specific HLAs, highlighting the potential of using vaccination as part of immunotherapy strategies for this cancer.
Antibodies to IL1β can enhance antitumor immunity, but inhibiting IL1α reduces antitumor effects. Thus, antagonists that block the shared IL1R1 do not improve antitumor immunity and are not equivalent to blocking IL1β alone.
The cross-reactivity of TCR-based therapies can lead to serious adverse events. PresentER is a high-throughput method for producing MHC-I peptide minigenes that can be used in in vitro immune assays to identify cross-reactive TCRs.
Compared to cytosolic antigens, mitochondrial tumor antigens prime a stronger antitumor immune response, instigated by enhanced cross-presentation and involvement of the STING pathway. Thus, cellular location of tumor antigens is relevant to improved cancer vaccine development.
Agonistic antibodies to GITR have antitumor effects. IL4-exposed CD4+ T cells activate c-Maf to generate IL21-expressing Tfh cells, which is required for antitumor activity and may be a surrogate marker for the effectiveness of GITR agonistic antibodies.
The immune-suppressive effects of tumor-associated macrophages (TAM) are partially controlled by metabolic reprogramming. RIPK3 shifts TAMs to an antitumor phenotype in hepatocellular carcinoma by modulating fatty acid metabolism, thus decreasing tumorigenesis.