What We're Reading
Cancer Immunol Res February 1 2020 8 (2) 159-159;
Posttranslational modifications of oncoproteins can promote tumor development, yet it is unclear what induces these alterations. In UC and CACC, M2-like macrophages produce CCL17 and IL13, which increases ST6GALNAC1 glycosyltransferase, leading to glycosylated MUC1 in colon cancer cells.
Elevated CMTM6 in patients with HNSCC predicted poor prognosis. Without CMTM6, cancer stem cell features and the proportion of exhausted T cells decrease, concomitantly improving antitumor immunity. Thus, CMTM6 may have potential as a therapeutic target.
Sibling mice from the same parental breeding pair and with similar microbiomes exhibit differing TCR repertoires. Thus, rejection of inoculated or chemically induced tumors differs, highlighting the important role of T-cell diversity in response to cancer.
Antigen-specific CD103+CD8+ T cells can self-regulate their CD103 expression by producing active TGFβ1 and have better TCR antigen sensitivity and enhanced effector functions versus CD103− populations. However, this population undergoes increased death with prolonged exposure to tumor cells.
Systemic effects of whole-body irradiation can fuel carcinogenesis by repressing antitumor immunity in a mouse model of breast cancer. Aggressive tumors lacking lymphocytic infiltrate can be prevented by dietary intervention with a nontoxic, immunomodulatory agent known as CAPE.
Blocking CD47/SIRPα interactions induces antitumor efficacy. A dual fusion protein incorporating SIRPα and CD40L potentiates tumor cell phagocytosis and type I interferon responses, improving control of established tumors and sensitivity to immune checkpoint blockade.
Systemic IL12 use is limited due to toxicity, yet intratumoral administration of an IL12 plasmid via electroporation is safe and efficacious, even at distant sites. In melanoma patients, this treatment induces local and systemic antigen-specific T-cell responses.
CD8+ T cells not only interact with tumor exosomes but also internalize them, providing a route by which miRNAs encapsulated in exosomes contribute to immune escape mechanisms.
Tumor immune evasion in NSCLC is promoted by overexpression of angiopoietin-2 (ANGPT2) and overaccumulation of M-MDSCs that express the ANGPT2-receptor, TIE2. The ANGPT2/TIE2+ M-MDSC axis could be useful for stratification of NSCLC patients and for therapy decisions.