Abstract

Highlights| May 04 2023 Selected Articles from This Issue Author & Article Information Online ISSN: 1538-8514 Print ISSN: 1535-7163 ©2023 American Association for Cancer Research2023American Association for Cancer Research Mol Cancer Ther (2023) 22 (5): 553. https://doi.org/10.1158/1535-7163.MCT-22-5-HI Related Content A commentary has been published: Discovery of a Small-Molecule Inhibitor Targeting the Androgen Receptor N-Terminal Domain for Castration-Resistant Prostate Cancer A commentary has been published: Novel Arginase Inhibitor, AZD0011, Demonstrates Immune Cell Stimulation and Antitumor Efficacy with Diverse Combination Partners A commentary has been published: Preclinical Evaluation of ON203, A Novel Bioengineered mAb Targeting Oxidized Macrophage Migration Inhibitory Factor as an Anticancer Therapeutic Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Article Versions Icon Versions Version of Record May 4 2023 Citation Selected Articles from This Issue. Mol Cancer Ther 1 May 2023; 22 (5): 553. https://doi.org/10.1158/1535-7163.MCT-22-5-HI Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest Search Advanced Search The oxidized macrophage migration inhibitory factor (oxMIF) is an emerging therapeutic target for many cancers due to oxMIF's selective occurrence in tumor lesions. Here, Rossmueller and colleagues describe ON203, a novel anti-oxMIF antibody with optimized physicochemical characteristics, in-vitro safety, and enhanced ADCC and ADCP effector functions. ON203 significantly reduced tumor growth and tumor cell proliferation as well as tumor cell intravasation and neo-angiogenesis in xenograft models. These findings highlight the potential of ON203 as a standalone immunotherapy or for enhancing efficacy in combination with angiogenesis and immune checkpoint-inhibitors in patients with solid tumors. Current mainstay treatment for prostate cancer is to suppress the androgen receptor (AR) signaling by castration and antiandrogens that target the ligand-binding domain (LBD). However, emergence of AR variants, such as AR-V7 lacking the LBD, have conferred severe drug resistance to all LBD-targeting AR inhibitors. AR-V7 has been established as a driver for the sustained AR signaling... You do not currently have access to this content.

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