{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nPTPRJ—also known as DEP‐1 or CD148—acts predominantly as a tumor suppressor that is frequently inactivated in a variety of human cancers. Positional cloning in animal models and analysis of human tumor samples have revealed that deletion, loss of heterozygosity and missense mutations affecting PTPRJ occur in colon, lung, breast, thyroid, pancreatic and meningioma cancers. In addition, certain low‐penetrance polymorphisms and specific haplotype configurations of the PTPRJ gene confer altered cancer risk and can even protect against or promote tumor progression. Together, these studies support a pivotal role for PTPRJ in restricting the onset and progression of neoplastic disease by counteracting oncogenic signals."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAt the molecular level PTPRJ modulates multiple receptor‐mediated signaling cascades by dephosphorylating key tyrosine residues on receptor tyrosine kinases and associated effectors. For example, PTPRJ can directly dephosphorylate the activation loop of receptors such as FLT3, VEGFR2, PDGFR and even the insulin receptor, thereby dampening downstream MAPK, PI3K‐Akt and Src family kinase signaling. In turn, such modulation affects cellular processes that include cell–cell adhesion, cytoskeletal dynamics and migration through substrates such as ERK1/2, p85 and cadherin–catenin complex molecules. This regulatory activity underlies its ability to inhibit mitogenic stimulation and control invasive behavior."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "14", "end_ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional layers of regulation further refine PTPRJ function. Alternative translational start sites and splicing events yield isoforms—including a secreted form with proangiogenic activity—that may modulate receptor signaling in a paracrine manner. Moreover, PTPRJ expression is subject to regulation by microRNAs and is influenced by specific polymorphisms that affect both its expression level and substrate affinities. Emerging data also demonstrate critical roles for PTPRJ in vascular and immune cell functions, as evidenced by its involvement in platelet biogenesis, endothelial barrier regulation, and even modulation of inflammatory responses. Collectively, these multifaceted regulatory mechanisms underscore the therapeutic potential of targeting PTPRJ in cancer as well as in metabolic and inflammatory disorders."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "33", "end_ref": "45"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Claudia A L Ruivenkamp, Tom van Wezel, Carlo Zanon, et al. 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