ArticleProceedings of the National Academy of Sciences of the United States of America2014
Loss of the tyrosine phosphatase PTPRD leads to aberrant STAT3 activation and promotes gliomagenesis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 92 citations in OpenAlex.
- Novel risk loci in LGI1-antibody encephalitis: genome-wide association study discovery and validation cohorts.Brain : a journal of neurology · 2025Pooled it
- Genome-wide meta-analysis, functional genomics and integrative analyses implicate new risk genes and therapeutic targets for anxiety disorders.Nature human behaviour · 2024Pooled it
- NetCIS: a network-based common insertion site pipeline for case-control Sleeping Beauty screens.Briefings in bioinformatics · 2026Article
- Cellular signaling meets bacterial infection: the integrative role of STAT3.Frontiers in cellular and infection microbiology · 2026Review
- Pathological neural and immune synapses in glioblastoma progression: mechanisms and therapeutic opportunities.Frontiers in neural circuits · 2026Review
- Comparison of asprosin immunoreactivity in endometrial hyperplasia and grade-1 endometrial adenocarcinoma: A retrospective case-control study.Turkish journal of obstetrics and gynecology · 2025Article
- Synaptic and Non-Synaptic Functions of PTPRD: A Receptor Tyrosine Phosphatase at the Crossroads of Neural Circuitry and Metabolism.Journal of neurochemistry · 2025Review
- Neurodevelopment Genes Encoding Olduvai Domains Link Myalgic Encephalomyelitis to Neuropsychiatric Disorders.Diagnostics (Basel, Switzerland) · 2025Article
- p53-regulated SESN1 and SESN2 regulate cell proliferation and cell death through control of STAT3.Cell communication and signaling : CCS · 2025Article
- Molecular genetic foundation of a sex-linked tailless trait in Hongshan chicken by whole genome data analysis.Poultry science · 2024Article
- Topological reorganization and functional alteration of distinct genomic components in gallbladder cancer.Frontiers of medicine · 2024Article
- Article
- The role of APOBEC3B in lung tumor evolution and targeted cancer therapy resistance.Nature genetics · 2024Article
- Neural conditional ablation of the protein tyrosine phosphatase receptor Delta PTPRD impairs gliogenesis in the developing mouse brain cortex.Frontiers in cell and developmental biology · 2024Article
- Manipulating PTPRD function with ectodomain antibodies.Genes & development · 2023Article
- Resveratrol Enhances Temozolomide Efficacy in Glioblastoma Cells through Downregulated MGMT and Negative Regulators-Related STAT3 Inactivation.International journal of molecular sciences · 2023Article
- Roles of STAT3 in the pathogenesis and treatment of glioblastoma.Frontiers in cell and developmental biology · 2023Review
- Epigenetic Regulation of Obesity-Associated Type 2 Diabetes.Medicina (Kaunas, Lithuania) · 2022Review
- PTPRD and CNTNAP2 as markers of tumor aggressiveness in oligodendrogliomas.Scientific reports · 2022Article
- Patients deriving long-term benefit from immune checkpoint inhibitors demonstrate conserved patterns of site-specific mutations.Scientific reports · 2022Article
7 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
PTPRD, which encodes the protein tyrosine phosphatase receptor-δ, is one of the most frequently inactivated genes across human cancers, including glioblastoma multiforme (GBM). PTPRD undergoes both deletion and mutation in cancers, with copy number loss comprising the primary mode of inactivation in GBM. However, it is unknown whether loss of PTPRD promotes tumorigenesis in vivo, and the mechanistic basis of PTPRD function in tumors is unclear. Here, using genomic analysis and a glioma mouse model, we demonstrate that loss of Ptprd accelerates tumor formation and define the oncogenic context in which Ptprd loss acts. Specifically, we show that in human GBMs, heterozygous loss of PTPRD is the predominant type of lesion and that loss of PTPRD and the CDKN2A/p16(INK4A) tumor suppressor frequently co-occur. Accordingly, heterozygous loss of Ptprd cooperates with p16 deletion to drive gliomagenesis in mice. Moreover, loss of the Ptprd phosphatase resulted in phospho-Stat3 accumulation and constitutive activation of Stat3-driven genetic programs. Surprisingly, the consequences of Ptprd loss are maximal in the heterozygous state, demonstrating a tight dependence on gene dosage. Ptprd loss did not increase cell proliferation but rather altered pathways governing the macrophage response. In total, we reveal that PTPRD is a bona fide tumor suppressor, pinpoint PTPRD loss as a cause of aberrant STAT3 activation in gliomas, and establish PTPRD loss, in the setting of CDKN2A/p16(INK4A) deletion, as a driver of glioma progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.