ArticleOncotarget2013
Germline PTPRD mutations in Ewing sarcoma: biologic and clinical implications.
Article in Oncotarget, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Pooled it
- IGF-1R inhibitors in cancer: A review of available evidence and future outlook.Critical reviews in oncology/hematology · 2025Review
- Advances in peripheral T cell lymphomas: pathogenesis, genetic landscapes and emerging therapeutic targets.Histopathology · 2025Review
- Genomic profiling identifies distinct genetic subtypes in extra-nodal natural killer/T-cell lymphoma.Leukemia · 2022Article
- Protein tyrosine phosphatases in skeletal development and diseases.Bone research · 2022Review
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- The Role of Tyrosine Kinases as a Critical Prognostic Parameter and Its Targeted Therapies in Ewing Sarcoma.Frontiers in cell and developmental biology · 2020Review
- Genetic Predisposition to Solid Pediatric Cancers.Frontiers in oncology · 2020Review
- Role of STAT3 in Genesis and Progression of Human Malignant Gliomas.Molecular neurobiology · 2017Review
- Germline Mutations in Cancer Predisposition Genes are Frequent in Sporadic Sarcomas.Scientific reports · 2017Article
- IGF-1R and mTOR Blockade: Novel Resistance Mechanisms and Synergistic Drug Combinations for Ewing Sarcoma.Journal of the National Cancer Institute · 2016Article
- RING1B contributes to Ewing sarcoma development by repressing the NaV1.6 sodium channel and the NF-κB pathway, independently of the fusion oncoprotein.Oncotarget · 2016Article
- Transgelin increases metastatic potential of colorectal cancer cells in vivo and alters expression of genes involved in cell motility.BMC cancer · 2016Article
- Review
- Targeted therapies for advanced Ewing sarcoma family of tumors.Cancer treatment reviews · 2015Review
- Missing-in-Metastasis regulates cell motility and invasion via PTPδ-mediated changes in SRC activity.The Biochemical journal · 2015Article
- Deletion of Ptprd and Cdkn2a cooperate to accelerate tumorigenesis.Oncotarget · 2014Article
- Article
- Novel secondary somatic mutations in Ewing's sarcoma and desmoplastic small round cell tumors.PloS one · 2014Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ewing sarcoma occurs in children, adolescents and young adults. High STAT3 levels have been reported in approximately 50% of patients with Ewing sarcoma, and may be important in tumorigenesis. Protein tyrosine phosphatase delta (PTPRD) is a tumor suppressor that inhibits STAT3 activation. To date, while somatic mutations in PTPRD have been reported in diverse tumors, germline mutations of PTPRD have not been investigated in Ewing sarcoma or other cancers. We identified a novel germline mutation in the PTPRD gene in three of eight patients (37.5%) with metastatic Ewing sarcoma. Although the functional impact in two of the patients is unclear, in one of them the aberration was annotated as a W775stop germline mutation, and would be expected to lead to gene truncation and, hence, loss of the STAT3 dephosphorylation function of PTPRD. Since STAT3 is phosphorylated after being recruited to the insulin growth factor receptor (IGF-1R), suppression of IGF-1R could attenuate the enhanced STAT3 activation expected in the presence of PTPRD mutations. Of interest, two of three patients with germline PTPRD mutations achieved durable complete responses following treatment with IGF-1R monoclonal antibody-based therapies. Our pilot data suggest that PTPRD germline mutations may play a role in the development of Ewing sarcoma, a disease of young people, and their presence may have implications for therapy.
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Registered trials
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