ArticleProceedings of the National Academy of Sciences of the United States of America2014
Frequent mutation of receptor protein tyrosine phosphatases provides a mechanism for STAT3 hyperactivation in head and neck cancer.
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 64 papers.
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Who cites it
64 citing papers in PubMed.
- Multi-cohort validation ofTranslational cancer research · 2026Article
- Constitutive EGFR Activation Induced by PTPRR Downregulation Confers Resistance to KRAS Inhibitors.Cancer research communications · 2026Article
- Innovative Strategies in Oral Carcinoma: Disrupting Cell Signaling for Therapeutic Advances.Asian Pacific journal of cancer prevention : APJCP · 2026Article
- Characterization of prevalent genetic variants in the Estonian Biobank body-mass index GWAS.Nature communications · 2025Article
- Evidence of mutations in tumour suppressor genes among oral cancer in Naswar, smokeless tobacco users.Acta odontologica Scandinavica · 2025Article
- [Research progress on the mechanisms of resistance to cetuximab targeted therapy in head and neck squamous cell carcinoma].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Review
- System analysis based on T-cell exhaustion-related genes identifies PTPRT as a promising diagnostic and prognostic biomarker for gastric cancer.Scientific reports · 2024Article
- A susceptibility gene signature for ERBB2-driven mammary tumour development and metastasis in collaborative cross mice.EBioMedicine · 2024Article
- Influence of point mutations on PR65 conformational adaptability: Insights from molecular simulations and nanoaperture optical tweezers.Science advances · 2024Article
- Downregulation of PTPRT elevates the expression of survivin and promotes the proliferation, migration, and invasion of lung adenocarcinoma.BMC cancer · 2024Article
- Assessing the validity of driver gene identification tools for targeted genome sequencing data.Bioinformatics advances · 2024Article
- Case Report: SMARCA4 (BRG1)-deficient undifferentiated carcinoma of gallbladder with genetic analysis.Frontiers in oncology · 2023Article
- STAT3 Activation as a Predictive Biomarker for Ruxolitinib Response in Head and Neck Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Elevated phosphorylation of EGFR in NSCLC due to mutations in PTPRH.PLoS genetics · 2022Article
- Review
- Outcomes and Molecular Features of Brain Metastasis in Gastroesophageal Adenocarcinoma.JAMA network open · 2022Article
- Genetic, Clinicopathological, and Radiological Features of Intrahepatic Cholangiocarcinoma with Ductal Plate Malformation Pattern.Gut and liver · 2022Article
- Review
- Molecular mechanism(s) of regulation(s) of c-MET/HGF signaling in head and neck cancer.Molecular cancer · 2022Review
- Association ofBioMed research international · 2022Article
4 more citing papers are in PubMed but not listed here.
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22 authors.
Funding
Abstract
The underpinnings of STAT3 hyperphosphorylation resulting in enhanced signaling and cancer progression are incompletely understood. Loss-of-function mutations of enzymes that dephosphorylate STAT3, such as receptor protein tyrosine phosphatases, which are encoded by the PTPR gene family, represent a plausible mechanism of STAT3 hyperactivation. We analyzed whole exome sequencing (n = 374) and reverse-phase protein array data (n = 212) from head and neck squamous cell carcinomas (HNSCCs). PTPR mutations are most common and are associated with significantly increased phospho-STAT3 expression in HNSCC tumors. Expression of receptor-like protein tyrosine phosphatase T (PTPRT) mutant proteins induces STAT3 phosphorylation and cell survival, consistent with a "driver" phenotype. Computational modeling reveals functional consequences of PTPRT mutations on phospho-tyrosine-substrate interactions. A high mutation rate (30%) of PTPRs was found in HNSCC and 14 other solid tumors, suggesting that PTPR alterations, in particular PTPRT mutations, may define a subset of patients where STAT3 pathway inhibitors hold particular promise as effective therapeutic agents.
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