期刊
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
卷 145, 期 3, 页码 599-607出版社
SPRINGER
DOI: 10.1007/s00432-018-2810-6
关键词
TCPTP; 18p deletion; PTPN2; Protein tyrosine phosphatase; Breast cancer; Gene copy number; Immunohistochemistry
类别
资金
- Swedish Cancer Society
- Cancer Research Foundations of Radiumhemmet
- Cancer Society in Stockholm
- King Gustav V Jubilee Clinical Research Foundation
- ALF grants Region Ostergotland
- Onkologiska Klinikernas i Linkoping Forskningsfond
Purpose The protein tyrosine phosphatase, non-receptor type 2 (PTNP2) regulates receptor tyrosine kinase signalling, preventing downstream activation of intracellular pathways like the PI3K/Akt pathway. The gene encoding the protein is located on chromosome 18p11; the 18p region is commonly deleted in breast cancer. In this study, we aimed to evaluate PTPN2 protein expression in a large breast cancer cohort, its possible associations to PTPN2 gene copy loss, Akt activation, and the potential use as a clinical marker in breast cancer. Methods PTPN2 protein expression was analysed by immunohistochemistry in 664 node-negative breast tumours from patients enrolled in a randomised tamoxifen trial. DNA was available for 146 patients, PTPN2 gene copy number was determined by real-time PCR. Results PTPN2 gene loss was detected in 17.8% of the tumours. Low PTPN2 protein expression was associated with higher levels of nuclear-activated Akt (pAkt-n). Low PTPN2 as well as the combination variable low PTPN2/high pAkt-n could be used as predictive markers of poor tamoxifen response. Conclusion PTPN2 negatively regulates Akt signalling and loss of PTPN2 protein along with increased pAkt-n is a new potential clinical marker of endocrine treatment efficacy, which may allow for further tailored patient therapies.
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