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PTPN2 deficiency along with activation of nuclear Akt predict endocrine resistance in breast cancer
Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.ORCID iD: 0000-0002-3084-7881
Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
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2019 (English)In: Journal of Cancer Research and Clinical Oncology, ISSN 0171-5216, E-ISSN 1432-1335, Vol. 145, no 3, p. 599-607Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
SPRINGER , 2019. Vol. 145, no 3, p. 599-607
Keywords [en]
TCPTP; 18p deletion; PTPN2; Protein tyrosine phosphatase; Breast cancer; Gene copy number; Immunohistochemistry
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Cancer and Oncology
Identifiers
URN: urn:nbn:se:liu:diva-154985DOI: 10.1007/s00432-018-2810-6ISI: 000459180600006PubMedID: 30515568OAI: oai:DiVA.org:liu-154985DiVA, id: diva2:1297561
Note

Funding Agencies|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

Available from: 2019-03-20 Created: 2019-03-20 Last updated: 2019-08-22

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Karlsson, ElinVeenstra, CynthiaGarsjö, JonNordenskjöld, BoStål, Olle
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