Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
PTK (protein tyrosine kinase)-6 and HER2 and 4, but not HER1 and 3 predict long-term survival in breast carcinomas.
Br. J. Cancer 96, 801-807 (2007)
The HER receptors are of therapeutic and prognostic significance in breast cancer, and their function is modulated by cytoplasmic tyrosine kinases like PTK6 (brk). We performed a retrospective study on archival breast cancer samples from patients with long follow-up and compared the protein expression between individual HERs and between HERs and the PTK6. Univariate and multivariate analyses were used to study the prognostic value of parameters. Metastases-free survival of patients for longer than 240 months was inversely associated (P< or =0.05) with nodal status, tumour size, and oestrogen receptor status, but was also directly associated with high protein expression levels of HER4 and PTK6 in Kaplan-Meier analysis. In multivariate analysis for metastases-free survival of >240 months, the stepwise selected parameters were tumour size (relative risk 3.1), PTK6 expression (0.4), and number of positive lymph nodes (1.2). Furthermore, we demonstrated a timedependence of the prognostic value attributed to the parameters. The HER receptors (HER2,4), but not PTK6, were independent prognostic markers for metastases-free survival at 60 months, whereas at 240 months PTK6 is the strongest prognostic marker. We demonstrate that PTK6 is a prognostic marker of metastases-free survival in breast cancer, and is independent of the classical morphological and molecular markers of lymph node involvement, tumour size, and HER2 status.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
PTK6 (BRK) expression; HER receptors; breast cancer; prognosis
ISSN (print) / ISBN
0007-0920
e-ISSN
1532-1827
Zeitschrift
British Journal of Cancer BJC
Quellenangaben
Band: 96,
Heft: 5,
Seiten: 801-807
Verlag
Springer
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Pathology (PATH)
Institute of Molecular Radiation Biology (IMS)
Institute of Molecular Radiation Biology (IMS)