Journal of Cancer Research and Clinical Oncology

, Volume 131, Issue 9, pp 591–596 | Cite as

High expression of skp2 correlates with poor prognosis in endometrial endometrioid adenocarcinoma

  • Yuko Kamata
  • Jun Watanabe
  • Yukari Nishimura
  • Tsutomu Arai
  • Miwa Kawaguchi
  • Manabu Hattori
  • Akane Obokata
  • Hiroyuki Kuramoto
Original Paper

Abstract

Purpose: Skp2 interacts with the degradation of cyclin-dependent kinase inhibitor p27. This study aimed to investigate the correlation of skp2 expression with the expression of p27 and other cell cycle regulators, and clinicopathological parameters in endometrial endometrioid adenocarcinoma. Methods: Tissue samples of 136 endometrioid adenocarcinomas, in addition to 20 endometrial hyperplasias and 20 normal endometria, were immunohistochemically stained for skp2. The expression was represented as a labeling index (LI), which indicates the percentage of positive nuclei. Results: Skp2 staining was localized in the nuclei of the glandular cells of the proliferative phase endometrium, and endometrial hyperplasia and carcinoma cells. Skp2 expression was increased significantly in those of higher histological grade. The high level of skp2 expression was significantly correlated with the presence of lymph node metastasis and lymph-vascular space involvement. The LI of skp2 in endometrial carcinoma was significantly correlated with that of p27, Ki-67, cdk2, cyclin A, cyclin D1, cyclin E, p53 and PTEN. The high level of skp2 expression (LI≧20%) was significantly correlated with the patients’ poor survival. Conclusions: The skp2 level might have increased due to p27 accumulation and may be a good indicator of proliferative activity and poor prognosis.

Keywords

skp2 p27 Cell cycle regulatory proteins Endometrial carcinoma 

Notes

Acknowledgements

This work supported by grants-in-aid for Project Research of the Graduate School of Medical Sciences, Kitasato University (Grants 2005 and 4007) and for Scientific Research from the Ministry of Education, Culture, Sports, Sciences and Technology (Grants 12670176 and 12671627), Japan.

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Copyright information

© Springer-Verlag 2005

Authors and Affiliations

  • Yuko Kamata
    • 1
  • Jun Watanabe
    • 2
  • Yukari Nishimura
    • 1
  • Tsutomu Arai
    • 1
  • Miwa Kawaguchi
    • 1
  • Manabu Hattori
    • 4
  • Akane Obokata
    • 1
  • Hiroyuki Kuramoto
    • 1
    • 3
    • 4
  1. 1.Department of Clinical Cytology, Graduate School of Medical SciencesKitasato UniversityKanagawaJapan
  2. 2.Department of Pathology, School of MedicineKitasato UniversityKanagawaJapan
  3. 3.Department of Obstetrics and Gynecology, School of MedicineKitasato UniversityKanagawaJapan
  4. 4.Department of Clinical Cytology, School of Allied Health SciencesKitasato UniversityKanagawaJapan

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