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Evolution in Endometrial Cancer: Evidence From an Immunohistochemical Study
  1. Ingrid Vandenput, MD*,
  2. Jone Trovik, MD,,
  3. Karin Leunen, MD*,
  4. Elisabeth Wik, MD,,
  5. Ingunn Stefansson, MD, PhD§,
  6. Lars Akslen, PhD§,
  7. Philippe Moerman, MD, PhD,
  8. Ignace Vergote, MD, PhD*,
  9. Helga Salvesen, MD, PhD, and
  10. Frédéric Amant, MD, PhD*
  1. * Leuven Cancer Institute (LKI), Gynecologic Oncology, UZ Gasthuisberg, Katholieke Universiteit Leuven, Leuven, Belgium;
  2. Department of Clinical Medicine, University of Bergen;
  3. Department of Obstetrics and Gynecology and
  4. § The Gade Institute, Section for Pathology, University of Bergen, Haukeland University Hospital, Bergen, Norway; and
  5. Department of Pathology, UZ Gasthuisberg, Katholieke Universiteit Leuven, Leuven, Belgium.
  1. Address correspondence and reprint requests to Frédéric Amant, MD, PhD, Leuven Cancer Institute (LKI), Gynecologic Oncology, UZ Gasthuisberg, Katholieke Universiteit Leuven, Herestraat 49, 3000 Leuven, Belgium. E-mail: frederic.amant{at}


Background: It is poorly described how endometrial cancer biology changes during tumor evolution. We hypothesize that characterization of molecular targets in recurrent lesions is more relevant for targeting treatment.

Methods: Paired biopsies from primary and recurrent endometrial cancer tumors (n = 85) were stained immunohistochemically for the following proteins: estrogen receptor (ER), progesterone receptor (PR), stathmin (correlating with phosphatidylinositol 3-kinase activity), HER-2/neu, WT1 (Wilms tumor gene 1), phospho-mammalian target of rapamycin (p-mTOR), and p53. Each tumor was scored, using a semiquantitative and subjective grading system. Discordance, a change in expression between primary and recurrent tumor, was defined as ≥2 step change; concordance was ≤1 step change. The frequency of change was correlated with established prognostic markers in endometrial cancer.

Results: Fifty-six patients (67%) were diagnosed with endometrioid carcinoma, 23 (27%) with serous/clear cell carcinoma. A change in expression between primary and recurrent tumor was noted in 7% to 31% of patients for ER, PR, stathmin, HER-2/neu, WT1, p-mTOR, and p53. Concordant-positive cases for PR were significantly correlated with stage, tumor grade, and histological subtype. Expression of ER, p53, and p-mTOR in cytoplasm in the recurrent tumor correlated significantly with survival.

Conclusions: Endometrial cancer biology changes over time. The decision on targeted treatment should preferably be based on recurrent tumor characteristics.

  • Endometrial cancer
  • Recurrence
  • Tumor biology
  • Targeted therapy

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