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749 Tumor cell dissemination is independent from endometrial carcinoma molecular subtypes
  1. L Volmer1,
  2. S Kommoss2,
  3. C Walter1,
  4. J Mcalpine3,
  5. A Lum4,
  6. A Talhouk3,
  7. S Matovina1,
  8. T Engler1,
  9. M Grube1,
  10. M Weiss1,
  11. A Staebler5,
  12. A Koch1 and
  13. A Hartkopf1
  1. 1Tübingen University hospital , Department of Women’s health, Tuebingen, Germany
  2. 2Tuebingen University Hospital , Department of Women’s Health, Tuebingen, Germany
  3. 3University of British Columbia, Department of Gynecology and Obstetrics, Division of Gynecologic Oncology, Vancouver, Canada
  4. 4BC Cancer Research Centre, Department of Molecular Oncology, Vancouver, Canada
  5. 5Tübingen University hospital, Institute of Pathology, Tübingen, Germany


Introduction/Background*Tumor cell dissemination is associated with a less favorable outcome in breast cancer patients. In contrast, only limited clinical significance was yet reported for other gynecologic malignancies. We have previously reported disseminated tumor cells (DTC) not to be associated with established risk factors, L1CAM immunoreactivity and outcome in endometrial carcinoma. It was the aim of this study to investigate potential associations of TCGA-derived molecular features such as POLE-mutation status, p53 abnormalities or MMR deficiency and the presence of DTC in the bone marrow of endometrial carcinoma patients.

Methodology Patients treated for primary endometrial carcinoma at Tuebingen University women’s hospital between 2003 and 2016 with bone marrow aspirates and FFPE tumor specimens were identified. For DTC detection, cytospins were stained for pan-cytokeratin (A45-B/B3 antibody). Molecular classification was performed according to the Proactive Molecular Risk Classifier for Endometrial Cancer (ProMisE).

Result(s)*A total of 402 patients with a complete set of bone marrow cytology, molecular and clinical data was evaluable. ProMisE molecular classification revealed 40(10.0%) POLEmut, 103(25,6%) MMRd, 52(12,9%) p53-abnormal and 207(51.5%) tumors with no specific molecular profile (NSMP). Overall DTC were detected in 71/402 (17.7%) patients. DTC occurrence was distributed equally among molecular groups (p=0.651). DTC were present in 7/40(17.5%) POLEmut, 21/103(20.4%) MMRd, 32/207(15.5%) NSMP and 11/52(21.2%) p53 abnormal tumors.

Conclusion*The scientific community widely agrees that molecular classification will be of key importance in future endometrial carcinoma patient care. In line with our previous findings, tumor cell dissemination is not associated with TCGA-inspired molecular groups in our large cohort of primary endometrial carcinoma patients. While DTC are detectable in a significant number of patients, even including cases with favorable POLEmut subtype, tumor cell dissemination seems not to play a role in disease progression and clinical outcome in endometrial carcinoma.

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