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#902 Synchronous endometrial and ovarian endometrioid carcinoma: an intricate clinical dilemma
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  1. Luisa Sánchez,
  2. Daniel Vázquez,
  3. Enrique Maria Chacon Cruz,
  4. Isabel Guereñu Panero,
  5. Teresa Iscar,
  6. Lidia Sancho,
  7. Felix Boria,
  8. Teresa Castellanos,
  9. Mónica Gutiérrez,
  10. Nabil Manzour,
  11. Jaime Espinos,
  12. Alejandro Gallego Martinez,
  13. José Angel minguez Milio,
  14. Mauricio Cambeiro,
  15. Juan Luis Alcázar,
  16. Antonio González Martin and
  17. Luis Chiva
  1. Clínica Universidad de Navarra, Madrid, Spain

Abstract

Introduction/Background Synchronous endometrial and ovarian carcinomas represent approximately 5% of endometrial cancers and about 10% of ovarian cancers.

Distinguishing between double primaries from metastatic tumors is essential for the selection of optimal adjuvant treatment and predicting patient prognosis.

Methodology We retrospectively reviewed 8 patients with pathologically confirmed synchronous endometrial and ovarian endometrioid carcinoma (SEO-EC) who underwent surgery at Clínica Universidad de Navarra between 2017 to 2023.

We analyzed the molecular profile, using next generation sequencing of 8 samples, from 5 patients. We subjected endometrial and ovarian tumors from 3 patients to parallel NGS with Oncomine Comprehensive Assay.

The clonal relationship between endometrial and ovarian carcinomas was assessed using the similarity index (SI).

Results Complete information on molecular subtype classification was available in 5 patients. Two were mismatch repair deficient (MMR-D), 1 POLE-mutated and 2 no specific molecular profile (NSMP), respectively. The classification was not available in 3 patients as POLE mutation analysis was omitted, of which 2 had an abnormal expression of p53.

During follow-up, 2 patients relapsed with 1 disease-specific death. The molecular profile of those who relapsed, 1 was NSMP and the other undetermined (NSMP vs POLE), respectively.

The SI ranges between 0 (completely different) and 1 (identical genomic profiles). The 3 patients subjected to parallel NGS analysis had a SI of 0.66, 0.75 and 1, respectively.

Conclusion Our data provide additional evidence to suggest that in patients with SEO-EC, these lesions are usually clonally related and probably there is only one primary tumors,

The other hypothesis is the synchronic origin, not necessarily dissemination. The fact that the 3 patients subjected to parallel NGS analysis shared one or more somatic mutations support clonal origin in these cases, as determined by the SI. Nevertheless, further research and a larger sample size are needed to validate this hypothesis.

Disclosures None

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