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OP008/#194 P53ABN molecular subtype encompasses a morphologically diverse subset of endometrial cancers and identifies therapeutic opportunities to improve outcomes
  1. A Jamieson1,
  2. E Thompson2,
  3. J Huvila3,
  4. S Leung2,
  5. A Lum4,
  6. L Helpman5,
  7. S Salvador6,
  8. J Irving7,
  9. K Grondin8,
  10. A Lytwyn9,
  11. C Parra-Herran10,
  12. S offman11,
  13. M Kinloch12,
  14. M Plante13,
  15. D Vicus14,
  16. A Talhouk4,
  17. S Scott15,
  18. D Huntsman4,
  19. C Gilks16 and
  20. J Mcalpine1
  1. 1University of British Columbia, Gynecologic Oncology, Vancouver, Canada
  2. 2Molecular Oncology, University of British Columbia, Vancouver, Canada
  3. 3University of Turku, Pathology, Turku, Finland
  4. 4University of British Columbia, Molecular Oncology, Vancouver, Canada
  5. 5McMaster University, Gynecologic Oncology, Hamilton, Canada
  6. 6McGill University, Gynecologic Oncology, Montreal, Canada
  7. 7University of British Columbia, Pathology, Victoria, Canada
  8. 8Laval University, Pathology, Quebec City, Canada
  9. 9McMaster University, Pathology, Hamilton, Canada
  10. 10University of Toronto, Pathology, Toronto, Canada
  11. 11Dalhousie University, Pathology, Halifax, Canada
  12. 12University of Saskatchewan, Pathology, Saskatoon, Canada
  13. 13Laval University, Gynecologic Oncology, Quebec City, Canada
  14. 14University of Toronto, Gynecologic Oncology, Toronto, Canada
  15. 15Dalhousie University, Gynecologic Oncology, Halifax, Canada
  16. 16University of British Columbia, Pathology, Vancouver, Canada


Objectives Molecular classification of endometrial cancer (EC) has important prognostic and therapeutic implications. p53abn EC represent the most aggressive molecular subtype, and recent data has shown a survival benefit from chemotherapy and targeted therapies. We describe the clinicopathologic diversity in presentation and outcomes of p53abn ECs.

Methods Molecular classification was performed on ECs diagnosed in 2016 from 30 Canadian centres. Clinicopathologic and outcome data were collected.

Results 190 ECs were p53abn subtype; 100 serous, 33 endometrioid, 29 carcinosarcomas, 20 mixed, 6 clear cell carcinoma, 2 undifferentiated. 13 p53abn endometrioid ECs were low grade (Gr1/2). There was a trend for worse outcomes with non-endometrioid histotypes(p=0.074). Non-endometrioid p53abn ECs were more likely to present with advanced stage (III-IV) disease compared to endometrioid p53abn ECs (43% vs 15%, p=0.003). There was significant variation in adjuvant treatment; 28% patients received no adjuvant therapy, 40% received no chemotherapy. of the patients who had no chemotherapy, 20/76 (26.3%) had a disease related event (progression/disease specific death). Stage I p53abn low grade ECs had worse outcomes (5-fold) than stage I low grade ECs of all other molecular subtypes combined.

Conclusions p53abn EC was observed across a range of histotypes including low grade ECs, with no significant difference in outcomes based on histotype. EC risk stratification based on histotype and stage failed to identify 25% of patients as high risk and 15% as intermediate risk based on the 2020 ESGO/ESTRO/ESP EC guidelines, which resulted in a missed opportunity for chemotherapy and targeted therapy.

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