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E-Poster Display

860P - Redefining prognosis in early-stage high-grade endometrial cancer

Date

17 Sep 2020

Session

E-Poster Display

Topics

Tumour Site

Endometrial Cancer

Presenters

Jorge Ramón

Citation

Annals of Oncology (2020) 31 (suppl_4): S551-S589. 10.1016/annonc/annonc276

Authors

J.L. Ramón1, I. Ruz Carancuel2, V. Heredia Soto3, L.E. García de la Calle4, Á. López Janeiro5, F.J. Escudero3, R. Crespo1, P. Ruiz6, M. Miguel6, A. Berjón5, A. Gallego Martínez4, A. Hernández7, A. Peláez-García6, D. Hardisson5, M. Mendiola6, A. Redondo4

Author affiliations

  • 1 Traslational Oncology Lab, Hospital Universitario La Paz, 28046 - Madrid/ES
  • 2 Department Of Pathology, Hospital Universitario Ramón y Cajal, 28034 - Madrid/ES
  • 3 Traslational Oncology Lab, Instituto de Investigación. Hospital Universitario La Paz, 28046 - Madrid/ES
  • 4 Department Of Medical Oncology, Hospital Universitario La Paz, 28046 - Madrid/ES
  • 5 Department Of Pathology, Hospital Universitario La Paz, 28046 - Madrid/ES
  • 6 Molecular Pathology And Therapeutic Targets, Instituto de Investigación. Hospital Universitario La Paz, 28046 - Madrid/ES
  • 7 Department Of Gynecology, Hospital Universitario La Paz, 28046 - Madrid/ES

Resources

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Abstract 860P

Background

Current clinicopathological risk stratification methods in endometrial cancer (EC) are not considered sufficiently accurate tools to address prognosis and adjuvant therapy. There is a high interobserver variation in the assignment of histotype, especially in high grade (HG) tumors. We investigate if molecular classification can be used to refine prognosis in early-stage HG-EC despite histological subtypes.

Methods

An early-stage (FIGO I & II) HG-EC patients cohort between 2003 to 2015 was collected in a Spanish hospital. Molecular surrogate classification was performed using immunohistochemistry for p53 (p53 wild-type “p53wt” or p53 aberrant “p53abn” expression) and mismatch repair (MMR) proteins (MLH1, PMS2, MSH2, and MSH6), considering MMR deficiency (MMRd) when a loss of MMR nuclear staining for at least one protein was identified. Identification of POLE mutations (POLE-EDM) was made by sequencing exons 9–14. Only pathogenic variants described in COSMIC database were considered for further analysis. Clinicopathological variables and survival ([RFS, relapse free survival; OS, overall survival]) correlations were assessed by the Kaplan Meier method and log rank.

Results

A cohort of 54 patients fulfilled clinical and pathological criteria. Distribution by histological subtype was: endometrioid (46.3%), serous (33.3%), undifferentiated (11.1%), mixed (5.6%), and clear cell (3.7%). Molecular profile was fully evaluable in 49 samples: MMRd (26.5%), POLE-EDM (12.2%), p53wt (22.5%), p53abn (38.8%). Regardless of molecular subtype, 5 year relapse rate was: POLE 0%, MMRd 31.6%, p53wt 35.7%, p53abn 48.9% (p=0.23), and 5 year OS rate was: POLE-EDM 100%, MMRd 76.2%, p53wt 48% and p53abn 38.5% (p=0.18). Considering only endometrioid subtype, there was a statistically significant correlation of the molecular classification with 5 year OS (p=0.02).

Conclusions

To our knowledge, this is the first series that has evaluated the molecular classification focused on early-stage HG-EC, including all histologies. Patients with POLE-EDM have an excellent prognosis, with no relapses in this subgroup, whereas patients with p53abn have the worst prognosis. The application of molecular classification in daily practice could be useful in a better design of adjuvant therapy.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

J.L. Ramón: Research grant/Funding (institution), Research grant: GEICO group. A. Gallego Martínez: Advisory/Consultancy, Travel/Accommodation/Expenses: PharmaMar; Travel/Accommodation/Expenses: Roche; Honoraria (self), Speaker: Clovis; Honoraria (self), Speaker: AstraZeneca; Honoraria (self), Travel/Accommodation/Expenses, Speaker: MSD; Travel/Accommodation/Expenses: Tesaro; Travel/Accommodation/Expenses: Pierre-Fabre. D. Hardisson: Leadership role, Principal Investigator: Molecular Pathology and Therapeutic Targets Lab. Hospital Universitario La Paz-IdiPAZ, Madrid, Spain. M. Mendiola: Honoraria (self), Speaker: AstraZeneca; Honoraria (self), Speaker: Tesaro. A. Redondo: Honoraria (self), Advisory/Consultancy, Speaker & Advisory role: Roche; Honoraria (self), Advisory/Consultancy, Speaker & Advisory role: PharmaMar; Honoraria (self), Advisory/Consultancy, Speaker & Advisory role: AstraZeneca; Honoraria (self), Advisory/Consultancy, Speaker & Advisory role: GSK; Honoraria (self), Advisory/Consultancy, Speaker & Advisory role: Clovis; Honoraria (self), Speaker: Novartis; Advisory/Consultancy: Amgen; Research grant/Funding (institution), Research funding: Roche; Research grant/Funding (institution), Research funding: PharmaMar; Research grant/Funding (institution), Research funding: Eisai; Non-remunerated activity/ies, PI of phase II Cecilia study (carboplatin-paclitaxel and bevacizumab in advanced cervical cancer): Roche; Officer/Board of Directors, Member of Executive Board and Secretary of Spanish Group of Ovarian Cancer Research (GEICO): GEICO group. All other authors have declared no conflicts of interest.

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