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711 Long-term survival women with advanced-stage high-grade serous carcinoma of the ovary, peritoneum, or fallopian tube: digging into their clinico-molecular features
  1. Roberta Mazzeo1,2,
  2. Carmen Garcia-Duran1,
  3. Víctor Navarro-Garcés3,
  4. Lorena Fariñas-Madrid1,
  5. Juan Francisco Grau-Bejar1,4,
  6. Lucia Musacchio1,5,
  7. Alba Meire-Barrio1,
  8. Olga Padrós-Rufete1,
  9. Ana Oaknin1 and
  10. David Garcia-Illescas1
  1. 1Gynecological Cancer Programme, Vall d’Hebron Institute of Oncology (VHIO), Hospital Universitari Val d’Hebron, Barcelona, Spain
  2. 2Department of Medicine (DAME), University of Udine, Udine, Italy
  3. 3Oncology Data Science (ODysSey) Group, Vall d’Hebron Institute of Oncology (VHIO), Barcelona, Spain
  4. 4Gynecological Cancer Translational Research Laboratory, Institut Gustave Roussy, Villejuif, France
  5. 5Department of Women and Child Health, Division of Gynecologic Oncology, Fondazione Policlinico Universitario Agostino Gemelli IRCCS, Rome, Italy

Abstract

Introduction/Background High-grade serous ovarian carcinoma (HGSC) remains the most lethal gynecologic cancer. However, there’s a patients’ subgroup with remarkable responses to treatment which have led to an exceptionally Long-Term Survival, namely >=10 years (LTS). How their clinical-molecular biomarkers might have determined their exceptionally long survival is ill-defined.

Methodology Between 2000–2023 46 consecutives LTS patients were identified from our electronic medical records. Patients’ clinicopathological characteristics, treatment history, germline BRCA status and tumor molecular features (by NGS) were reviewed (data cut-off 01-oct-2023).

Results At diagnosis, median age was 53.3 years (IQR 49.5–60.2), and most patients had FIGO stage IIIC (45.5%) and IVB (13.6%). Tumor NGS was available for 39 patients. Most frequent tumor alterations were TP53 (31 patients, 91.2%), BRCA1 (15, 40.5%), BRCA2 (5, 14.3%), NF1 (4, 12.1%), RB1 (2, 6.3%), BRIP1 and RAD51d (1, 3.1% for both). Median Tumor Mutational Burden (TMB) was 7.1 (IQR 4.5–8.8). Tumors harboring CCNE1 amplification (5, 17.8%) had a slightly higher TMB (8.8, IQR 8.1–10.0), without mutations in homologous recombination (HR) genes.

While 5 patients had no disease recurrence at data cut-off, the median number of relapses in the patients’ journey was 5 (IQR 2–7). Data regarding therapy are shown in table 1. With a median follow-up of 12 years (95%CI, 11.4–13.2), 37 patients were still alive, 32 of them with disease. Six patients died of disease (median interval diagnosis-death: 11.2 years, IQR 10.7–12.4), two died of myelodysplastic syndromes after PARPi maintenance at the platinum-sensitive relapse, and one patient died of infection.

Conclusion Acknowledging the limitations of a small sample size and retrospective nature, our results suggest extensive primary TFIp (>24 months) as a common characteristic leading to LTS. Indeed, this cohort is enriched in tumors harboring HR mutations which support the exquisite response to platinum. Increased TMB may have contributed to a better prognosis. Further analyses are warranted.

Disclosures Nothing to declare.

Abstract 711 Table 1

Summary of 46 long-term survival patient’s treatment characteristic

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