972PD - Efficacy of platinum plus gemcitabine (G) in platinum-resistant (R) compared to platinum-sensitive (S) ovarian cancer: the Royal Marsden Experience

Date 30 September 2012
Event ESMO Congress 2012
Session Gynecological cancers
Topics Cytotoxic agents
Ovarian Cancer
Therapy
Biological therapy
Presenter Angela George
Authors A. George1, N. Tunariu2, S. Gupta3, N. Wilkinson4, M.E. Gore5, S.B. Kaye6, S. Banerjee7
  • 1Gynaecology, Royal Marsden NHS Foundation Trust and Institute of Cancer Research ICR, SM2 5PT - Sutton/UK
  • 2Radiology Department, Royal Marsden NHS Foundation Trust and the Institute of Cancer Research ICR, SM2 5PT - Sutton/UK
  • 3Statistics Department, Royal Marsden NHS Foundation Trust, SW3 6JJ - London/UK
  • 4Gynaecology Unit, Royal Marsden NHS Foundation Trust and Institute of Cancer Research ICR, SM2 5PT - Sutton/UK
  • 5Department Of Medicine, Royal Marsden Hospital NHS Foundation Trust, SW3 6JJ - London/UK
  • 6Dept. Of Medicine, Institute of Cancer Research, GB-SM2 5PT - Sutton/UK
  • 7Department Of Medicine, Royal Marsden HospitalNHS Foundation Trust, GB-SW3 6JJ - London/UK

 

Abstract

Background

Carboplatin plus gemcitabine (GC) is approved in S relapsed ovarian cancer. The likelihood of response to platinum in R relapse (< 6months treatment free interval) is perceived to be low. Rechallenge with platinum-based chemotherapy is not routinely used in this setting. However, recent experience suggests that GC should be considered. Our aims were to assess the efficacy of GC in R patients, compare this with S patients and explore potential factors predicting clinical outcome.

Method

Patients who started GC (C AUC 4 D1, G 800-1000 mg/m2 D1, D8 q3wk) for relapsed ovarian, peritoneal or fallopian tube carcinoma between 01/01/10 and 01/04/12 were analysed retrospectively. The primary endpoint was response rate (RR). Secondary endpoints included GCIG CA125 response and time to progression. The time between last platinum and first dose of GC (LPGCI) was assessed as a predictor of response to treatment.

Results

63 patients (33 S; 29 R; 1 platinum-refractory) were evaluable: age (median, range) S 57 (34-74), R 58 (34-79); prior lines of chemotherapy (median, range) S 1.5 (1-12), R 3.5 (1-6); 83% high grade serous; 22% BRCA 1/2 germline mutation; 19% prior PARP inhibitor, 11% received cisplatin due to carboplatin hypersensitivity. The LPGCIs were (median, range) S 12.3 months (7.0-138), R 11.2 months (2.3-40). The differences in RR between S and R patients were not statistically significant (RECIST RR S 74%, R 57% p = 0.17; GCIG CA125 S 79% R 67% p = 0.31). Treatment was generally well tolerated. However, omission of D8 G on ≥2 cycles was required in 16% due to toxicity (myelosuppression and fatigue). At the time of analysis, 78% had no evidence of disease progression. LPGCI was not predictive of response (p = 0.60, 95% CI 0.97 – 1.04).

Conclusions

The level of activity of GC in R patients is equivalent to that expected in S patients. This may relate to the potential for G to overcome platinum resistance. The relevance of LPGCI needs to be explored further. Further clinical outcome analyses and data on potential predictive factors will be presented. GC should now be considered a valid option for patients with platinum-resistant ovarian cancer.

Disclosure

All authors have declared no conflicts of interest.