e-Poster Presentation Clinical Oncology Society of Australia Annual Scientific Meeting 2020

Long-term Haematologic Toxicity of 177Lu-PRRT CAPTEM Chemotherapy of GEPNET (#227)

Piyush Grover 1 , Murali Kesavan 2 , Wei-Sen Lam 3 , Phillip Claringbold 3 , Harvey Turner 3
  1. Sir Charles Gairdner Hospital, Perth, WA, Australia
  2. School of Medicine, The University of Western Australia, Perth, WA, Australia
  3. Medical Oncology, Fiona Stanley Hospital, Perth, WA, Australia


Thirty-seven patients with advanced gastroenteropancreatic neuroendocrine tumors (GEPNETs) were treated on a prospective phase II single-center study with 4 cycles of 7.9 GBq 177Lu-octreotate combined with capecitabine and temozolomide chemotherapy (CAPTEM). Each 8-week cycle combined radiopeptide therapy with 14 days of capecitabine (1,500 mg/m2) and 5 days of temozolomide (200 mg/m2). The median progression-free survival was 48-months and median overall survival was 86-months. Of the 27 patients who progressed, 11 (41%) were successfully salvaged with further PRRT. The incidence of grade ³3 haematologic toxicity was analysed.  


At a median follow-up of 7-years (range 1-10), 6 (16%) patients developed persistent haematologic toxicity ([PHT] defined as sustained grade ≥3 haematologic toxicity beyond 36-months follow up) and 3 (8%) developed MDS/AL with a median time-to-event of 46 and 34-months respectively.  Development of PHT was the only significant risk factor for secondary MDS/AL (RR, 32; 95% CI: 1.85 to 552.18; p<0.001). The addition of temozolomide conferred an increased risk of MDS/AL, however it was not statistically significant.  The 21 deaths recorded included 13 (62%) from progressive disease and all 3 (14%) patients with MDS/AL.  


177Lu-octreotate CAPTEM therapy for GEPNETs demonstrates long-term efficacy and hematological safety. Secondary MDS/AL following treatment is a stochastic event without correlation with baseline risk factors.  Testing for clonal haematopoiesis may provide a means for stratification of prospective patients based on genetic risk for development of long-term haematologic toxicity.