P-0118 - FOLFIRINOX in pancreatic cancer: the National Cancer Institute of Milan single experience

Date 28 June 2014
Event World GI 2014
Session Poster Session
Topics Anti-Cancer Agents & Biologic Therapy
Pancreatic Cancer
Presenter Fiorella Dotti Katia
Citation Annals of Oncology (2014) 25 (suppl_2): ii14-ii104. 10.1093/annonc/mdu165
Authors F. Dotti Katia1, L. Celio1, F. AgustonI1, S. Damian1, M. Niger1, F. Ricchini1, M. Duca1, F. de Braud2
  • 1Fondazione IRCCS Istituto Nazionale dei Tumori, Milan/IT
  • 2Fondazione I.R.C.C.S. Istituto Nazionale Tumori, Milan/IT



FOLFIRINOX regimen is an effective therapeutic option in the treatment of advanced pancreatic cancer in patients with good PS with a significant survival benefit compared to gemcitabine. (Conroy et al., N Engl J Med 2011;364:1817). However, the toxicity profile can be relevant. In this retrospective analysis, we reviewed our experience to assess the feasibility of the regimen.


All patients who received FOLFIRINOX consecutively from Sep 2011 to Feb 2014 were considered. The doses were identical to the Conroy's trial; dose reductions were at the discretion of the physician. Patients were treated until progression, unacceptable toxicity, or surgical resection. Primary end point was tolerability (CTCAE criteria, v. 4.03). Secondary end point was tumor response.


Between 09/2011 and 02/2014, 37 pts were treated consecutively. The median age was 58 y (range 30-71), 23 were male and all had a PS 0/1. 21 pts had metastatic disease, 14 unresectable locally advanced PC and 2 had borderline disease. Pancreatic tumor location was head in 17 (46%) with 7 pts required the placement of a biliary stent. The median number of cycles per patient was 5 (range 1-12). The majority of patients (57%) received full doses of all drugs with cycle 1 whereas 16 patients received dose attenuation of FOLFIRINOX in cycle 1 to assess tolerability. 13 (35%) patients had a dose reduction due to toxic effects. Only one patient permanently discontinued due to toxicity. Of the 181 cycles administered, 100 (55%) had some dose modifications. CPT-11 dosage was modified in 91 cycles, Oxaliplatin in 34, bolus 5-FU in 39 and infusion 5-FU in 29. Bolus fluorouracil was omitted in 54 cycles. Sixteen pts (43%) received prophylactic G-CSF after the first cycle. Grade 3-4 chemotherapy-related toxicities occurred in 20 patients (54%). The most common G3-4 adverse events were neutropenia (32%), infections (11%), fatigue (8%), diarrhea (5%) and febrile neutropenia (3%). Among 35 evaluable patients, 9 (26%) achieved PR. Stabilization occurred in 14 (40%) patients. Five patients with locally advance PC and one with borderline disease underwent resection.


In our experience, FOLFIRINOX is reasonably feasible with manageable toxicity in patients in good general condition. This regimen, in our opinion, should be evaluated in other settings and in combination with innovative agents. A dose reduction and an appropriate supportive care may improve the tolerability of the treatment.