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e14661 Background: FOLFIRINOX is an important addition to our therapeutic armamentarium for the treatment of aPDAC; however, safety and tolerability issues (hematologic toxicity, increased risk of AE in pts carrying biliary stents) may limit its use in routine clinical practice. Methods: We reviewed the clinical charts of 36 aPDAC pts receiving first-line FOLFIRINOX at two different institutions and analyzed toxicity and outcomes according to the presence or absence of a biliary stent and whether they received (n=21) or not (n=15) primary prophylactic G-CSF (d 7-9-11). Results: 36 pts (M/F: 22/14; median age: 57 yrs, range: 37-70; stage III/IV: 10/26; ECOG PS 0/1: 33/3) and 241 cycles were analyzed. Toxicity was mild with G3/4 adverse events (AE) in 50% reduction in CA19.9 occurred in 61% of pts. Median PFS was 8 mos (95% CI: 6-9 mos). Conclusions: FOLFIRINOX is well tolerated and easily manageable on an outpatient basis in young (

Pancreatic cancer is the only human malignancy for which patients' survival has not improved substantially during the past 30 years. Despite advances in the comprehension of the molecular mechanisms underlying pancreatic carcinogenesis, current systemic treatments offer only a modest benefit in tumor-related symptoms and survival. Over the past decades, gemcitabine and its combination with other standard cytotoxic agents have been the reference treatments for advanced pancreatic cancer patients. The recent introduction of the three-drug combination regimen FOLFIRINOX or the new taxane nab-paclitaxel represent key advances for a better control of the disease. Novel agents targeting molecular mechanisms involved in cancer development and maintenance are currently under clinical investigation. This review describes the most important findings in the field of systemic combination therapies for the treatment of pancreatic cancer. We discuss the emerging evidences for the clinical activity of combination treatments with standard chemotherapy plus novel agents targeting tumor cell-autonomous and tumor microenvironment signaling pathways. We present some of the most important advances in the comprehension of the molecular mechanisms responsible for the chemoresistance of pancreatic cancer and the emerging therapeutic targets to overcome this resistance.

Background: TemCap is an option for treatment of NENs; benefit of treatment until progression rather than a fixed 6-month (mo) course remains unclear.Methods: Patients (pts) diagnosed with advanced NEN (pathology-confirmed), treated with TemCap with follow-up and available radiological response data were eligible for this retrospective study. Efficacy was assessed by RECIST v1.1.Results: Of 62 pts identified (Jan’12-Jan’17), 60 were eligible. Median (med) age at starting TemCap was 63.6 yrs; 50% were male; Performance Status (PS) 0-1 (83.3%), 2 (16.7%); with NEN of lung (33.3%), pancreas (21.7%), small bowel (16.7%), colorectal (3.3%) and other (25.0%) origin. The med Ki-67 was 12% (range 1-29); most (83.3%) were well-differentiated [grade (G)1/typical (18.3%); G2/atypical (65%); G3 (16.7%)], non-functional (75.0%) and metastatic (90.0%). Pts received TemCap as first- (33.3%) or second- (35.0%) line, for a med of 5.58 mo (95%CI 5.33-5.78). After 6 cycles, 38 pts (63.3%) were progression-free (i.e. eligible for maintenance TemCap [mTemCap]); 11 received mTemCap, 27 did not. Rationale for mTemCap was good response (n = 7), good tolerance (n = 3) or pts’ wishes (n = 1). Overall, 29 pts (48.3%) had stable disease and 14 pts (23.3%) achieved a partial response (PR); med reduction in responding pts was -56.7% (95%CI -76.4 to -33.3); 4 additional pts (6.67%) achieved a reduction >20% but