570 Introduction: Capecitabine (Xeloda [X]) shows synergy with taxanes and adding X to docetaxel (T) extends overall survival (OS), response rate (RR) and progression free-survival (PFS) beyond T alone. Sequential single-agent therapy could confer convenience benefits and may be more appropriate than combination chemotherapy for some pts. Methods: Pts with anthracycline-pretreated MBC received 3-weekly cycles of 1 of the following regimens: X→taxane (X 1250mg/m2 bid d1–14, followed after progression (PD) by T 100mg/m2 or paclitaxel [P] 175mg/m2 day 1; X+P (X 825mg/m2 bid days 1–14 + P 175mg/m2 day 1) or X+T (X 825mg/m2 bid days 1–14 + T 75mg/m2 day 1). Results: Of the 368 pts enrolled, 91 are either still on therapy or not evaluable. The table shows baseline characteristics, efficacy and safety in evaluable pts. Median follow up is 15.5 months. Median doses for X in each arm (1st cycle vs. 8th cycle, mg/m2 bid): 1218 vs. 1054; 948 vs. 900; 846 vs. 751. Median doses for P and T (1st cycle vs. 8th cycle, mg/m2): 173 vs. 169 and 75 vs. 72, respectively. In the X→taxane arm, 58 pts (64%) received sequential taxane; the remainder did not receive a taxane, either because they were still on X, had CR or had rapid PD. Conclusions: RR is higher with XP and XT, but PFS and OS are similar at a median follow-up of 15.5 months. All regimens were well tolerated with minimal grade 4 AEs. Because there is no clear superiority of sequential vs. combined therapy, pt characteristics are likely to be used to decide which regimen is the most appropriate. [Table: see text] [Table: see text]
WSE is associated with better response to Erlotinib and improved progression-free survival in patients with NSCLC. Additional studies in epidermal growth factor receptor signaling pathway in WSE-associated NSCLC are warranted.
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Background: BV (Avastin®) is a monoclonal antibody to VEGF that significantly improved PFS and response rate when combined with 1st-line taxane chemotherapy (CTx) in two randomised phase III studies in patients (pts) with LR or mBC: E2100 (weekly paclitaxel ± BV) and double-blind, PL-controlled study AVADO (D ± two different BV doses). Preclinical data suggest that BV inhibits tumour neovascularisation and can limit tumour vascular regrowth. Both above trial protocols recommended BV use until PD, even after discontinuation of concomitant CTx. In the NO16966 trial in metastatic colorectal cancer, PFS was longer for pts continuing BV following cessation of CTx than for those where BV and CTx were stopped at the same time. We report results of an exploratory analysis of time to PD or death after cessation of D in pts in AVADO.
 Methods: AVADO compared BV 7.5 or 15mg/kg + D 100mg/m2 with PL + D in 736 pts with inoperable LR or mBC, ECOG PS 0–1 and adequate LVEF. D and BV/PL were administered q3w, with D given for up to 9 cycles and BV/PL continued until PD or unacceptable toxicity.
 Results: The table presents median time from discontinuation of D until PD or death in different subgroups in the AVADO study. Approximately 70% of pts in each arm discontinuing D went on to receive at least one dose of BV or PL before PD.
 
 Conclusions: Continuation of single-agent BV at either dose after discontinuation of D significantly delayed PD or death compared with single-agent PL. These results support the hypothesis that BV may inhibit tumour neovascularisation and progression following CTx and suggests that clinical benefit may be maximised by treatment with BV until progression.
Citation Information: Cancer Res 2009;69(2 Suppl):Abstract nr 903.
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