In recent years, oral fluoropyrimidines have been evaluated in oesophagogastric cancer. Capecitabine has been shown to have equivalent activity to 5-FU, with a different selleck bio safety profile (Cunningham et al, 2008). It is likely that modification of the wTCF regimen by substituting an oral fluoropyrimidine for 5-FU would maintain activity, while potentially improving safety and convenience. Novel biological targeted agents, such as bevacizumab, cetuximab, and panitumumab, have also improved outcomes in a range of cancers including colorectal, breast, and lung cancer (Hurwitz et al, 2004; Sandler et al, 2006; Jonker et al, 2007; Miller et al, 2007; Van Cutsem et al, 2007). Some of these agents are currently being evaluated in advanced oesophagogastric cancer.

Weekly docetaxel-based chemotherapy provides a useful chemotherapy backbone for evaluation of targeted agents, and the AGITG is currently evaluating the efficacy and safety of adding the epidermal growth factor receptor-targeted antibody, panitumumab, to wTCF chemotherapy as treatment for this disease. Acknowledgments This study was supported by an unrestricted educational grant by Sanofi-Aventis. Drugs were provided by Sanofi-Aventis and Roche. Numerous individuals from many institutions participated to complete this study. We thank everyone involved for their efforts.
Liver cancer, especially hepatocellular carcinoma (HCC), is a malignancy of worldwide significance (1,2). Although the increased global incidence of HCC is correlated with the increasing prevalence of chronic infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) (2,3), some of the mechanisms associated with the initiation and progression of this disease remain elusive.

Dysregulation of the hedgehog (HH) pathway is implicated in the carcinogenesis of multiple tissue types (1,4). HH was first identified in Drosophila during screening of genes that are important in early embryonic development (5). This pathway is activated during binding of sonic HH (SHH) or Indian hedgehog (IHH) ligand to their receptors, Patched (PTCH). The unbound PTCH acts as a tumor suppressor that can bind to and repress smoothened (SMOH), thereby preventing the SMOH proto-oncoprotein from activating downstream of the transcription factors, such as glioma-associated oncogene-1 (GLI1). By contrast, the ligand-bound PTCH facilitates the release of SMOH and activation of GLI1 resulting in the transcription of target genes including PTCH and GLI1 (1). The HH activation AV-951 has been observed in other types cancers such as basal cell carcinomas of the skin (6-9), prostate cancer (10,11), lung cancer (12,13), gastrointestinal cancers (14-19), breast cancer (20,21), and ovarian cancer (22).