Reliability of platelet-derived endothelial cell growth factor as a prognostic factor for oral and oropharyngeal carcinomas.

Objective: To identify a strong prognostic biological marker for patients with oral and oropharyngeal squamous cell carcinomas.

Design: We evaluated the protein expressions of 26 tumor-associated factors, including cytokines and cytokine receptors (granulocyte colony-stimulating factor [G-CSF], interleukin 10 [IL-10], G-CSF receptor [G-CSFR], and IL-12 receptor); angiogenic factors (platelet-derived endothelial cell growth factor [PD-ECGF] and vessel count); cell cycle-related proteins (p27, cyclin D1, and cyclin E); apoptosis-related factors (wild-type p53, Bax, Bcl-2, apoptotic index, Fas, and Fas ligand); oncogene proteins (c-fos and c-Myc); cell-surface proteins (P-glycoprotein, multidrug resistance-associated protein, nm23, and CD40); intracellular proteins (aryl hydrocarbon receptor nuclear translocator, aryl hydrocarbon receptor, and heat shock protein 27); and DNA mismatch-repair genes (protein encoded by human mutL homologue 1 and the human mutS homologue of the chromosome 2p gene) by means of immunohistochemical analysis.

Setting: Department of Otorhinolaryngology-Head and Neck Surgery, University of Fukui, Fukui, Japan.

Combined treatment of cisplatin and overexpression of caspase-activated deoxyribonuclease (CAD) promotes apoptosis in vitro and in vivo.

Recent studies have demonstrated that a caspase-activated deoxyribonuclease (CAD) causes DNA degradation in nuclei after treatment of cells with caspase-3. In this study, we evaluated the effect of CAD overexpression on tumor cells treated with a chemotherapeutic agent in vitro and in vivo. In an in vitro study, we transfected mouse fibroblast L cells with a vector encoding mouse CAD and evaluated the therapeutic potential of CAD gene transfer to L cells treated with cisplatin (CDDP).