Precise assessment of the extent of nasopharyngeal carcinoma (NPC) represents the basic step towards optimal treatment. We compared the capacity of CT and MRI in assessing the extent of NPC in 67 patients. MRI was superior to CT in demonstrating lesions in the retropharyngeal node, skull base, intracranial area, carotid space, longus colli muscle and levator palatini muscle. Of 25 cases in which retropharyngeal adenopathy was recognised only on MRI, seven had been reported as showing oropharyngeal involvement and 18 as primary extension to the carotid space on CT. MRI showed skull-base involvement in 40 patients compared with 27 on CT and intracranial involvement in 38 patients versus 24 on CT. There was not a single case in which skull base invasion was seen on CT but not on MRI. MRI enabled improved recognition of tumour infiltration of longus colli muscles (34 cases compared with 15 on CT). It allowed us to clarify 12 questionable sinonasal opacities on CT. Overall, T-staging was changed in 18 of 67 patients (26.9%), including upstaging in 15 cases and down-staging in 3 cases, after comparing CT with MRI. The nodel status was changed from negative on CT to positive on MRI in 4 of 67 patients (6%). We believe that MRI allows more accurate evaluation of the extent of NPC than CT and should be the primary mode of investigation.

Oral squamous cell carcinoma (OSCC) is highly invasive and is associated with frequent tumour recurrences and lymph node metastases. Identification of genes involved in the aggressiveness of OSCC may provide new targets for clinical intervention. A genome-wide study based on the Sty1 250K SNP array indicated the involvement of the Talin-1 (TLN1) gene in the 9p13.3 amplicon, which was further validated by dual colour fluorescence in situ hybridization (FISH). Comparative analyses revealed that TLN1 was the most highly expressed integrin-cytoskeleton cross-linker that can trigger integrin activation. IHC analyses and mouse study also revealed an association between TLN1 overexpression and advanced OSCC with invasion to adjacent tissues. Survival analyses indicated a significant association between TLN1 genetic gain/overexpression and a reduced overall survival in patients. Functional knockdown by a dominant negative TLN1 fragment reduced cell growth and invasiveness in TLN1-overexpressing cells via inactivation of downstream oncogenic signalling. The present study suggests an important role for TLN1 in oral cancer development. TLN1 overexpression could serve as a diagnostic marker for aggressive phenotypes and a potential target for treating OSCC.

Oral squamous cell carcinoma has a striking tendency to migrate and metastasize. Cyclooxygenase (COX)-2, the inducible isoform of prostaglandin (PG) synthase, has been implicated in tumor metastasis. However, the effects of COX-2 on human oral cancer cells are largely unknown. We found that overexpression of COX-2 or exogenous PGE 2 increased migration and intercellular adhesion molecule 1 (ICAM)-1 expression in human oral cancer cells. Using pharmacological inhibitors, activators, and genetic inhibition of EP receptors, we discovered that the EP1 receptor, but not other PGE receptors, is involved in PGE 2 -mediated cell migration and ICAM-1 expression. PGE 2 -mediated migration and ICAM-1 up-regulation were attenuated by inhibitors of protein kinase C (PKC)␦, and c-Src. Activation of the PKC␦, c-Src, and AP-1 signaling pathway occurred after PGE 2 treatment. PGE 2 -induced expression of ICAM-1 and migration activity were inhibited by a specific inhibitor, siRNA, and mutants of PKC␦, c-Src, and AP-1. In addition, migration-prone sublines demonstrated that cells with increased migration ability had higher expression of COX-2 and ICAM-1. Taken together, these results indicate that the PGE 2 and EP1 interaction enhanced migration of oral cancer cells through an increase in ICAM-1 production.