to stroma, suggesting a role for invadopodia in local invasiveness. At ameloblastoma invasion sites cortactin would recruit MT-MMP, inducing focal degradation in stroma. Correlating cortactin and MT1-MMP presence in ameloblastoma with our previous findings on MMPs and growth factors, 3,4 we suggest that cortactin, MT1-MMP, proteases and growth factors would combine forces to regulate ameloblastoma invasiveness.We demonstrated cortactin and MT1-MMP expression in ameloblastoma. These proteins were increased significantly compared to CCOT, a non-invasive odontogenic tumour. Our results indicate that invadopodia proteins cooperate to regulate ameloblastoma invasion. acknowledgements This investigation was supported by the State of São Paulo Research Foundation (FAPESP grants 2006 ⁄ 57079-4 and 2008 ⁄ 57103-8) and the Brazilian National Council for

Carcinoma cuniculatum (CC) is a rare variant of extremely well differentiated squamous cell carcinoma. We present the clinicopathological features of two cases of CC; one lingual and one esophageal case with a molecular genetic study regarding the TP53 gene mutational status. Case 1 was a 62 year old male with enlarging chronic ulcer in the tongue. Case 2 was a 77 year old male with progressive dysphagia and odynophagia. Both patients were treated surgically. Both tumors showed deeply invaginating, keratin-filled, burrowing crypts lined by very well differentiated squamous epithelium. The esophageal tumor showed varying degrees of reactive nuclear atypia largely limited to the areas with dense intratumoral infiltration of neutrophils. No mutation of TP53 was identified in the esophageal case. Cytologic atypia limited to areas of significant acute inflammation may occur in CC and should, in the absence of aggressive stromal invasion, not preclude a diagnosis of CC.

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Symptoms and signs of gallbladder cancer may be insidious. Thorough workup is needed if the patient presents with symptoms and signs of a paraneoplastic syndrome.