Oral squamous carcinogenesis is a multistep process in which multiple genetic events occur that alter the normal functions of oncogenes and tumour suppressor genes. This can result in increased production of growth factors or numbers of cell surface receptors, enhanced intracellular messenger signalling, and/or increased production of transcription factors. In combination with the loss of tumour suppressor activity, this leads to a cell phenotype capable of increased cell proliferation, with loss of cell cohesion, and the ability to infiltrate local tissue and spread to distant sites. Recent advances in the understanding of the molecular control of these various pathways will allow more accurate diagnosis and assessment of prognosis, and might lead the way for more novel approaches to treatment and prevention. (J Clin Pathol: Mol Pathol 2000;53:165-172)

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The immunocytochemical expression of cadherins and catenins was examined during the process of oral carcinogenesis by comparing their expression in normal and dysplastic epithelium with primary and metastatic carcinomas. While control epithelium showed normal distribution for P and E cadherin and the catenins, in severe dysplasia P‐cadherin was upregulated. In other cases and in carcinoma‐in‐situ adjacent to infiltrating carcinomas, membranous expression of the cadherins and catenins was reduced or lost. The changes in expression of E‐cadherin and the catenins suggest that disruption of the E‐cadherin/catenin complex is a late event associated with invasion. In primary carcinomas reduced membranous and cytoplasmic staining were observed for both cadherins and catenins. Abnormal localisation of E‐cadherin occurred in the more superficial parts of the better differentiated carcinomas, suggesting abnormality to the E‐cadherin complex(es). In contrast, membranous expression of cadherins and catenins was reduced or lost in the deep invasive margin of primary carcinomas and in most poorly differentiated carcinomas. For E‐cadherin at least, this reduction appears associated with differentiation, invasion and possibly prognosis. Possible mechanisms involved for changes in expression of the cadherins and associated catenins and areas for further study are discussed.

Juvenile ossifying fibroma (JOF) is a well-defined clinical and histological entity that has recently been separated from other fibro-osseous lesions, including cemento-ossifying fibromas. Its biological behaviour is well defined, but unexplained. Its behaviour, clinical and histological appearance, however, bears resemblance to osteofibrous dysplasia of long bones, a lesion that in some cases has been reported to be part of a spectrum of diseases associated with adamantinoma, thus accounting for its variable biological behaviour. Eight cases of JOF were examined for islands of epithelium or single epithelial cells using immunocytochemistry. While these cases of JOF could clearly be separated from other fibro-osseous lesions, and were histologically similar to osteofibrous dysplasia, the absence of cytokeratin-positive cells in all cases suggests that another reason for its biological behaviour has still to be found.

Tectonic models for the latest Paleoproterozoic to earliest Mesoproterozoic evolution of eastern Australia (circa 1620–1500 Ma) are diverse and either emphasize plume or plate margin activity, neither of which satisfactorily explains all geological observations. The dichotomy is largely attributed to geochemical, spatial and temporal data that suggest voluminous A‐type felsic magmas are plume related, whereas distribution of arc‐related magmas and intense orogenic overprint suggest plate margin activity. The salient geological events include arc‐related magmatism at circa 1620–1610 Ma followed by a magmatic hiatus coincident with north‐south crustal shortening (1610–1590 Ma) and a magmatic flare‐up of A‐type felsic magmas throughout the Gawler Craton (circa 1595–1575 Ma). These magmas form the oldest component of a northward younging hot spot track that extends to the Mount Isa Inlier. At circa 1590–1550 Ma, arc magmatism resumed along the northern margin of the Gawler Craton and the rest of eastern Australia records a 90° shift in the regional shortening direction related to activity along the eastern margin of the Australian continent. A plume‐modified orogenic setting satisfies all of the spatial and temporal relationships between magma generation and orogenic activity. In this model, the Gawler Craton and the adjacent subduction zone migrated over a mantle plume (circa 1620–1610 Ma). Resultant flat subduction caused transient orogenesis (1610–1595 Ma) in the overriding plate. Slab delamination and thermal assimilation of the plume and the subducting slab caused a switch to crustal extension in the overriding plate, resulting in extensive mantle‐derived and crustal melting in the Gawler Craton (1595–1575 Ma).