Odontogenic tumours are a heterogeneous group of lesions that develop in the oral cavity region and are characterized by the formation of tumoural structures that differentiate as teeth. Due to the diversity of their histopathological characteristics and clinical behaviour, the classification of these tumours is still under debate. Alterations in morphogenesis pathways such as the Hedgehog, MAPK and WNT/β-catenin pathways are implicated in the formation of odontogenic lesions, but the molecular bases of many of these lesions are still unknown. In this study, we used genetically modified mice to study the role of IKKβ (a fundamental regulator of NF-κB activity and many other proteins) in oral epithelial cells and odontogenic tissues. Transgenic mice overexpressing IKKβ in oral epithelial cells show a significant increase in immune cells in both the oral epithelia and oral submucosa. They also show changes in the expression of several proteins and miRNAs that are important for cancer development. Interestingly, we found that overactivity of IKKβ in oral epithelia and odontogenic tissues, in conjunction with the loss of tumour suppressor proteins (p53, or p16 and p19), leads to the appearance of odontogenic tumours that can be classified as ameloblastic odontomas, sometimes accompanied by foci of secondary ameloblastic carcinomas. These tumours show NF-κB activation and increased β-catenin activity. These findings may help to elucidate the molecular determinants of odontogenic tumourigenesis and the role of IKKβ in the homoeostasis and tumoural transformation of oral and odontogenic epithelia.

UV radiation is the most important environmental skin aggressor, causing cancer and other problems. This paper reports the use of oligonucleotide microarray technology to determine changes in gene expression in human keratinocytes after UVB treatment. Examination of the effects of different doses at different times after irradiation gave a global picture of the keratinocyte response to this type of insult. Five hundred thirty-nine regulated transcripts were found and organized into nine different clusters depending on behavior patterns. Classification of these genes into 23 functional categories revealed that several biological processes are globally affected by UVB. In addition to confirming a majority up-regulation of the transcripts related to the UV-specific inflammatory and stress responses, significant increases were seen in the expression of genes involved in basal transcription, splicing, and translation as well as in the proteasome-mediated degradation category. On the other hand, those transcripts belonging to the metabolism and adhesion categories were strongly downregulated. These results demonstrate the complexity of the transcriptional profile of the UVB response, describe several cellular processes previously not known to be affected by UV irradiation, and serve as a basis for the global characterization of UV-regulated genes and pathways. T he epidermis is a physiological barrier that protects the organism against pathogens and chemical or physical damage. UV radiation is the most important physical carcinogen in the environment, and the skin is its main target. In this tissue, UV induces photochemical changes that may lead to acute effects such as erythema or sunburn (1), or chronic effects that include premature skin aging (2, 3) and skin tumors (4, 5). In recent years, the importance of UV radiation has increased because of the thinning of the ozone layer (6) and increasing skin cancer rates (7). UV light affects the skin in different ways depending on its wavelength. UVA (320 -400 nm) effects are primarily oxidative in nature. UVC (200 -290 nm) hardly ever reaches the surface of the earth. UVB (290 -320 nm) is the most important and is considered the causative agent of many of the effects attributed to UV (8), giving rise to mutations in DNA and modifying the pattern of gene expression. This transcriptional regulation is part of the cellular reaction to UV-induced stress and operates as a defense mechanism. The known UV response comprises, for instance, the rapid activation of genes with reparative, protective, or apoptotic functions and the communication of stress to other cells via secreted signaling molecules (9).Although a number of UV-regulated genes and processes have been described (see refs. 9 and 10 for review), many of the molecular events involved in the UV response remain unknown. However, many studies on UV lack physiological relevance because they were performed by using UVC and established epithelial cell lines or fibroblasts. Habitually exposed to UV radiation, keratinocytes a...