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Abstract Odontogenic tumors (OT) are considered rare events and their epidemiologic data are scarce and under-estimated in developing countries because there is no systematic collection of clinical features including histological analyses of the tissue samples. Furthermore, there is an underestimation of the disease relevance and affected people are often marginalized in spite of severe functional impairment of aero-digestive tract. Etiology of OT in humans is still unknown and it represents an important therapeutic and diagnostic challenge. Lassa fever is an acute viral haemorrhagic illness caused by Lassa virus, a member of the arenavirus family of viruses. The disease is endemic in the rodent population in West-East Africa. Humans usually become infected with Lassa virus through exposure to the food or household items contaminated with urine or feces of infected rats. It is also reported person-to-person infections. About 80% of people infected by Lassa virus have no symptoms but the virus establishes a life-long persistent infection. The present commentary significance is to start, for the first time ever, a systematic collection of clinical features and tissue sample collection at the St. Mary’s Hospital in Lacor (Gulu) North Uganda where the considered pathologies have an important frequency. The systematic collection will allow to corroborate the possible association between arenaviruses infection and pathogenesis of odontogenic tumors in humans.

Abstract The tumor suppressor p53 plays a critical role to preserve DNA fidelity from diverse insults through the regulation of cell-cycle checkpoints, DNA repair, senescence and apoptosis. The TP53 is the most frequently inactivated gene in human cancers. This leads to the production of mutant p53 proteins that loose wild-type p53 tumor suppression functions and concomitantly acquire new oncogenic properties among which deregulated cell proliferation, increased chemoresistance, disruption of tissue architecture, promotion of migration, invasion and metastasis and several other pro-oncogenic activities. Mouse models show that the genetic reconstitution of the wild type p53 tumor suppression functions rescues tumor growth. This strongly supports the notion that either restoring wt-p53 activity or inhibiting mutant p53 oncogenic activity could provide an efficient strategy to treat human cancers. In this review we briefly summarize recent advances in the study of small molecules and compounds that subvert oncogenic activities of mutant p53 protein into wt-p53 tumor suppressor functions. We highlight inhibitors of signaling pathways aberrantly modulated by oncogenic mutant p53 proteins as promising therapeutic strategies. Finally, we consider the clinical applications of compounds targeting mutant p53 and the use of currently available drugs in the treatment of tumors expressing mutant p53 proteins.

Abstract This commentary wishes to highlight the latest discoveries in the mutant p53 field that have been discussed in the 8th p53 Mutant Workshop 2019, held in Lyon. TP53 mutant (mutp53) proteins are involved in the pathogenesis of most human cancers. Mutp53 proteins not only lose wild-typ53 function but, in some circumstances, may acquire novel oncogenic functions, namely gain-of-function (GOF), which lead to aberrant cell proliferation, chemoresistance, disruption of tissue architecture, migration, invasion and metastasis. Decoding the TP53 mutational spectrum and mutp53 interaction with additional transcription factors will therefore help to developing and testing novel and hopefully more efficient combinatorial therapeutic approaches.