SummaryAlthough TGF- suppresses early stages of tumour development, it later contributes to tumour progression when cells become resistant to its suppressive effects. In addition to circumventing TGF--induced growth arrest and apoptosis, malignant tumour cells become capable of undergoing epithelial-to-mesenchymal transition (EMT), favouring invasion and metastasis. Therefore, defining the mechanisms that allow cancer cells to escape from the suppressive effects of TGF- is fundamental to understand tumour progression and to design specific therapies. Here, we have examined the role of Snail1 as a suppressor of TGF--induced apoptosis in murine non-transformed hepatocytes, rat and human hepatocarcinoma cell lines and transgenic mice. We show that Snail1 confers resistance to TGF--induced cell death and that it is sufficient to induce EMT in adult hepatocytes, cells otherwise refractory to this transition upon exposure to TGF-. Furthermore, we show that Snail1 silencing prevents EMT and restores the cell death response induced by TGF-. As Snail1 is a known target of TGF- signalling, our data indicate that Snail1 might transduce the tumour-promoting effects of TGF-, namely the EMT concomitant with the resistance to cell death.

Lichen planus (LP) is an idiopathic disorder that presents with cutaneous and genital manifestations. Esophageal LP (ELP) was first described by Al-Shihabi and Jackson [J Laryngol Otol 1982;96:567-571] in 1982. Only approximately 80 cases have been documented in the literature since. It is a rare and underrecognized disorder, leading to a delay in diagnosis and a lack of standardized management. We describe the presentation, diagnosis, and management of 6 cases of ELP, at a tertiary institution, because we believe that an increasing awareness of this condition can help identify more cases and increase our understanding of this interesting condition.

Analysis of performance across a subset of segmental and prosodic variables illustrated that "The Caterpillar" passage showed promise for extracting individual profiles of impairment that could augment current assessment protocols and inform treatment planning in motor speech disorders.

Most cells are naturally resistant to TNF-a-induced cell death and become sensitized when NF-kB transactivation is blocked or in the presence of protein synthesis inhibitors that prevent the expression of anti-apoptotic genes. In this report we analyzed the role of osmotic stress on TNF-a-induced cell death. We found that it sensitizes the naturally resistant HeLa cells to TNF-a-induced apoptosis, with the involvement of an increase in the activity of several kinases, the inhibition of Bcl-2 expression, and a late increase on NF-kB activation. Cell death occurs regardless of the enhanced NF-kB activity, whose inhibition produces an increase in apoptosis. The inhibition of p38 kinase, also involved in NF-kB activation, significantly increases the effect of osmotic stress on TNF-a-induced cell death.