Early stage adenoid cystic carcinoma of the posterior nasal septum: a rare manifestation

Adenoid cystic carcinomas are rare malignant tumors that commonly arise from major and minor salivary glands and are characterized by slow growth, frequent local recurrences, and high incidence of distant metastasis, especially reported in patients with advanced stage tumors. Adenoid cystic carcinomas can rarely occur in other areas of the head and neck region, notably in the nasal cavity. Moreover, adenoid cystic carcinoma limited to the nasal septum is particularly unusual and has been the subject of a small number of published cases only. We discuss here a case of a 42 year-old woman diagnosed with early stage adenoid cystic carcinoma of the posterior nasal septum, treated solely with surgical resection via endoscopic approach. During five years of follow-up, no local recurrence or distant metastasis has been detected

Early stage adenoid cystic carcinoma of the posterior nasal septum: a rare manifestation

Adenoid cystic carcinomas are rare malignant tumors that commonly arise from major and minor salivary glands and are characterized by slow growth, frequent local recurrences, and high incidence of distant metastasis, especially reported in patients with advanced stage tumors. Adenoid cystic carcinomas can rarely occur in other areas of the head and neck region, notably in the nasal cavity. Moreover, adenoid cystic carcinoma limited to the nasal septum is particularly unusual and has been the subject of a small number of published cases only. We discuss here a case of a 42 year-old woman diagnosed with early stage adenoid cystic carcinoma of the posterior nasal septum, treated solely with surgical resection via endoscopic approach. During five years of follow-up, no local recurrence or distant metastasis has been detected

CD36 Participates in PrP106–126-Induced Activation of Microglia

Microglial activation is a characteristic feature of the pathogenesis of prion diseases. The molecular mechanisms that underlie prion-induced microglial activation are not very well understood. In the present study, we investigated the role of the class B scavenger receptor CD36 in microglial activation induced by neurotoxic prion protein (PrP) fragment 106–126 (PrP106–126). We first examined the time course of CD36 mRNA expression upon exposure to PrP106–126 in BV2 microglia. We then analyzed different parameters of microglial activation in PrP106–126-treated cells in the presence or not of anti-CD36 monoclonal antibody (mAb). The cells were first incubated for 1 h with CD36 monoclonal antibody to block the CD36 receptor, and were then treated with neurotoxic prion peptides PrP106–126. The results showed that PrP106–126 treatment led to a rapid yet transitory increase in the mRNA expression of CD36, upregulated mRNA and protein levels of proinflammatory cytokines (IL-1β, IL-6 and TNF-α), increased iNOS expression and nitric oxide (NO) production, stimulated the activation of NF-κB and caspase-1, and elevated Fyn activity. The blockade of CD36 had no effect on PrP106–126-stimulated NF-κB activation and TNF-α protein release, abrogated the PrP106–126-induced iNOS stimulation, downregulated IL-1β and IL-6 expression at both mRNA and protein levels as well as TNF-α mRNA expression, decreased NO production and Fyn phosphorylation, reduced caspase-1 cleavage induced by moderate PrP106–126 –treatment, but had no effect on caspase-1 activation after treatment with a high concentration of PrP106–126. Together, these results suggest that CD36 is involved in PrP106–126-induced microglial activation and that the participation of CD36 in the interaction between PrP106–126 and microglia may be mediated by Src tyrosine kinases. Our findings provide new insights into the mechanisms underlying the activation of microglia by neurotoxic prion peptides and open perspectives for new therapeutic strategies for prion diseases by modulation of CD36 signaling

Primers used for real-time PCR and cloning.

<p>Primers used for real-time PCR and cloning.</p

Role of CD36 in PrP_106–126-induced production of nitric oxide and iNOS expression in BV2 and primary microglia.

<p>Cells were first pre-incubated or not with anti-CD36mAb (1 µg/ml) or irrelevant rabbit IgG (Ab) and then treated for 12 hours with PBS, 50 µM PrP_106–126 (PrP), or scrambled PrP_106–126 (Scr). A. The level of NO was measured in supernatant from primary microglia culture with nitrite assay as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030756#s2" target="_blank">Materials and Methods</a>. The amount of nitric oxide is expressed as U/l cell supernatant. B. ELISA was performed on supernatant from culture of BV2 microglia as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030756#s2" target="_blank">Materials and methods</a>. All data in A and B are means ± s.d. of triplicate samples and are representative of an experimental n of 3 or 4, * P<0.05. C. Cytoplasmic extracts from primary microglia were prepared and immunoblotted with anti-iNOS antibody as described in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0030756#s2" target="_blank">Materials and Methods</a>. The blot was stripped and reprobed with anti-β-actin antibody to estimate the total amount of protein loaded in gel. Representative blots of iNOS and actin are shown. Bars represent the relative levels of iNOS, compared with β-actin, and were expressed as arbitrary units. Data are the means±S.D of three independent experiments. * P<0.05, significantly different from control cells. 1-PBS, 2–50 µM PrP_106–126, 3- PrP_106–126+irrelevant rabbit IgG (Ab), 4- Prpscr (50 µM), 5- Anti-CD36mAb (1 µg/ml), 6- PrP_106–126+Anti-CD36mAb.</p