Mucoepidermoid (MEC) salivary gland tumors arise from a t(11;19) rearrangement which generates a fusion oncogene, Mect1-Maml2, that functions to activate CREB-responsive target genes. To determine if sustained expression of Mect1-Maml2 is required for tumor cell growth, we first showed that ectopic expression of Mect1-Maml2 in rat epithelial RK3E cells is tumorigenic in vivo in nude mice and that excised xenografts continue to express the fusion oncogene. We then generated a hairpin RNAi vector that selectively suppressed the fusion peptide and showed that ectopic expression in either parotid or pulmonary MEC tumor cell lines containing the t(11;19) rearrangement resulted in at least 90% colony growth inhibition. In contrast, single nucleotide changes within this RNAi sequence abolished the ability to suppress Mect1-Maml2 protein and abolished all growth inhibition of these MEC tumor lines. In addition, the RNAi-specific vector had no effect on colony growth of non-MEC tumors including a lung tumor or two other salivary gland cell lines that do not express Mect1-Maml2. We also generated a mutant Mect1-Maml2 expression plasmid that carried silent nucleotide changes within the RNAi target sequence and observed that co-transfection of this mutant, but not wild-type Mect1-Maml2, could partially rescue RNAi growth inhibition in the MEC tumor line. The recent detection of acquired fusion oncogenes in epithelial solid tumors has suggested new possibilities for the diagnosis and therapy of these cancers. Our data show that the 'gain-of-function' activity from aberrant Mect1-Maml2 expression is a candidate therapeutic target for this group of malignant salivary gland tumors.

the expense of higher numbers of deaths in both groups than in the actual scenario, and a lesser improvement in absolute inequality. The differences between the two scenarios raised ethical questions. Conclusion When talking about health inequalities, defining desirable reductions in them, assessing trends and judging success and failure, it is important, on social justice and other grounds, to consider both absolute and relative inequality. Objective To assess the influence of social circumstances at 12 yrs on c-section delivery. Methods Women (n¼6827) were consecutively recruited during the assembling of a birth-cohort. Interviews were used to obtain data on social and demographic characteristics and current pregnancy events. Financial childhood circumstances were classified as low (LF) or high (HF) based on the number of amenities reported. Parents' education was defined as low (#6 years, LPE) and high (HPE). The effect of participants' financial socioeconomic conditions on csection risk was computed using logistic regression stratified by parents 'education. Results Women with both high financial and educational childhood circumstances were significantly older, more educated and more frequently primiparous, with normal or underweight and reporting private antenatal care. The overall c-section rate was 35.6% varying from 32.2% (LF-LE) to 41.3% (HF-HE). After adjustment and considering women in LF-LPE as reference, we obtained OR¼0.92; 95% CI 0.66 to 1.28 for LF-HPE group, OR¼1.19; 95% CI 1.04 to 1.37 for HF-LPE group and OR¼1.38; 95% CI 1.16 to 1.64) for HF-HPE group. Stratifying by parents' education and compared with women in LF group, those in HF group showed higher risk of csection either in the LPE group (OR¼1.19; 95% CI 1.04 to 1.37) or in the HPE group (OR¼1.42; 95% CI 0.99 to 2.02). Conclusions Our results suggest that, independently of the parents' education and the current socio-demographic conditions, the childhood financial environment may influence the mode of delivery. P1-353