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, 2010). For coculture studies, isolated SPC+ AECIIs and BASCs were plated in nonadherent dish seeded with 10-fold more MAPK+Akt ECs. Conditioned medium from MAPK+Akt ECs was added to AECs. After coculture, AECIIs and BASCs were quantified by flow cytometric analysis. After PNX, total RNA was isolated from Ribonucleotide reductase the mouse lungs to perform qPCR using Taqman expression systems (Applied Biosystems). HB-EGF concentration in BALF was examined by sandwich ELISA and western blot using anti-HB-EGF antibodies (Santa Cruz), and cleavage of laminin5 ��2 chain was tested with antibody against ��2 chain (Santa Cruz). All data are presented as mean �� SEM. Differences between groups were tested for statistical significance using Student's t test or analysis of variance (ANOVA). Statistical significance was set at p?VX-770 mouse S). M.S. is supported by R01HL53793. VE-Cad-CreERT2 mice were gift from Dr.?Ralf H. Adams (Max Planck Institute). SPC/CCSP-rtTA and (tetO)-cre mice were provided by Drs. Jeffrey A. Whitsett and Anne-Karina T. Perl (Cincinnati Children's Hospital Medical Centre). Fgfr1loxP/loxP mice were offered by Drs. Michael Simons and Masahiro Murakami (Yale University). The authors are grateful to Ms. Biin Sung for assistance in lung mechanics measurement. ""Insights into the molecular pathogenesis of cancer have led to successful therapies. Recent technological advances greatly facilitate the genome-wide detection of genetic and epigenetic changes in cancer cells. For example, sequencing studies have cataloged somatic mutations that occur in several cancers and paired-end sequencing and array-CGH studies provide?a genome-level view of complex genomic CH5424802 aberrations that occur?in tumorigenesis (Velculescu, 2008). These studies have revealed a diversity of genetic changes that likely account for some of the clinical heterogeneity seen in pathologically similar tumors. Analyses of larger numbers of patient samples have also uncovered common and recurrent changes that may be considered as key drivers of malignant transformation (Chin and Gray, 2008). Notably, tumors often acquire complex genomic aberrations including gains and losses of large sections or even entire chromosomes. Identifying the target gene(s) from such complex genomic changes remains a significant challenge. RNA-interference (RNAi) technology has greatly facilitated loss-of-function studies in mammalian cells and even in animal models (Dickins et?al.