Parallels between oncogene-induced cardiac neoplasia and heart regeneration in zebrafish

We used a cardiac-specific tamoxifen-dependent Gal4-ERT2/UAS model to achieve uniform but conditionally regulated expression of the oncogene HRASG12V in zebrafish cardiomyocytes. We found that the inhibition of TOR signaling using rapamycin treatment counteracts neoplasic growth. We analyse the transcriptome of neoplasic ventricles after exposure to DMSO and rapamycin and we applied bioinformatic analysis to determine common and distinctive molecular signatures of neoplasia versus regeneration of the heart. Overall design: Adult zebrafish ventricles of regenerating and neoplasic hearts were isolated for RNA-sequencing