Inhibition of microRNA-203 by oncogenic HRas mutations promotes skin cancer initiation.

NFATc2 maintains the drug-induced TIC phenotypes through trans-activating SOX2/ALDH1A1 expression and scavenging stress from ROS.

DNA-PK and PTEN protect breast cancer cells from lethal replication stress induced by the WEE1 inhibitor AZD1775 and constitute new potential biomarkers for AZD1775 sensitivity.

Pre-neoplastic cells in the brain release SDF1, which mediates an immediate infiltration of macrophages that differentiate into microglia-like cells and promote proliferation of pre-neoplastic cells.

The earliest steps of tumor initiation in the cerebellum are regulated by critical interactions between pre-tumor cells and stromal cells, which can be manipulated by targeting the Norrin/Frizzled4 signaling axis.

Analyses of genetically engineered mouse models reveal the androgen receptor-independent properties of a luminal stem/progenitor cell in the prostate epithelium, and its ability to serve as a cell of origin for castration-resistant prostate cancer.

Mutational inactivation of the JNK signaling pathway causes genomic instability and breast cancer development.

The Rho kinases ROCK1 and 2 act redundantly in regulating cell proliferation and their depletion causes cellular senescence.

Aberrant phosphorylation of tyrosine 78 on Atoh1 via Jak2 is responsible for sonic hedgehog type medulloblastoma growths in vivo.

The presented primary epithelial acinus-based platform for studying interactions between normal and malignant cells will enable in depth analysis of the tumor initiation process on a molecular level.