Loss-of-function screening identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway and revealed that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two critical barriers that prevent oncogenic transformation.

The protein IFI6 regulates DNA replication via the transcription factor E2F2, which is necessary for transformation and growth of melanomas induced by the NRASQ61K mutant oncogene product.

ST recruitment of STRIPAK facilitates PP2A-mediated dephosphorylation of MAP4K4 and induces cell transformation highlighting that STRIPAK complex plays a key role in defining PP2A specificity and activity.

Transformation mediated by oncogenic BRAF requires transcriptional activation of TWIST at the earliest stage of neoplastic transformation.

Cancer-associated changes in small nucleolar RNAs and site-specific pseudouridine modifications impact ribosome activity.

Sequentially expressed temporal transcription factors in neural stem cells during early development determine which progeny can undergo malignant transformation upon dedifferentiation.

Myc expression is shown to cause sublethal activation of Caspase-3 and downstream endonuclease G, which causes DNA double strand breaks and oncogenic transformation in human cells.

Overexpression of PLK1 triggers oncogenic transformation and transcriptional reprogramming of prostate epithelial cells, which stimulates cell migration and invasion.

By regulating acinar cell differentiation, the transcription factor PTF1A acts as a novel class of tumor suppressor in pancreatic cancer.

The study of a recurrent breast cancer MAGI3 truncation reveals the role of MAGI3 in regulating the Hippo effector YAP and highlights premature mRNA cleavage and polyadenylation as a mechanism underlying cancer development.