The development of Drosophila somatosensory neurons is spared under nutrient deficiency so that they grow more dendrites and make animals more sensitive to environmental stimuli.

The combination of ceritinib with CGM097 demonstrates remarkable antitumor activity in TP53 wild-type neuroblastoma models with ALK aberrations and is able to overcome the resistance acquired during ceritinib treatment.

Deletion of the ATM cofactor ATMIN reduces PDGFRA expression and strongly suppresses tumorigenesis in a TP53-deficient mouse model of glioblastoma.

The secreted molecules FAM150A and FAM150B bind to the ALK RTK extracellular domain, potently activating the receptor activation and driving downstream signaling events.

Nutrient limitation elicits differential responses in cells lacking the tumor suppressor PTEN and in normal cells, resulting in hyperplastic overgrowth of PTEN mutant tissue independent of additional mutations.