Growth and Tracheogenesis are Separable Traits in Drosophila Cancers

Drosophila clonal cancer models provide an excellent contribution to the study of the molecular basis of tumourigenesis. A number of human cancer hallmarks are indeed functionally conserved; among them, overgrowth and vessel remodelling are particularly relevant to primary mass formation and cell dissemination throughout the organism. We have previously identified MYC as a Hippo downstream target in Drosophila and demonstrated that cells with defects in polarity genes require MYC expression to overwhelm wild-type neighbours and develop into malignant masses. Recent data from our lab also showed that neo-tracheogenesis does occur in Drosophila cancers, and it is either functionally or molecularly analogous to mammalian tumour neo-angiogenesis. Here I extended on previous work showing that, in Drosophila epithelial tumours, mass expansion and tracheogenesis are separable traits, dependent on MYC and FOS activity respectively. These two transcription factors are found at the intersection of the Hippo, JNK and Ras/MAPK signalling cascades, which are recognised as central actors in cancer progression.