Complex interplay between oncogenic pathways. Changes in tumor malignancy from hyperplasia to metastatic cancer result from the accumulation of numerous alterations of normal cellular functions. Cell polarity, cell proliferation and apoptosis are key targets of neoplastic mutations. Proteins such as Scribble, aPKC or JNK (see text) can simultaneously participate in several signaling pathways (dotted arrows) controlling these different cell functions. Consequently, changes in their activity are likely to have dramatic effects on tumor progression. In the case of Scribble, mutations lead to loss of cell polarity, to increased cell proliferation and to the induction of pro-apoptotic pathways via a subset of these intertwined signaling cascades (highlighted in red).