Abstract
Tumor-microenvironment (TME) interactions are among the main causes of drug resistance, may be mediated by soluble factors or direct cell-to-cell interactions, and are profoundly modulated by the mutational landscape of the cancer cells. In colorectal cancer (CRC), interactions between cancer cells and TME may modulate sensitivity or resistance to molecularly targeted treatments even in the presence of strong mutational drivers (e.g. BRAF mutations). While PTEN-loss has an established role as a negative prognostic factor in CRC, a detailed understanding of its function and role in determining sensitivity/resistance to inhibitors of the PI3K/mTOR pathway is currently lacking.
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