Amelia D'Alessio

TL;DR: A large-scale characterization of the cancer genome might offer personalized cancer genomic information, which may improve the anti-tumor efficacy of signalling inhibitors.

TL;DR: Clinical trials failed to attend the promising expectations deriving from preclinical studies with anti-VEGF agents, and potential strategies might be the employment of combinatory therapies with immune checkpoint inhibitors or agents that inhibit signaling pathways and proangiogenic factors activated in response to V EGF blockade, and the identification of novel targets in the VEGF cascade.

TL;DR: It is found that both MEK/MAPK and the PI3K/AKT signaling pathways mediate the ability of TGF‐α to induce secretion of angiogenic factors in MSCs.

TL;DR: Overexpression of a constitutively activated form of p42-MAPK in SK-Br-3 cells resulted in an approximately 50% increase in the IC50 to gefitinib, and culture of ZD10 resistant cells in absence of gef itinib led to reversion of the resistant phenotype, suggesting that MAPK signaling might play a role in the resistance that develops in breast cancer cells after long-term exposure to gfitin ib.

TL;DR: The results demonstrate that breast cancer cells with acquired resistance to lapatinib have a more aggressive phenotype compared with their parental counterpart, and that Src signaling and CXCR4 play an important role in this phenomenon, thus representing potential targets for therapeutic intervention in lapatinIB-resistant breast cancer patients.