Proffered Paper - Basic Science

LINK to Proffered Paper - Basic Science

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1O - A study of cancer dissemination from metastatic intermediates of hypermethylated colorectal patients reveals a new mode of collective migration

The abstract concludes: By studying primary cancer specimens and cell lines from colorectal cancer, we demonstrate the existence of a second mode of collective migration, presenting the hallmarks of amoeboid migration, that we named collective amoeboid. This mode could be use by other cancer clusters when confronted to non-adhesive interfaces like the lumen of lymphatic vessels. This work suggests that therapies targeting adhesive properties of cancer cells might be unsuccessful and unravels a new therapeutic avenue to limit the metastatic spread of CRCs.


1977O - Functional inactivation of E-cadherin drives EMT-less metastasis

The abstract concludes: We identify functional inactivation of E-cadherin by Trop-2 as a pivotal driver of EMT-less metastatic diffusion in human cancer. This global, Trop-2/E-cadherin/b-catenin–driven pro-metastatic program profoundly impacts on the survival of patients bearing breast, colon, uterus, ovary, stomach, lung, pancreas tumours, paving the way for novel diagnostic procedures and anti-cancer therapies.


2O - Growth differentiation factor 15 (GDF-15) neutralization reverses cancer cachexia, restores physical performance and mitigates emesis associated with platinum-based chemotherapy

The abstract concludes: Our findings indicate GDF-15 is a key regulator of cancer cachexia and chemotherapy-induced malaise. GDF-15 inhibition holds the potential as an effective therapeutic approach in combination with chemotherapy to alleviate GDF-15 mediated malaise, declined physical function and cachexia in patients.


3O - Efficacy of the triple combination of Estrogen Receptor, CDK4/6 and PI3K pathway inhibitors in ex-vivo models of breast cancer

The abstract concludes: The results showed an encouraging activity of the triple combination of ER, CDK4/6, and PI3K pathway inhibitors in ex vivo models of ER-positive BC. The different effect of the treatments could suggest a correlation between mutation setting and individual response.