10/01/20

Hizlaria / Ponente: Laura Gómez-Cuadrado – PhD student at Cancer Research UK Edinburgh Centre, UK. Cancer Therapeutics lab. Supervisor: Professor Val Brunton

Data / Fecha: 2020ko urtarrilak 10 / 10 de enero de 2020.
Ordua / Hora:  13:30-14:30.
Lekua / LugarBiodonostia OIIko OIIko Formakuntza Aretoan, 3.Solairua. / IIS Biodonostia, Sala de Formación, Planta 3.

Laburpena / Resumen:
Invasive Lobular Carcinoma (ILC) is the second most common histological subtype of breast cancer, after Invasive Ductal Carcinoma (IDC), which account for 10-15% and 80% of diagnosed breast cancers, respectively. ILC has an unusual pattern of metastatic dissemination, spreading to distinct sites such as the gastro-intestinal tract, peritoneum and ovary. Despite prognosis and survival rates being originally favourable, patients with lobular histology appear to have a worse survival in multivariate analysis after a prolonged follow-up.

There is strong evidence supporting the importance of the Tumour Microenvironment (TME) in influencing tumour progression, metastatic spread and therapeutic response. However, little is known about the molecular mechanisms by which the TME influences the behaviour of ILC. We hypothesise that the interaction of ILC with the TME is critical for driving a disease distinct from IDC. As previous studies have been performed in whole ILC tissue samples, it would be more meaningful to isolate the tumour from the surrounding stroma. In order to better understand how the TME may drive the unique features of ILC, we have performed gene expression microarray analysis of primary cultured Cancer Associated Fibroblasts (CAFs) and Laser Capture Microdissected (LCM)- Tumour Epithelium (TE) and Tumour Stroma (TS) from 23 primary ILC patients. Two-class-paired Rank Products analysis identified 1,082 genes increased in the TS of ILC compared to TE. These data have been compared to existing LCM-separated datasets of normal and IDC, and have revealed a set of genes that are increased specifically in the tumour microenvironment of ILC. Mechanistic studies of these candidate genes will help us to elucidate how changes in the TME affect ILC progression, metastasis, and response to therapy.