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Giulia Trimaglio

Biography

I was born on July 21st 1991 in Cuneo (CN), Italy.

 

In July 2013, I received my Bachelor degree in Biological Sciences at the University of Torino, Italy.

During my BSc thesis, I studied the role of the adaptor protein p140Cap in different physiological and pathological contexts (neurons, neuroblastoma and breast cancer) under the supervision of Prof. Paola Defilippi (MBC-Molecular Biotechnology Center, Torino, Italy).

 

In October 2015, I received my Master degree in Cellular and Molecular Biology (University of Torino, Italy). My Master thesis was performed half at the University of Torino (Italy) and half at the Inserm (Université de Lille 1, France) under the supervision of Prof. Alessadra Fiorio Pla and Prof. Dimitra Gkika. The aim of my research was to investigate the functional role of TRP channels in prostate tumor-derived endothelial cells.

 

In March 2016, I started my PhD studies in the Neyrolles lab at the IPBS, Toulouse, France. My PhD project is supervised by Dr. Yoann Rombouts and is part of the European Innovative Training Network (ITN) “GlyCoCan” whose aim is to expand the knowledge on the structure-function relationship of glycosylation in colorectal cancer (CRC) for finding improved diagnostic and prognostic biomarkers and pave the way for novel therapeutic targets. In this context, my thesis project aims at studying the impact of immune lectins and cancer glycosignature(s) involved in the development of colorectal cancer.

 

Research Project

Colorectal cancer (CRC) is a major health burden being the third and second most common cancer in men and women respectively and accounting for 1.4 million cases and 694,000 deaths world-wide in 2012. In addition to the quality-of-life consequences and the severe prognosis it has also reached elevated health care costs and therefore there is a strong need for new diagnostic and prognostic biomarkers as well as an improvement of the current treatments. Cancers develop in complex tissue microenvironments, mainly composed of stromal, endothelial and immune cells, which they depend upon for sustained growth, invasion and metastasis. In this context, the complex interaction existing between the tumor cells and the local immune response, resulting in a balance between tumor-promoting and tumor-controlling effects, is gaining a particular interest. Indeed, promising new treatments for CRC target tumors’ microenvironment immune subpopulations. Among the infiltrating immune cells, the innate immune cells, like tumor-associated macrophages (TAMs) and dendritic cells (DCs), have been described to heavily infiltrate the tumor. A well-known feature of DCs and TAMs is the secretion/membrane expression of multiple glycan binding receptors (lectins), especially C-type lectins, that are involved, among other receptors, in the recognition of tumor-associated antigens. Indeed, it is now well-known that aberrant glycosylation is an hallmark of malignant transformation/progression and that is exploitable by cancer cells, via interaction with lectin-expressing immune cells, to elude or modulate the immune response. In this context, we are interested in understanding if aberrant glycosylations of the CRC cells could interact with the innate immune lectins driving to a polarization of the immune system towards an immune-suppressive phenotype.