Professor Giorgio Stassi MD started his research activity in 1989 as researcher with the Laboratory of Immunological medicine at the Institute of Clinical Medicine of the University of Palermo. In 1997 he started work at the Rangos Research Center (PA) USA, under the supervision of Prof. Trucco and working on the pathogenesis of Diabetes Mellitus. He returns to Italy in 2000 and thanks to a AIRC financing, was able to create a Laboratory of Cellular and Molecular Biology at the Department of experimental Medicine at the University of Palermo.

In 2002 he takes position as Head of the Cellular and Molecular Pathophysiology Laboratory at the Department ofgiorgio_stassi4 Surgical and Oncological Sciences of the University of Palermo. In the last years his scientific interest has been focused on the study of the role that cancer stem cells have in the onset and the progression in different tumors of epithelial origin such as colon, breast and thyroid tumors.

Recently, Stassi and his collaborators published a series of articles on top journals such as Cell Stem Cell and Nature in which he clarified one of the main mechanisms in regard to the resistance to chemotherapy of the cancer stem cells of the colon and proposing a new strategy for the cure of these tumors.

He has brought mechanisms to light that regulate epithelial tumor cells’ s
urvival and resistance to conventional therapy. These results have significantly contributed to cancer research, allowing him to issue a patent that enables the development of innovative cancer therapies. 

He was appointed one of the first to isolate stem cells from colon and thyroid tumors. The advanced development of this system has ulteriorly confirmed its innovative contribution to cancer research leading to attractive discoveries, which have paved the way to designing new “tailored” and more effective anti-cancer strategies.

stassi_giorgio3Recently, he identified CD44v6 as a colon cancer stem cells (CSCs) marker required for the metastatic potential of CSCs. Moreover, he has established that the tumor niche reprograms CD44v6- CRC progenitors in metastatic CD44v6+ stem cells concluding that CD44v6 is an independent negative prognostic marker. 

He determined that CD44v6 cells are dependent upon the activation of the PI3K/AKT pathway. PI3K promotes the expression of CD44v6 in colorectal cancer progenitors, while its inhibition impairs migration and survival of CD44v6+ CRC cells. On the bases of these results, a clinical trial with available drugs that target the PI3K pathway, has been designed for CRC patients.

Career ultima modifica: 2015-10-09T12:37:00+00:00 da admin