Daniele Baiz received his MSc in Molecular Biology (2004) and a PhD in Cancer Cell Biology (2009) from the University of Trieste (Italy), where he started challenging the areas of Cancer Biology and Cell Signalling by working on a model of hepatocellular carcinoma. He moved to the United States in 2010 as postdoctoral fellow (Wake Forest School of Medicine, NC) where, under the supervision of Dr G. Kulik, he pioneered a preclinical study for castration-resistant prostate cancer, by developing and combining the first prostate cancer-targeted PI3K inhibitor prodrug (in collaboration with Dr. M. Welker and Dr. Salisbury, WFU) and the first PSMA-targeted immunotoxin (in collaboration with Dr. W. Debinski, BTCOE). In 2012 he was awarded with a T32 training grant from the NIH/NCI by which he continued working on projects on prostate cancer and started exploring how glioblastoma (a devastating brain tumour with poor diagnosis) may receive benefits from the tumour microenvironment. At the end of 2013, supported by a postdoctoral fellowship from the International Centre for Genetic Engineering and Biotechnology, he joined the Molecular Haematology Group (ICGEB, Rome - Italy), where he continue studying abnormal cancer signalling pathways in CLL and B-cell lymphomas, acquiring a strong interest on studying miRNA signatures as potential biomarkers. At the end of 2014, he moved to the Plymouth University where he joined the team of Prof. O. Hanemann as Research Fellow. Dr. Baiz is a member of the AACR, EACR, AAAS/Science, Biochemical Society and reviewer for several international journals.
Brief description of reserach project
This project in the area of stratified medicine is aiming to discover new diagnostic/prognostic meningioma signatures to correlate the established pathological grade of the tumour, residual tumour and early recurrence with the selected biomarkers.
We identified a potential meningioma signature that may accelerate diagnosis of meningioma patients. In particular, gene expression analysis on blood serum exosomes showed increased expression of STAT1 in meningioma patients when compared to healthy controls, in line with our previous results that revealed STAT1 protein constitutively over-expressed in all meningioma grades and playing a pivotal role in its growth (Ferluga S. et al, manuscript in preparation). In addition, the paralleled development of a cancer microRNA profiling in meningioma cells suggested that microRNA signatures, differentially expressed within grades (especially WHO I versus III), might represent prognostic biomarkers. We identified two miRNAs (belonging to signalling pathways controlling cell growth, differentiation and apoptosis) differentially de-regulated in meningioma samples that might represent a diagnostic/prognostic signature to identify tumour progression.
In summary, we have preliminary data that might support early diagnosis and prognosis. Their correlation with clinical data will represent a robust advancement of personalised and stratified medicine for meningioma patients.