Dr Daniele Baiz
Profiles

Dr Daniele Baiz

Marie Curie Fellow

Biomedical Research - Institute of Translational & Stratified Medicine (Plymouth University Peninsula Schools of Medicine and De

Role

Marie Curie Cascade Fellow

Qualifications

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 United States in 2010 as postdoctoral fellow (Wake Forest School of Medicine, NC) joining a preclinical study in a model of castration-resistant prostate cancer, using the first prostate cancer-targeted PI3K inhibitor prodrug and the first PSMA-targeted immunotoxin. 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 with a postdoctoral fellowship from the International Centre for Genetic Engineering and Biotechnology, he joined the Molecular Haematology Group, 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.

Professional membership

2014 – present: American Association for the Advancement of Science; 2014 – present: European Association for Cancer Research, UK; 2013 – present: Biochemical Society, UK; 2010 – present: American Association for Cancer Research, US

Roles on external bodies

2014 – present: Kidscan Children’s Cancer Research Charity (Scientific Committee). University of Salford, Manchester, http://www.kidscan.org.uk/

Teaching interests

Cancer Biology, Molecular and Cellular Biology, Cancer Signalling Networks, Translational Research.

Research interests

The discovery of circulating biomarkers to provide early diagnosis represents an urgent priority for brain tumor research. In fact, at the time in which they cause symptoms they are can be difficult to treat due to the location or size, resulting in their relapse eventually becoming an incurable disease. MicroRNAs are a large class of small RNAs forming a signaling network called “miRNome”, regulating the gene expression at the post-transcriptional level and playing an important role in many physiological and pathological processes including cancer. Many studies suggest that exosomes, micro-vesicles secreted by cells (including cancer cells) and circulating in the blood and body fluids, transport proteins and nucleic acids, including miRNAs. Currently, I am applying my expertise in proteomics and in gene expression analysis to discover novel diagnostic and/or prognostic biomarkers in common brain tumors (meningiomas) based on circulating proteins and miRNA signatures, to facilitate early diagnosis, recurrence and/or prediction to a higher grade tumor.

Grants & contracts

29/03/2016 – present: FP7 Marie Curie Actions (PCOFUND-GA-2012600181, £ 101391/year. “The CASCADE International Fellowship Program”, University of Plymouth & Nottingham), UK (http://www.cascade-fellows.eu/daniele-baiz). 12/01/2013 – 11/30/2014: “The Arturo Falaschi” ICGEB Fellowship Programmes (€ 24000/year). Postdoctoral Training Fellowship in Molecular Hematology, International Centre for Genetic Engineering and Biotechnology, Trieste, IT. 12/01/2012 – 11/30/2013: NIH/NCI 5T32CA079448 ($ 46092/year), “Ruth L. Kirschstein” National Research Service Award. Postdoctoral Training Fellowship in Cancer Biology, Wake Forest School of Medicine, Department of Cancer Biology, NC, USA. 01/1/2006 – 31/12/2009: PhD Fellowship in Biomolecular Sciences, XXIº Cycle (€ 31200/3 years), University of Trieste, Department of Life Sciences, Trieste, IT.

Peer-reviewed publications: Farra R*, Dapas B*, Baiz D, Tonon F, Chiaretti S, Del Sal G, Rustighi A, Elvassore N, Pozzato G, Grassi M and Grassi G.“The down-modulation of the Pin-1/E2F-1 axis accounts for the anti-proliferative effect of Bortezomib in hepatocellular carcinoma cells” Biochimie, 2015 May;112:85-95 (*These authors contributed equally). Baiz D, Dapas B, Farra R, Scaggiante B, Pozzato G, Zanconati F, Fiotti N, Consoloni L, Chiaretti S and Grassi G. “Bortezomib effect on E2Fs and related genes in hepatocellular carcinoma cell lines”World J Gastroenterol. 2014 Jan 21;20(3):795-803. Baiz D, Hassan S, Choi Y A, Flores A, Karpova Y, Yancey D, Pullikuth A, Sui G, Sadelain M, Debinski W and Kulik G. “Combination of the PI3K inhibitor ZSTK474 with a PSMA-targeted immunotoxin accelerates apoptosis and regression of prostate cancer” Neoplasia. 2013 Oct; 15(10):1172-83. Yancey D*, Nelson KC*, Baiz D, Hassan S, Flores A, Pullikuth A, Karpova Y, Axanova L, Moore V, Sui G and Kulik G. “BAD dephosphorylation and decreased expression of MCL-1 induce rapid apoptosis in prostate cancer cells”. PLoS One. 2013 Sep 5; 8(9):e74561 (*These authors contributed equally). Hassan S, Karpova Y, Baiz D, Yancey D, Pullikuth A, Flores A, Register T, Cline JM, D’Agostino R Jr, Danial N, Datta SR and Kulik G. “Behavioral stress accelerates prostate cancer development in mice”. J Clinical Invest. 2013, Feb. 1; 123(2):874-86 (Featured on FORBES Magazine, 1/29/2013). Baiz D, Pinder TA, Hassan S, Karpova Y, Salsbury F, Welker ME and Kulik G.“Synthesis and characterization of a novel prostate cancer-targeted Phosphatidylinositol-3-kinase inhibitor prodrug”. J Med Chem 2012, Sept. 27; 55(18):8038-46 (Cover of JMC). Baiz D, Pozzato G, Dapas B, Farra R, Scaggiante B, Grassi M, Uxa L, Giansante C, Guarnieri G and Grassi G. “Bortezomib arrests the proliferation of hepatocellular carcinoma cells HepG2 and JHH6 by differentially affecting E2F1, p21,and p27 levels” Biochimie 2009, Mar; 91(3):373-82. Grassi G, Scaggiante B, Farra R, Dapas B, Agostini F, Baiz D, Rosso N and Tiribelli C. “The expression levels of the translational factors eEF1A 1/2 correlate with cell growth but not apoptosis in hepatocellular carcinoma cell lines with different differentiation grade” Biochimie 2007, Dec; 89(12):1544-52. Book Chapters and Reviews: Grassi M, Cavallaro G, Scirè S, Scaggiante B, Dapas B, Farra R, Baiz D, Giansante C, Guarnieri G,Perin D, and Grassi G “Current strategies to improve the efficacy and the delivery of nucleic acid based drugs” Current Signal Transduction Therapy 2010, 5(2):92-120. Scaggiante B, Dapas B, Farra R, Baiz D and Grassi G “Antisense, siRNA, ribozyme and aptamer oligonucleotides as molecular tools for the control of cell proliferation in the prospective of supporting therapies” Handbook of cell proliferation. Pages 107-149. Nova Science Publishers (2009). Published Abstracts: Baiz D, Pozzato G, Farra R, Dapas B, Scaggiante B, Guarnieri G, and Grassi G “Potential application of proteasome inhibitor bortezomib for treatment of hepatocellular carcinoma”. Hepatology International (2008). Volume 2: supplement 2, page S69. Farra R, Dapas B, Baiz D, Pozzato G, Scaggiante B, Guarnieri G, and Grassi G. “siRNAs targeted against cyclin E1, cyclin E2 and E2F1 downregulate te growth of hepatocellular carcinoma showing their potential use on the prevention of this type of tumor” Hepatology International (2008). Volume 2: supplement 2, page S108

Reports & invited lectures

Invited Lectures and Presentations: (June 13, 2013) Wake Forest School of Medicine, Dept. of Cancer Biology, Winston-Salem, NC, USA. External Advisory Committee Review. “Development of strategic targeted therapies against abnormal cancer signaling”. (October 16, 2012)Wake Forest School of Medicine, Dept. of Cancer Biology, Winston-Salem, NC, USA. “Combination of the PI3K inhibitor ZSTK474 with a PSMA-targeted cytotoxin promotes apoptosis and regression of PTEN-deficient prostate cancer”. (April 2, 2012)103rd AACR Annual Meeting. Chicago, IL. “Prostate-specific inhibition of PI3 Kinase and protein synthesis as a therapy for hormone-refractory prostate cancer”. (April 3, 2011)102nd AACR Annual Meeting. Orlando, FL. “Loss of Bad phosphorylation and Mcl-1 expression is necessary for rapid apoptosis induced by combination of TGFα-PE and ZSTK474 in prostate cancer cells”. (January 14, 2009)Invited speaker: Eberhard Karls Universität Tübingen, Dept. of Molecular Pathology, Tübingen, Germany “Bortezomib arrests the proliferation of hepatocellular carcinoma cells HepG2 and JHH6 by differentially affecting E2F1, p21,and p27 levels”.(June 24, 2008) Invited speaker: The Young Scientist Marathon 2008-University of Trieste, School of Medicine and Surgery-Merck-Serono, Italy. “Potential application of proteasome inhibitor bortezomib for treatment of hepatocellular carcinoma”. (June 13, 2008) EASL Monothematic Conference – Liver Cancer: from molecular pathogenesis to new therapies. Prague, Czech Republic “Potential application of proteasome inhibitor bortezomib for treatment of hepatocellular carcinoma”. Conference Proceedings: Lyons Rimmer J, Zhou L, Baiz D, Ercolano E, and Hanemann CO “Elucidating the roles and regulation of nuclear KSR1 in Merlin-deficient low grade brain tumour growth”. (FEBS Advanced Lecture Course/co-founded EACR, “Molecular mechanisms of signal transduction and cancer”, Spetses-Greece, August 16-24, 2015). Baiz D, Choi YA, Karpova Y, Yancey D, Hassan S, Sadelain M, Debinski W, and Kulik G “Prostate-specific inhibition of PI3 Kinase and protein synthesis as a therapy for hormone-refractory prostate cancer”. (American Association for Cancer Research, 103rd Annual Meeting. Chicago, IL, March 31-April 4, 2012). Baiz D, Choi Y, Baurin V, Karpova Y, Yancey D, Hassan S, Gibo D, Debinski W, and Kulik G. “Loss of Bad phosphorylation and Mcl-1 expression is necessary for rapid apoptosis induced by combination of TGFα-PE and ZSTK474 in prostate cancer cells”. (American Association for Cancer Research, 102nd Annual Meeting. Orlando, FL, April 2-6, 2011). Baiz D, Farra R, Scaggiante B, Dapas B, Pozzato G, Consoloni L, Giansante C, Fiotti N, Altamura N, Guarnieri G, and Grassi G “Evaluation of Bortezomib impact on cell-cycle related genes in the hepatocellular carcinoma cell lines HepG2 and JHH6 by means of microarray analysis” (EASL Special Conference on Hepatocellular Carcinoma: from Genomics to Treatments. Dubrovnik, Croatia, June 25-26, 2010). Baiz D, Pozzato G, Farra R, Dapas B, Scaggiante B, Guarnieri G, and Grassi G. “Potential application of proteasome inhibitor bortezomib for treatment of hepatocellular carcinoma” (EASL Monothematic Conference – Liver Cancer: from molecular pathogenesis to new therapies. Prague, Czech Republic, June 12-14, 2008). Baiz D, Pozzato G, Farra R, Dapas B, Scaggiante B, Guarnieri G, and Grassi G “Potential application of proteasome inhibitor bortezomib for treatment of hepatocellular carcinoma” (International Liver Congress. Hong Kong, Shanghai, June 12-15, 2008). Farra R, Dapas B, Baiz D, Pozzato G, Scaggiante B, Guarnieri G, and Grassi G “siRNAs targeted against cyclin E1, cyclin E2 and E2F1 downregulate te growth of hepatocellular carcinoma showing their potential use on the prevention of this type of tumor”. (International Liver Congress. Hong Kong, Shanghai, June 12-15, 2008). Farra R, Pozzato G, Dapas B, Baiz D, Scaggiante B, Guarnieri G, and Grassi G. “SFR depletion by siRNA reduces hepatocellular carcinoma cell proliferation, showing its involvement in the biology of this type of tumor”. (Ireland Society of Gene and Cell Therapy Conference. Galway, Ireland, May 18, 2007)

Other academic activities

I am involved in the Plymouth University Research In Action program (SSU 008), where I am responsible for the Special Study Unit theme "Targeting signalling pathways in low-grade brain tumours". I am also involved in the supervision and training of PhD students joining our research team.

Links

See: http://www.cascade-fellows.eu/daniele-baiz and https://www1.plymouth.ac.uk/research/crtb/Pages/postdocs.aspx