Dr. Giovannino Silvestri, Ph.D - Marlene and Stewart Greenebaum Comprehensive Cancer Center University of Maryland School of Medicine - Research Associate

Dr. Giovannino Silvestri

Ph.D

Marlene and Stewart Greenebaum Comprehensive Cancer Center University of Maryland School of Medicine

Research Associate

Baltimore, Maryland | United States

Main Specialties: Biology, Blood Banking - Transfusion Medicine, Hematology, Hematology & Oncology, Oncology

Additional Specialties: Chronic Myelogenous Leukemia

ORCID logohttps://orcid.org/0000-0001-5911-6997


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Dr. Giovannino Silvestri, Ph.D - Marlene and Stewart Greenebaum Comprehensive Cancer Center University of Maryland School of Medicine - Research Associate

Dr. Giovannino Silvestri

Ph.D

Introduction

Dr. Giovannino Silvestrireceived his M.S. in Pathology and Molecular Biology (Summa cum laude) from the University of Calabria in 2009, Italy. In 2013, he earned his Ph.D. in Molecular and Cellular Biology and Pathology from the University of Verona, Italy, working in Dr. Sorio’s laboratory on assessing the role of the Protein Tyrosine Phosphatase Receptor Gamma (PTPRG) in Chronic Myelogenous Leukemia (CML). Dr. Silvestri's research has been dealing with malignant hematology since 2009. His interest has been focused for the past ten years on understanding the molecular mechanisms responsible for the emergence, maintenance and progression of leukemias in particular on CML. In 2013, he joined Prof. Perrotti’s laboratory at University of Maryland Baltimore (UMB), Marlene and Stewart Greenebaum Comprehensive Cancer Center, Baltimore MD, USA where he is studying the role of miRNAs in the cross-talk between leukemic stem, stromal and immune cells. Dr. Silvestri has broad background in the molecular biology of cancer with specific training in chronic myelogenous leukemia (CML) research. During the few years spent in the USA, he has focused his efforts in identifying novel mechanisms of stemness in CML. Currently, Dr. Silvestri’s research interest is on the role of non-coding RNAs as regulators of normal and leukemic stem and progenitor cell function and to develop new therapeutic drugs that will improve outcome of CML patients resistant to tyrosine kinase inhibitor-based therapies and eradicate the disease at stem cell level.

Primary Affiliation: Marlene and Stewart Greenebaum Comprehensive Cancer Center University of Maryland School of Medicine - Baltimore, Maryland , United States

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Experience

Publications

11Publications

384Reads

14Profile Views

7PubMed Central Citations

Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.

Curr Drug Targets 2017 ;18(4):377-388

Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD 21201, United States.

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http://dx.doi.org/10.2174/1389450117666160615074120DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5970649PMC
September 2017
30 Reads
1 Citation
3.021 Impact Factor

Unsupervised explorative data analysis of normal human leukocytes and BCR/ABL positive leukemic cells mid-infrared spectra.

Analyst 2015 Jul;140(13):4407-22

Azienda Ospedaliera Universitaria Intergrata di Verona, Department of Pathology and Diagnostics - Unit of Immunology, Policinico G. Rossi, P.le L.A. Scuro 10, I-37134 Verona, Italy.

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http://dx.doi.org/10.1039/c5an00148jDOI Listing
July 2015
3 Reads
1 Citation
4.110 Impact Factor

Rapid recognition of drug-resistance/sensitivity in leukemic cells by Fourier transform infrared microspectroscopy and unsupervised hierarchical cluster analysis.

Analyst 2013 Jul;138(14):3934-45

Azienda Ospedaliera Universitaria Integrata Verona, Department of Pathology and Diagnostics - Unit of Immunology, Policlinico G. Rossi, P.le L.A. Scuro, 10, I-37134, Verona, Italy.

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http://dx.doi.org/10.1039/c2an36393cDOI Listing
July 2013
13 Reads
2 Citations
4.110 Impact Factor

Chronic Myelogenous Leukemia (CML): Current Research Focus

ESH EDUCATION BOOK

The use of imatinib mesylate, second and third generation Abl tyrosine kinase inhibitors (TKI) (i.e. dasatinib, nilotinib, bosutinib and ponatinib) made CML a clinically manageable and, in a small percentage of cases, a cured disease. TKI therapy also turned CML blastic transformation into a rare event; however, disease progression still occurs in those patients who are refractory, not compliant with TKI therapy or develop resistance to multiple TKIs. In the past few years, it became clear that the BCR-ABL1 oncogene does not operate alone to drive disease emergence, maintenance and progression. Indeed, it seems that bone marrow (BM) microenvironment-generated signals and cell autonomous BCR-ABL kinase-independent genetic and epigenetic alterations all contribute to i. persistence of a quiescent leukemic stem cell (LSC) reservoir, ii. innate or acquired resistance to TKIs, and iii. progression into the fatal blast crisis stage. Herein, we review the intricate leukemic network in which aberrant, but finely tuned, survival, mitogenic and self-renewal signals are generated by leukemic progenitors, stromal cells, immune cells and metabolic microenvironmental conditions (e.g. hypoxia) to promote LSC maintenance and blastic transformation.

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9 Reads