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Giovannino Silvestri, PhD

Academic Title:

Research Associate

Primary Appointment:

Medicine

Additional Title:

Research Associate at Institute of Human Virology

Location:

Institute of Human Virology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, Laboratory of Stem Cell & Cancer Biology

Phone (Primary):

tel:410-706-6168

Education and Training

2003-2006, B.S., Biology, University of Calabria, Italy.             

2006-2009, M.S., Biology, University of Calabria, Italy (Magna cum Laude).   

2010-2013, Ph.D.,Molecular and Cellular Biology and Pathology, University of Verona, Italy. Thesis Advisor – Dr. Claudio Sorio.“Biochemical and functional characterization of the oncosuppressor gene Protein Tyrosine Phosphatase Receptor Gamma in Chronic  Myelogenous Leukemia”.

2013-2018, Post-Doctoral Fellow, Program in Oncology, University of Maryland, Greenebaum CCC, Baltimore, USA.

2018-2018, Research Associate, Program in Oncology, University of Maryland, Greenebaum CCC, Baltimore, USA.

2019- Present, Research Associate, Institute of Human Virology, University of Maryland, Baltimore, USA.

Biosketch

Dr. Giovannino Silvestri received 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  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.

 

Research/Clinical Keywords

Hematology Malignancies, Chronic Myeloid Leukemia, Ph+ALL, Tumor Microenvironment, MicroRNAs, Non-long coding RNAs, Signal Transduction, mouse models.

Highlighted Publications

  1. Bellisola G., Cinque G., Vezzalini M., Moratti E., Silvestri G., Redealli S., Gambacorti Passerini C., Wehbe K., and C. Sorio. Rapid recognition of drug-resistance/sensitivity in leukemic cells by Fourier transform infrared microspectroscopy and unsupervised hierarchical cluster analysis, Analyst, 138:3934-3945, 2013.

  2. Bellisola G, Bolomini Vittori M, Cinque G, Dumas P, Fiorini Z, Laudanna C, Mirenda M, Sandt C, Silvestri G, Tomasello L, Vezzalini M, Wehbe K, Sorio C. Unsupervised explorative data analysis of normal human leukocytes and BCR/ABL positive leukemic cells mid-infrared spectra. Analyst,140:4407-22, 2015

  3. Perrotti D, Silvestri G, Stramucci L. Chronic Myelogenous Leukemia (CML): Current Research Focus. The Hematology Journal, 9:91-102, 2015.  

  4. Laidlaw K., Berhan S., Liu S, Silvestri G, Holyoake T, Frank D, Aggarwal B.B., Perrotti D., Jørgensen H., Arbiser J. Cooperation of imipramine blue and tyrosine kinase blockade demonstrates activity against chronic myeloid leukemia. Oncotarget, 7:51651, 2016.

  5. Perrotti D, Silvestri G, Stramucci L, Yu J, Trotta R. Cellular and Molecular Networks in Chronic Myeloid Leukemia: the leukemic stem, progenitor and stromal cell interplay. Current drug targets, 18:377-388, 2017.

  6. Srutova K, Curik N, Burda P, Savvulidi F, Silvestri G, Trotta R, Klamova H, Pecherkova P, Sovova Z, Koblihova J, Stopka T, Perrotti D and Machova Polakova K. BCR-ABL1 mediated miR-150 downregulation throught MYC contributed to myeloid differentiation block and resistance in chronic myeloid leukemia. Haematologica, 103(12):2016-2025. doi: 10.3324/haematol.2018.193086, 2018.

  7. G Silvestri, R Trotta, L Stramucci, JJ Ellis, JG Harb… -Persistence of Drug-Resistant Leukemic Stem Cells and Impaired NK Cell Immunity in CML Patients Depend on MIR300 Antiproliferative and PP2A-Activating Functions, Blood Cancer Discovery,, 2020.

  8.  Giuseppe Palma, Teresa Pasqua, Giovannino Silvestri, Carmine Rocca, Paola Gualtieri, Antonio Barbieri, Anna De Bartolo, Antonino De Lorenzo, Tommaso Angelone; Ennio Avolio;Gerardo Botti. PI3Kδ inhibition as a potential therapeutic target in COVID-19 . Frontiers in Immunology, section Vaccines and Molecular Therapeutics. ahead of print, 2020.

     

 

Awards and Affiliations

Memberships:

2014-present   Member, American Society of Hematology (ASH).

2015-present   Member, American Association for the Advancement of Science (AAAS).

2015-present   Member, The International CML Foundation (iCMLf)

2017-present   Associate Member, American Association for Cancer Research (AACR).

 

Honors and Awards:

2009, Best Graduate Award 2009, University of Calabria, Italy, awarded for distinguished  performance in biology.

2010-13, Ph.D. Student Fellowship, Italian Ministry of Health, University of Verona, Italy.

2012, 14th ESH-iCMLf Travel Award, Baltimore, USA.

2014, 16th ESH-iCMLf Travel Award, Philadelphia, USA.

2015, Award for Best poster presentation, University of Maryland, USA.

2015, American Society of Hematology Abstract achievement Award winner, Orlando, USA.  

2017, September Postdoc Appreciation Month, program in Oncology, University of Maryland, USA.

2018, Member Memory Board and Membership Testimonial, Selected from The American Association for Cancer Research (AACR), Chicago, USA.

In the News

Dr Silvestri  on March 11th, 2019 released an interview to an italian science magazine OGGIScienza.it that interviewed him to tell to the italian community the research he is performing in the United States of America.

https://oggiscienza.it/2019/03/11/leucemia-mieloide-cronica/

Translation is written below:

OGGISCIENZA.IT.           SEARCHING ABROAD

 Chronic myeloid leukemia, the research to destroy cancer stem cells.

Two directions of CML research: study drug-resistant cancer stem cells and develop new molecules to treat patients resistant to therapies. 

by Luisa Alessio

11 March 2019 at 7:00pm

 Chronic myeloid leukemia (CML) is a disorder of the hematopoiesis, the production process of blood cells, which develops in the bone marrow and is due to the transformation of the stem cells from which the blood cells originate. At the genetic level, CML is characterized by a reciprocal translocation between chromosome 9 and chromosome 22, an exchange of genetic material that gives rise to the Philadelphia chromosome and the BCR-ABL fusion gene.Chronic myeloid leukemia is diagnosed around the age of 50 and, although not curable, is a clinically manageable disease with chemotherapy drugs.

Giovannino Silvestriis an Italian researcher today at the University of Maryland School of Medicine, where he studies the molecular mechanisms underlying CML. The goal of his work is to provide new information for the development of drugs aimed at destroying cancer stem cells in patients' bone marrow.

Name: Giovannino Silvestri

Age: 34 years

Born in: Rende (CS), Italy.

I live in: Baltimore, United States.

Ph.D.: molecular and cellular biology and pathology, Verona, Italy.

Research: Approaches of stem cells biology at the Laboratory of Stem Cell & Cancer Biology, Institute of Human Virology, University of Maryland School of Medicine.

Interests: traveling, hike, running.

I like Baltimore for: the strong local identity, the retro charm, the inhabitants.

I don't like Baltimore for: it's very dangerous.

Thought: If you can dream it, you can do it. (Walt Disney).

 What are the limits of the drugs currently on the market?

The treatment of chronic myeloid leukemia consists in keeping the progression of the disease under control. CML, in fact, is characterized by three phases: the chronic phase can last for years and manifests itself with an abnormal production and accumulation in the blood of a particular type of white blood cells, the neutrophils; the accelerated phase occurs when the progenitor cells begin to proliferate in an uncontrolled manner both in the blood and in the bone marrow; the blast phase occurs after a few weeks or months and presents an excessive accumulation of blasts (large undifferentiated cells with pathological changes) in the blood and bone marrow.CML drugs work by "clearing" blood from blasts and preventing the evolution of the disease: at the molecular level, this occurs through the selective inhibition of tyrosine kinase enzymes, a class of proteins to which BCR-ABL belongs. The first inhibitor used for the treatment of chronic myeloid leukemia was Imatinib: its introduction has revolutionized the treatment of CML and has greatly improved the quality and life expectancy of patients. Unfortunately, the limit of these drugs lies in the fact that they work only in the peripheral blood and cannot reach the bone marrow, where the cancer stem cells reside from which the blasts originate. For this reason therapies are very effective in the chronic phase but insufficient in patients in accelerated and blast phase. The purpose of my research is to understand how cells work in this stem cell niche and to find a way to destroy them. CML therapy urgently needs new drugs because many patients develop resistance to current treatments, although is available today the fifth generation of tyrosine kinase inhibitors. 

What kind of molecular mechanisms are you studying?

Our laboratory deals with RNA, in particular with microRNAs (or miRNAs), that is small non-coding RNAs. We found that in CML there is a group of dysregulated miRNAs involved in the progression of the disease towards the blast phase and in the fate regulation of cancer stem cells (or CSC, cancer stem cell). In particular we focused on a miRNA whose expression drops dramatically in the chronic phase and almost completely disappears in the blast phase, because we wanted to understand what happens to the cells in case of its reactivation.At the level of myeloid progenitors, that is the most differentiated cells present in our blood, we have seen that this miRNA behaves as a tumor suppressor and its over-expression leads to the death of leukemic cells. Furthermore, when used in combination with Imatinib, it enhances the chemotherapy effect.In the bone marrow, however, the situation is different: first, the expression of miRNA is extremely high, almost 700 times more than normal. This data has greatly surprised us, because the role of tumor suppressors is to kill cancer cells and, usually, leukemia cells eliminate or extinguish everything that is harmful to their survival. Probably the CSCs turn the situation to their advantage and maintain high expression of the miRNA just to exploit its action of blocking the cell cycle and remain in a dormant state. They will only reactivate when an uncontrolled proliferation stimulus arrives. Furthermore, they do not undergo cell death because they are able to block the apoptotic activity of miRNA thanks to the presence of a very long non-coding RNA that behaves like a sponge and seizes it.We have tried to treat human leukemic cells in order to hyper-express miRNA and at the same time reduce the expression of the long non-coding RNA. It was found that, in mice, this combination is able to completely destroy cancer stem cells and eradicate the disease.

  What are the future prospects of your work?

We want to study the role of other miRNAs and their mechanism of action in the progression of leukemia; in particular, we are focusing on a microRNA that also has a specific activity on natural killer cells of natural immunity. The idea is to identify as many ways as possible to restore cell defense mechanisms against CML to be more likely to eliminate the disease.Furthermore, we are thinking of including in our research also acute myeloid leukemia (AML), a very aggressive disease for which few treatments exist and in which patients quickly develop resistance to the few drugs available. We want to use our leukemic transgenic mouse models to study the role of miRNAs and long non-coding RNAs in AML, given that at the molecular level there are many similarities with CML.

Professional Activity

2012, MicroFTIR stage and performing experiments at the Synchrotron Soleil, Paris, France.

2013, Organized laboratory planning and maintenance, University of Maryland, USA.   

2015, Mentor laboratory for The Nathan Schnaper Summer Intern Program (NSIP) in cancer Research at Universityof Maryland Baltimore Greenebaum CCC, Baltimore, USA  

2018-present, Postdoc Peer Mentor Program, University of Maryland, USA.

2018-present Judge, Undergraduate Poster Competition 2018, Stevenson University and Johns Hopkins Medical Institution, Baltimore, USA.Selected by the Collaborative Teaching Fellows Program to evaluate research posters of undergraduate students.

2019, Judge, 42nd   Medical Research Day (MSRD), University of Maryland, USA.

Links of Interest

Proffered Communications: oral (O) and poster (P) presentation

  1. Morsi H., El Ayoubi H., Moratti E., Vezzalini M., Silvestri G., Stradoni R., Murineddu M., Gabbas A., Monne M. and C. Sorio.  High Resistance Rate of Chronic Myeloid Leukaemia (CML) to Imatinib Myselate (IM) Might be related to Protein Tyrosine Phosphatase Receptor Type Gamma (PTPRG) Down-Regulation. Proceedings Qatar Foundation Annual Research Forum Epub: November 2011 (O).
  2. Bellisola G., Cinque G., Vezzalini M., Silvestri G., Redaelli S., Gambacorti Passerini C., Wehbe K. and C. Sorio. Rapid identification of drug-resistance/sensitivity in leukemic cells by Fourier Transform InfraRed microspectroscopy (microFTIR) and unsupervised Hierarchical Cluster Analysis (HCA) Proceeding of the Synchrotron Radiation UserMeeting Oxford, UK, September 2012. (P).
  3. Silvestri G*., Mirenda M., Vezzalini M., Moratti E., Laudanna C.and C. Sorio. Molecular mechanisms of the antiproliferative effect of Protein Tyrosine Phosphatase Receptor-like Gamma (PTPRG):  BCR/ABL and LYN kinase as key targets. Proceeding of the 14th ESH-iCMLf International Conference on CML Biology and Therapy. Baltimore, Usa, September 2012 (P) (*): recipient of the iCMLF travel award.
  4. Bellisola G., Cinque G., Vezzalini M., Moratti E., Silvestri G., Redaelli S., Wehbe K. and C. Sorio. Rapid identification of drug-resistance/sensitivity in leukemic cells by Fourier transform infrared microspectroscopy (microFTIR) and unsupervised pattern recognition. Proceeding of the 14th ESH-iCMLf International Conference on CML Biology and Therapy. Baltimore, USA, September 2012 (P).
  5. Bellisola G., Cinque G., Sandt C., Dumas P., Silvestri G. and C. Sorio. Oncosuppressive effect of direct transduction of receptor-type tyrosine-protein phosphatase gamma (PTPRG) intracellular catalytic domains in K562 cells. Proceeding of the 15th ESH-iCMLf International Conference on CML Biology and Therapy. Estoril, Portugal, September 2013 (P).
  6. Tomasello L., Silvestri G., Della Peruta M., Fiorini Z., Vezzalini M. and Claudio Sorio. Protein Tyrosine Phosphatase Receptor Type Gamma is an inhibitor of critical BCR/ABL driven pathways in Chronic Myeloid Leukemia. Societa’ Italiana di Cancerologia. Ferrara, Italy, September 2014 (O).
  7. Bellisola G., Tomasello L., Fiorini Z., Silvestri G., Vezzalini M. and Claudio Sorio. Direct transduction of Receptor-Type Protein Tyrosine-Phosphatase Gamma (PTPRG) intracellular catalytic domains in K562 cells. Societa’ Italiana di Cancerologia. Ferrara, Italy, September 2014 (P).
  8. Silvestri G*., Ellis J., Stramucci L., Harb J.G., Neviani P., Marcucci G., Reid A., Milojkovic D., Apperley J., Baer M., Trotta R., and D. Perrotti. MicroRNAs as regulators of stem and progenitor CML cells function. Peer reviewed and printed in the Proceedings of the 2014 ESH-iCMLf International Conference on CML-Biology and Therapy, Philadelphia (O).     (*): Invited Speaker.                                                                      
  9. Silvestri G., Ellis J.J., Stramucci L., Harb J.G., Neviani P., Marcucci G., Roy D-C., Hokland P., Milojkovic D., Reid A., Apperley J.F., Livak F.M., Baer M.R., Trotta R., and D. Perrotti. miR-300 acts as a tumor suppressor in Ph+ progenitors by Modulating the JAK2-SET/PP2A-B catenin interplay. Peer Reviewed and Published in Blood (Suppl.) dedicated to the 56th ASH Annual Meeting 2014 (P).
  10. Silvestri G*., Justin Ellis, Lorenzo Stramucci, Jason G Harb, Paolo Neviani, Guido Marcucci, Denis-Claude Roy, Peter Hokland, Dragana Milojkovic, Alistair Reid, Jane F. Apperley, Ferenc M. Livak, Maria R. Baer, Rossana Trotta, and Danilo Perrotti. miR-300 acts as a tumor suppressor in Ph+ progenitors by Modulating the JAK2-SET/PP2A-B catenin interplay. UMB Cancer Center Retreat, Baltimore, USA, May 18, 2015.(P)                             (*): Best Poster Presentation.
  11. Silvestri G*., Stramucci L, Ellis J., Yu J., Harb J.G., Neviani P., Marcucci G., Srutova K., Machova Polakova K., Roy D-C.,  Hokland P., Deininger MW., Bhatia R.,  Gambacorti-Passerini C., Milojkovic D., Reid A.G., Apperley J.F., Livak F., Baer M.R., Trotta R. and Perrotti D. Role of the MSC-derived exosomal and endogenous JAK2-SET/PP2A-beta-catenin-modulator miR-300 in leukemic stem/progenitor and NK cell proliferation and survival in CML. Peer reviewed and printed in the Proceedings of the 2015 ESH-iCMLf International Conference on CML-Biology and Therapy, Estoril, Portugal (O).                                                                                              (*): Best scored Biology Abstract.
  12. Silvestri G*., Stramucci L., Ellis J., Yu J., Harb J.G., Neviani P., Marcucci G., Srutova K., Machova Polakova K.,   Roy D-C,  Hokland P., Deininger MW., Bhatia R.,  Gambacorti-Passerini C., Milojkovic D., Reid A.G., Apperley J.F., Livak F., Baer M.R., Trotta R., and Perrotti D. Role of the MSC-Derived Exosomal and Endogenous JAK2-SET/PP2A-Beta Catenin-Modulator Mir-300 in Leukemic Stem/Progenitor Proliferation and Survival in CML. Peer Reviewed and Published in Blood (Suppl.) dedicated to the 57th ASH Annual Meeting 2015 (O). (*): ASH travel award.
  13. Trotta R., Silvestri G., Stramucci L., Ellis J., Yu J., Harb J.G., Neviani P., Marcucci G., Srutova K., Machova Polakova K.,  Roy D-C., Hokland P., Deininger M.W., Bhatia R.,  Gambacorti-Passerini C., Milojkovic D., Reid A.G., Apperley J.F., Livak F., Baer M.R., and Perrotti D. Role of the MSC-Derived Exosomal and Endogenous JAK2-SET/PP2A-Beta Catenin-Modulator Mir-300 in Leukemic Stem/Progenitor Proliferation and Survival in CML.  Proceeding of the AACR Annual Meeting (New Orleans, LA) 2016 (P).
  14. Silvestri G., Stramucci L., Ellis J., Yu J., Harb J.G., Neviani P., Marcucci G., Srutova K., Machova Polakova K.,  Roy D-C.,  Hokland P., Deininger M.W., Bhatia R.,  Gambacorti-Passerini C., Milojkovic D., Reid A.G., Apperley J.F., Livak F., Baer M.R., Trotta R., and Perrotti D. Role of Mir-300 in Leukemic Stem/Progenitor Proliferation and Survival in CML. Peer Reviewed and Published in the Haematologica (Suppl.) dedicated to the European Hematology Association (EHA) Annual Meeting. Copenhagen, Danmark. 2016. (O).
  15. Yu J.E., Silvestri G., Stramucci L., Livak F.M., Baer M.R., Trotta R., and Perrotti, D. The Role of SETBP1 in Leukemia-Initiating Cell Survival and Self-Renewal in Adult Ph+ B-ALL. ESH-iCMLF ESH-iCMLf International Conference on CML-Biology and Therapy, Houston TX Sept. 2016 (O).
  16. Yu J.E., Silvestri G., Stramucci L., Sanada M., Yamaguchi T., Du Y., Westermarck J., Caligiuri M.A., Garzon R., Milojkovic D., Apperley J.F., Roy D-C., Marcucci G., Calabretta, B., Baer M.R., Trotta R. and Perrotti D. Potential Targeting Ph+ Acute Lymphoblastic Leukemia Stem and Progenitor Cells By Modulating the CIP2A-SET-SETBP1 –Mediated Suppression of PP2A Activity Peer Reviewed and Published in Blood (Suppl.) dedicated to the 58th ASH Annual Meeting 2016 (P).
  17. P. Burda, N. Čuřík, K. Šrůtová, F. Savvulidi, G. Silvestri, H. Klamová, P. Pecherková, Ž. Sovová, J. Koblihová, T. Stopka, D. Perrotti, K. Machová Poláková Myc-dependent repression mechanism of the mir-150 transcriptional regulation in chronic myeloid leukemia. Peer Reviewed and Published in the Leukemia (Suppl.) dedicated to the European Hematology Association (EHA) Annual Meeting. Madrid, Spain. 2017 (P).
  18. Silvestri G., Stramucci L., Ellis J., Yu J., Harb J.G., Neviani P., Zhang B., Srutova K., Gambacorti-Passerini C., Pineda G., Jamieson C., Calabretta B., Stagno F., Vigneri P., Nteliopoulos  G., May P., Reid A.G., Garzon R.,  Roy D-C.,  Guimond M., Hokland P., Deininger M., Fitzgerald G., Harman C., Dazzi F., Milojkovic D., Apperley J.F., Marcucci G., Qi J., Fan X., Machova-Polakova K., Baer M.R., Trotta R., and Perrotti D.The BM Niche Uses Mir-300 As a Biological Rheostat to Selectively Control Stem Cell-Driven Malignant Hematopoiesis and Innate Anti-Cancer Immunity. UMB CCC Retreat, September 2017 (P).
  19. Silvestri G*., Stramucci L., Ellis J., Yu J., Harb JG, Neviani P., Zhang B., Srutova K., Gambacorti-Passerini C., Pineda G., Jamieson C., Calabretta B., Stagno F., Vigneri P., Nteliopoulos  G., May P., Reid A.G., Garzon R.,  Roy D-C.,  Guimond M., Hokland P., Deininger M., Fitzgerald G., Harman C., Dazzi F., Milojkovic D., , Apperley J.F., Marcucci G., Qi J., Fan X., Machova-Polakova K., Baer M.R., Trotta R., and Perrotti D.The BM Niche Uses Mir-300 As a Biological Rheostat to Selectively Control Stem Cell-Driven Malignant Hematopoiesis and Innate Anti-Cancer Immunity. ESH-iCMLf International Conference on CML-Biology and Therapy, Estoril, Portugal Oct. 2017 (O). (*): selected for Key note lecture.
  20. Silvestri G., Stramucci L., Ellis J., Yu J., Harb J.G., Neviani P., Zhang B., Srutova K., Gambacorti-Passerini C., Pineda G., Jamieson C., Calabretta B., Stagno F., Vigneri P., Nteliopoulos G., May P., Reid A.G., Garzon R., Roy D-C.,  Guimond M., Hokland P., Deininger M., Fitzgerald G., Harman C., Dazzi F., Milojkovic D.,  Apperley J.F., Marcucci G., Qi J., Fan X., Machova-Polakova K., Baer M.R., Trotta R., and Perrotti D.The Bone Marrow Niche Uses Mir-300 As a Biological Rheostat to Selectively Control Stem Cell-Driven Malignant Hematopoiesis and Innate Anti-Cancer Immunity. Peer Reviewed and Published in Blood (Suppl.) dedicated to the 59th ASH Annual Meeting 2017 (O).
  21. Silvestri G., Stramucci L., Ellis J., Yu J., Harb J.G., Neviani P., Zhang B., Srutova K., Gambacorti-Passerini C., Pineda G., Jamieson C., Calabretta B., Stagno F., Vigneri P., Nteliopoulos G., May P., Reid A.G., Garzon R.,  Roy D-C.,  Guimond M., Hokland P., Deininger M., Fitzgerald G., Harman C., Dazzi F., Milojkovic D., Apperley J.F., Marcucci G., Qi J., Fan X., Machova-Polakova K., Baer M.R., Trotta R., and Perrotti D. The tumor suppressor activity of miR-300 is detrimental for leukemia development but required for leukemia stem cell maintenance. Proceeding of the AACR Annual Meeting, Chicago, 2018 (P).
  22. Trotta R., Silvestri G., Stramucci L., Guimond M., Marcucci G., Fan X., Baer M.R., and D. Perrotti. Bone marrow microenvironment-induced miR-300 expression impairs natural killer cell proliferation and anti-tumor activity. Proceeding of the AACR Annual Meeting Chicago, 2018 (P).
  23. Trotta R., Silvestri G., Stramucci L., Guimond M., Marcucci G., Fan X., Baer M.R., and D. Perrotti. Bone marrow microenvironment-induced miR-300 expression impairs natural killer cell proliferation and anti-tumor activity. JAIDS Journal of Acquired Immune Deficiency Syndromes. 81():63, DOI: 10.1097/01.qai.0000558015.84504.53, April 2019.
  24. Silvestri G. et al. The 14q32.31 MIR300 DLK1-DIO3 oncosuppressor induces CML and AML cancer stem cell quiescence and inhibits NK cell Immunity. 21st ESH-iCMLf International Conference on CML-Biology and Therapy, Bordeaux, France Sep. 2019 (O). (*): selected abstract.
  25. Giovannino Silvestri, Rossana Trotta, Lorenzo Stramucci, Shuzhen Wang, Ann-Kathrin Eisfeld, Bin Zhang, Klara Srutova, Gabriel Pineda, Catriona Jamieson, Fabio Stagno, Paolo Vigneri, Georgios Nteliopoulos, Martin Guimond, Peter Hokland, Michael W Deininger, Francesco Dazzi, Dragana Milojkovic, Jane Apperley, Guido Marcucci, Xiaoxuan Fan, Maria R Baer, Bruno Calabretta, Danilo Perrotti. A 14q32.31 Genomic-Imprinted DLK1-DIO3 microrna promotes Leukemogenesis By Inducing Stem Cell Quiescence and Inhibiting NK Cell Anti-Cancer ImmunityBlood, The Journal of the American Society of Hematology. (2019) 134 (Supplement_1): 4141.