Angela Bentivegna

 CURRICULUM

  • 1999: Degree in Biology (University of Milan). Thesis on Neurofibromatosis type 1. “Utilizzo di sonde locus-specifiche per la caratterizzazione di delezioni sporadiche e familiari: identificazione di una nuova sindrome da microdelezioni centrata sul gene NF1”.
  • 2004: Specialization in Medical Genetics (University of Milan). Thesis title: “Ricerca di alterazioni del Gene CREBBP (CREB Binding Protein) in pazienti con sindrome di Rubinstein-Taybi”.
  • 2008: PhD in experimental Pathology and Neuropathology (University of Milan). Thesis title: “Base molecolare della sindrome di Chromatin remodelling Rubinstein-Taybi: un sistema modello per lo studio dei deficit funzionali di acetilazione istonica”
  • 2020: Professor in Medical Genetics (MED/03).

Current position:

Professor of Medical Genetics at the University of Milano-Bicocca.

RESEARCH INTERESTS

  • Cancer research

Isolation of cancer stem cells from biopsies of patients with high-grade gliomas; study of genetic, genomic and epigenomic profiles, at the basis of solid tumors (urothelial, brain, thyroid tumors). 

  • Non-oncological research

Role of specific chromosomal and / or genetic aberrations in the development of complex genetic diseases in neurosciences, such as developmental disability, speech disorder, psychoses.

RESEARCH PROGRAM

Gliomas are malignant tumors of glial origin classified, according to WHO2016, from II to IV degree. Grade II tumors are more indolent while Grade III and IV tumors are very aggressive. Grade IV tumors are named Glioblastoma Multiforme (GBM) which represents approximately 70% of all gliomas and 12-14% of all brain tumors. Currently, GBM is untreated and has a prognosis that is variable and that is influenced by the molecular characteristics of the tumor as well as by its histological characteristics, but which maintains a median of survival of approximately 14-16 months. GBM are tumors supported by the presence of a small group of stem cells, the Cancer Stem Cells (CSC) which, given their stem characteristics, support the continuous renewal of the cellular elements that make up the tumor mass. Furthermore, they are also able to develop mechanisms of resistance to chemotherapy and radiation therapy through DNA repair mechanisms. This dual role (maintenance of tumor mass and resistance to treatments) causes CSCs to be responsible for tumor recurrence during neuro-oncological follow-up. Recently, this cell population has proven capable of communicating with other cells through a network of micro vesicles (MV) capable of transporting fragments of tumor DNA, microRNA (miRNA) and proteins, capable of influencing cell replication and invasiveness, the response anti-tumor immune and to induce resistance to adjuvant treatments. Through the analysis of the MV, isolated from peripheral blood samples of the patients through the liquid biopsy, it would be possible to identify these precious messages and therefore find new therapeutic strategies for this type of tumor. The aim is to determine the genetic profile of the tumor mass, of the tumor margins (peritumoral zone) as well, and of the respective isolated stem cell cultures, by array-CGH technique and / or Next Generation Sequencing (NGS). This profile will be useful to re-search for genetic mutations identified as more representative, using them as tumor markers, in plasma-isolated MVs via liquid biopsy in pre and post-operative samples and during patient follow-up, to establish the disease recurrence.

PUBLICATIONS SELECTED FROM THE LAST 5 YEARS

  1. Instability of Short Arm of Acrocentric Chromosomes: Lesson from Non-Acrocentric Satellited Chromosomes. Report of 24 Unrelated Cases. Redaelli S, Conconi D, Villa N, Sala E, Crosti F, Corti C, Catusi I, Garzo M, Romitti L, Martinoli E, Patrizi A, Malgara R, Recalcati MP, Dalprà L, Lavitrano M, Riva P, Roversi G, Bentivegna A. Int J Mol Sci. 2020 May 13;21(10):E3431. doi: 10.3390/ijms21103431.
  2. Unbalanced X;Autosome Translocations May Lead to Mild Phenotypes and Are Associated with Autoimmune Diseases. Ciaccio C, Redaelli S, Bentivegna A, Marelli S, Crosti F, Sala EM, Cavallari U. Cytogenet Genome Res. 2020;160(2):80-84. doi: 10.1159/000506097. Epub 2020 Feb 5.
  3. A Ploidy Increase Promotes Sensitivity of Glioma Stem Cells to Aurora Kinases Inhibition. Cilibrasi C, Guzzi A, Bazzoni R, Riva G, Cadamuro M, Hochegger H, Bentivegna A. J Oncol. 2019 Aug 19;2019:9014045. doi: 10.1155/2019/9014045. eCollection 2019.
  4. UGT1A1 mutations and psychoses: towards understanding the relationship with unconjugated bilirubin. Bentivegna A, Santambrogio J, Clerici M. CNS Spectr. 2019 Jul 24:1-3. doi: 10.1017/S1092852919001251. Online ahead of print.
  5. Refining the Phenotype of Recurrent Rearrangements of Chromosome 16. Redaelli S, Maitz S, Crosti F, Sala E, Villa N, Spaccini L, Selicorni A, Rigoldi M, Conconi D, Dalprà L, Roversi G, Bentivegna A. Int J Mol Sci. 2019 Mar 4;20(5):1095. doi: 10.3390/ijms20051095.
  6. Role of Notch Signaling Pathway in Glioblastoma Pathogenesis. Bazzoni R, Bentivegna A. Cancers (Basel). 2019 Mar 1;11(3):292. doi: 10.3390/cancers11030292.
  7. Specific Expression of a New Bruton Tyrosine Kinase Isoform (p65BTK) in the Glioblastoma Gemistocytic Histotype. Sala L, Cirillo G, Riva G, Romano G, Giussani C, Cialdella A, Todisco A, Virtuoso A, Cerrito MG, Bentivegna A, Grassilli E, Ardizzoia A, Bonoldi E, Giovannoni R, Papa M, Lavitrano M. Front Mol Neurosci. 2019 Jan 24;12:2. doi: 10.3389/fnmol.2019.00002. eCollection 2019.
  8. Valproic Acid Inhibits Proliferation and Reduces Invasiveness in Glioma Stem Cells Through Wnt/β Catenin Signalling Activation. Riva G, Cilibrasi C, Bazzoni R, Cadamuro M, Negroni C, Butta V, Strazzabosco M, Dalprà L, Lavitrano M, Bentivegna A. Genes (Basel). 2018 Oct 26;9(11):522. doi: 10.3390/genes9110522.
  9. Resveratrol Impairs Glioma Stem Cells Proliferation and Motility by Modulating the Wnt Signaling Pathway. Cilibrasi C, Riva G, Romano G, Cadamuro M, Bazzoni R, Butta V, Paoletta L, Dalprà L, Strazzabosco M, Lavitrano M, Giovannoni R, Bentivegna A. PLoS One. 2017 Jan 12;12(1):e0169854. doi: 10.1371/journal.pone.0169854. eCollection 2017.
  10. Epigenetic targeting of glioma stem cells: Short-term and long-term treatments with valproic acid modulate DNA methylation and differentiation behavior, but not temozolomide sensitivity. Riva G, Butta V, Cilibrasi C, Baronchelli S, Redaelli S, Dalprà L, Lavitrano M, Bentivegna A. Oncol Rep. 2016 May;35(5):2811-24. doi: 10.3892/or.2016.4665. Epub 2016 Mar 9.

COLLABORATION WITH FOREIGN UNIVERSITIES

  • Dr Helfrid Hochegger  (Genome Damage and Stability Center, University of Sussex, Brighton, UK)
  • Prof. Georgios Giamas (University of Sussex -School of Life Sciences, Brighton, UK)
  • CNR , Istituto di Tecnologie Biomediche, LITA, Milano Dr. Ida Biunno
  • IST- Istituto Nazionale Ricerca sul Cancro, Genova, Dr. Antonio Daga
  • Università di Cagliari, Sezione di  Biochimica, Biologia e Genetica, Prof. Roberta Vanni

FURTHER INFO

Please visit the following links:

 

Elisabetta Donzelli
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