• Istituto di Biologia e Patologia Molecolari

Tel :+390649917515
Fax :+39064457529
Senior Researcher

Istitute of Molecular Biology and Pathology - National Research Council
Sapienza University of Rome
Laboratorio di Genetica I\u00b0 piano stanza 4 Via degli Apuli,4 00185 Roma

Ataxia Telangiectasia (AT) is a recessive genetic disease caused by mutation and/or inactivation of the ATM gene and characterized by neurological defects, immunodeficiency, radiosensitivity and tumor proneness. Parents of AT patients are estimated to represent 1.69-3.43% of the Italian population. They have an apparently normal phenotype and ignore to be healthy carriers until the birth of their first AT affected child. They are however more susceptible to tumors and more radiosensitive than the normal population. 

We showed that, during mitotic division, ATM induces p53 localization at centrosomes, the major organizers of the mitotic spindle poles. In AT patient-derived cells, the percentage of p53 dissociation from centrosomes (p53cd) ranges from 70% to 100%, whereas in normal individuals it drops to 10-25%. Interestingly, in cells derived from parents of AT patients (healthy carriers), p53cd ranges from 45% to 60%. Based on these findings, we have developed a method for the diagnosis of AT and, most importantly, for the identification of healthy carriers (patent RM2010A000015)


1.Cherubini G, Naim V, Caruso P, Burla R, Bogliolo M, Cundari E, Benihoud K, Saggio I and Rosselli F. (2011) The FANC pathway is activated by adenovirus infection and promotes viral replication-dependent recombination. Nucleic Acids Res. 39:5459-73.

2.Cundari E., Chessa L., Prodosmo A., Soddu S., (2010) “Methods for the identification of Ataxia telangectasia healthy carriers and relative kits”. Patent n. ITRM2010A000015.

3.Decordier I, Cundari E and Kirsch-Volders M. (2008) Survival of aneuploid, micronucleated and/or polyploid cells: crosstalk between ploidy control and apoptosis. Mutat Res. 651:30-39. 

4.Decordier I, Cundari E and Kirsch-Volders M. (2008) Mitotic checkpoints and the maintenance of the chromosome karyotype. Mutat Res. 651:3-13. 

5.Stagni V, di Bari MG, Cursi S, Condò I, Cencioni MT, Testi R, Lerenthal Y, Cundari E and Barilà D. (2008) ATM kinase activity modulates Fas sensitivity through the regulation of FLIP in lymphoid cells. Blood. 111:829-837. 

6.Oricchio E, Saladino C, Iacovelli S, Soddu S, and Cundari E. (2006) ATM is Activated by Default in Mitosis, Localizes at Centrosomes and Monitors Mitotic Spindle Integrity. Cell Cycle. 5(1): 88-92.

7.Cherubini G, Petouchoff T, Grossi M, Piersanti S, Cundari E and Saggio I. (2006) E1B55K-deleted adenovirus (ONYX-015) overrides G1/S and G2/M checkpoints and causes mitotic catastrophe and endoreduplication in p53-proficient normal cells. Cell Cycle. 5(19): 2244-2252

8.Tritarelli A, Oricchio E, Ciciarello M, Mangiacasale R, Palena A, Lavia P, Soddu S, and Cundari E. (2004) p53 Localization at Centrosomes during Mitosis and Postmitotic Checkpoint are ATM-Dependent and Require Serine 15 Phosphorylation. Mol Biol Cell. 15: 3751-3757

9.Mangiacasale R., Tritarelli A., Sciamanna I., Cannone M., Lavia P. Barberis M., Lorenzini R. and Cundari E. (2001). Normal and cancer-prone human cells respond differently to extremely low frequency electromagnetic fields. FEBS Letters, 487: 397-403.

10.Ciciarello M., Mangiacasale R., Casenghi M., D’Angelo M., Soddu S., Lavia P. and Cundari E. (2001). p53 Displacement from Centrosomes and p53-Mediated G1 Arrest Following Transient Inhibition of the Mitotic Spindle. J. Biol. Chem., 276: 19205-19213.

Si possono inserire: 

Ricercatori CNR/universitari, Post-Doc, PhD stud, e Laureandi

Within IBPM

•Prof. Isabella Saggio, IBPM associate 


External collaborations 


•Dr. Silvia Soddu, Istituto Regina Elena, Roma


•Dr. Maurizio Fanciulli, Istituto Regina Elena, Roma


•Prof. Rodolfo Negri, Università “La Sapienza”, Roma.


•Prof. Micheline Kirsh-Volders, Free Unversity of Brussels, Brussels (Belgium)


•Dr. Laetitia Gonzalez, Free Unversity of Brussels, Brussels (Belgium)


•Dr. Filippo Rosselli, Institut Gustave Roussy, Villejuif (France)



1978: Post-graduate course "Techniques for mutagenesis evaluation", C.N.R. Institute of Mutagenesis and Differentiation in Pisa.

1977: Degree (Laurea) cum Laude in Biological Sciences, “Sapienza” University of Rome.



Current: Invited professor at the Laboratory of Cell Genetics (Brussels) and associate professor at the Graduate School of Molecular Biology and Biotechnology (Brussels) of the Free University of Brussels (VUB)

2003-present: CNR Senior Scientist (Primo Ricercatore) at IBPM, Rome

1996-2009: visiting scientist, three months per year, at the Laboratory of Cell Genetics, Free University of Brussels (VUB) directed by Prof. M. Kirsch-Volders; project “Apoptosis and the Control of the Mitotic Ceckpoint”. 

1995: visiting scientist (two month research stage), Institut Curie- Section de Recherche, Paris 

1994: visiting scientist (three month research stage), Institut Curie- Section de Recherche, Paris; project “Role of Apoptosis in the Fanconi Anemia Syndrome”  (host scientist Dr. E. Moustacchi).

1990: Short-term research Fellowship from the French Medical Research Foundation (three months), Institut Curie, Paris (supervisor Dr. D. Averbeck).

1988: moves to the Center of Evolutionary Genetics, Rome (currently part of IBPM).

1985-86: Long-term research Fellow supported by European Science Foundation, Institut  Curie, Paris.

1982: CNR Research Scientist appointment, Institute of Mutagenesis and Differentiation, Pisa.

1978: CNR post-graduate research fellow, National Institute of Nutrition, Rome.


Main fields of interest: Cell biology; cell-cycle regulation; role of apoptosis in the regulation of cell growth; flow-cytometry; genetic toxicology