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Overview | Research directions | Group members | Collaborations | Selected Publications

Overview

Metastasis is the leading cause of death in cancer patients. The formation of metastasis, or even secondary tumors, is remarkably influenced by different types of tumor-stroma interactions, in which stromal components of the tumor microenvironment can influence the behavior of cancer cells.
The main interest of our group is based in understanding the molecular mechanisms important in the metastatic process, particularly in breast cancer. A particular attention is based on the gene expression network reprograming driven by master regulator transcription factors with a prominent role in tumor biology, such as p53 and NFkB. Since chemotherapy regimens within inflamed microenvironment is a condition often found in tumor patients and can activate gene expression reprogramming leading to increased migratory capability, we hypothesized that "in vitro education" of breast adecarcinoma-derived cells can lead to the acquisition of a mesenchymal phenotype, more aggressive in term of tumorigenesis and metastasis potential.
Moreover, the laboratory interests are also based on the transcriptional regulation of cancer-associated genes mediated by other transcription factor master regulators such as c-Myc, Estrogen and Androgen Receptors.

The activity of the Laboratory of Molecular Cancer Genetics is primarily focused on the development of genome-wide, 3D and transcription-based assays using cancer-derived cell lines, primary cells and in vivo model systems.

Research directions

The main research directions are focused on the analysis of gene expression in breast cancer patients and cell lines, in vitro 3D as well as in vivo models of metastasis and angiogenesis.

  • Identification of the molecular mechanisms underlying the transcriptional cooperation between p53 and NFkB.
  • Definition of prognostic value of identified gene signatures in breast cancer patients.
  • Role of EMT as mechanism of resistance to chemotherapy.
  • Determination of the p53 isoforms expression in cancer cells.
  • Defining the role of microenvironment in tumor angiogenesis and metastasis formation.

Group members

  • Yari Ciribilli, PI
  • Laura Pezzè, Master student
  • Francesca Precazzini, Master student
  • Silvia D’Ambrosi, Bachelor student

Motivated candidates, including undergraduate, master and doctoral students interested in the research topics, are encouraged to contact the PI (ciribilli [at] science.unitn.it).

Collaborations

  • Juergen Borlak, Hannover Medical School (MHH), Germany
  • Daniel Menendez, National Institute for Environmental Health Sciences (NIEHS, NIH), Research Triangle Park, NC, USA
  • Michael A. Resnick, National Institute of Environmental Health Sciences (NIEHS, NIH), Research Triangle Park, NC, USA
  • Jean-Christophe Bourdon, Dundee Cancer Centre, University of Dundee, Scotland
  • Thierry Soussi, Karolinska Institutet, Stockholm, Sweden
  • Mattia Barbareschi, Santa Chiara Hospital, Trento, Italy
  • Antonella Ferro, Santa Chiara Hospital, Trento, Italy
  • Gilberto Fronza, National Institute for Cancer research (IST), Genoa, Italy
  • Antonella Motta, Department of Industrial Engineering, University of Trento, Italy

Selected publications

  • Garritano S.*, Romanel A.*, Ciribilli Y.*, Bisio A., Gavoci A., Inga A., Demichelis F. In-silico identification and functional validation of allele-dependent AR enhancers. 2015 In press, Oncotarget.
  • Bisio A., Zámborszky J., Zaccara S., Lion M., Tebaldi T., Sharma V., Raimondi I., Alessandrini F., Ciribilli Y.*, Inga A.*. Cooperative interactions between p53 and NFkB enhance cell plasticity. Oncotarget. 2014 Oct 21.
  • Zaccara S., Tebaldi T., Pederiva C., Ciribilli Y., Bisio A., Inga A. p53-directed translational control can shape and expand the universe of p53 target genes. Cell Death and Differentiation. 2014 Oct;21(10):1522-34.
  • Monti P.*, Ciribilli Y.*, Bisio A.*, Foggetti G., Raimondi I., Campomenosi P., Menichini P., Fronza G., Inga A. ΔN-P63a and TA-P63a exhibit intrinsic differences in transactivation specificities that depend on distinct features of DNA target sites. Oncotarget. 2014 Apr 30;5(8):2116-30.
  • Bisio A.*, Ciribilli Y.*, Fronza G.*, Inga A.*, Monti P.*. P53 mutants in the Tower of Babel of cancer progression. Human Mutation. 2014 Jun;35(6):689-701. doi: 10.1002/humu.22514.
  • Bisio A., De Sanctis V., Del Vescovo V., Jegga A.G., Denti M.A., Inga A. and Ciribilli Y. MiRNA-based, p53 dependent post-transcriptional circuits: mechanisms, targets and inter-individual variation. BMC Cancer, 2013 Nov 21;13:552.
  • Ciribilli Y., Monti P., Bisio A., Nguyen H.T., Ethayathulla A.S., Ramos A., Foggetti G., Menichini P., Menendez D., Resnick M.A., Viadiu H., Fronza G. and Inga A. Transactivation specificity is conserved among p53 family proteins and depends on a response element sequence code. Nucleic Acids Res. 2013 Oct;41(18):8637-53.
  • Lion M, Bisio A, Tebaldi T, De Sanctis V, Menendez D, Resnick MA, Ciribilli Y, Inga A. Interaction between p53 and estradiol pathways in transcriptional responses to chemotherapeutics. Cell Cycle. 2013 Apr 15;12(8):1211-24.

* = equal contribution