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Faculty Profile

Antonio Di Cristofano, Ph.D.

Dr. Antonio Di Cristofano

Professional Interests

Phosphatidylinositol-3-kinase (PI3K) is a crucial mediator of receptor-initiated signaling cascades, through the production of phosphatidylinositol (3,4,5)-triphosphate (PIP-3).  Among the major effectors of PI3K is the AKT kinase, which is activated upon PIP-3-mediated membrane recruitment and, in turn, phosphorylates an ever-growing list of target proteins, regulating key processes such as proliferation, survival, cell size, genome stability, metabolism, and mRNA translation.  This cascade is counteracted by the PTEN tumor suppressor, which opposes PI3K activity by dephosphorylating PIP-3 to PIP-2.  Somatic deletions, mutations and epigenetic inactivation of PTEN have been identified in a large fraction of tumors (endometrial, glioblastoma, prostate, thyroid, melanoma), placing PTEN among the most commonly mutated genes in human cancer. 

The central focus of my laboratory is the identification and characterization of the specific biological processes and signaling pathways that are controlled by the PI3K/PTEN/AKT cascade. Our research is centered on tumors originating in the thyroid gland: we utilize genetically engineered mouse models to identify and deconstruct the signaling cascades altered during early neoplastic transformation, to understand through which signaling nodes the PI3K cascade intersects with other growth-promoting pathways, and to design and test in vivo innovative, rationally designed therapeutic approaches.



Selected Publications

  1. Champa, D., Russo, M.A., Liao, X-H., Refetoff, S., Ghossein, R.A., and Di Cristofano, A. Obatoclax overcomes resistance to cell death in aggressive thyroid carcinomas by countering Bcl2a1 and Mcl1 overexpression. Endocr. Relat. Cancer, in press.
  2. Antico Arciuch V.G., Russo, M.A., Kang, K.S, and Di Cristofano, A. Inhibition of AMPK and Krebs cycle gene expression drives metabolic remodeling of Pten-deficient preneoplastic thyroid cells.  Cancer Res., 73: 5459-5472, 2013.
  3. Russo, M.A., Kang, K.S., and Di Cristofano, A. The PLK1 inhibitor GSK461364A is effective in poorly differentiated and anaplastic thyroid carcinoma cells, independent of the nature of their driver mutations.  Thyroid, 23:1284-1293, 2013. 
  4. Antico Arciuch V.G., Russo, M.A., Dima, M., Kang, K.S., Dasrath, F., Liao, X-H., Refetoff, S., Montagna, C., and Di Cristofano, A. Thyrocyte-specific inactivation of p53 and Pten results in anaplastic thyroid carcinomas faithfully recapitulating human tumors. Oncotarget, 2:1109-1126, 2011.
  5. Dima, M., Miller, K.A., Antico-Arciuch V.G., and Di Cristofano, A. Establishment and characterization of cell lines from a novel mouse model of poorly differentiated thyroid carcinoma: powerful tools for basic and preclinical research. Thyroid, 21:1001-1007, 2011.
  6. Antico-Arciuch VG, Dima, M., Liao, X-H., Refetoff, S., and Di Cristofano, A. Cross-talk between PI3K and estrogen in the mouse thyroid predisposes to the development of follicular carcinomas with a higher incidence in females. Oncogene, 29:5678-5686, 2010.
  7. Miller, K., Yeager, N., Baker, K., Liao, X-H., Refetoff, S., and Di Cristofano, A. Oncogenic Kras Requires Simultaneous PI3K Signaling to Induce ERK Activation and Transform Thyroid Epithelial Cells in Vivo. Cancer Res., 69:3689-3694, 2009.

More Information About Dr. Antonio Di Cristofano

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Albert Einstein College of Medicine
Michael F. Price Center
1301 Morris Park Avenue , Room 302
Bronx, NY 10461

Tel: 718.678.1137
Fax: 718.678.1020

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