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Sotillo - ERC InvestigatorPublications

Mad2 is a critical mediator of the chromosome instability observed upon Rb and p53 pathway inhibition.
Schvartzman, J.M., Duijf, P.H., Sotillo, R., Coker, C. & Benezra, R.
Cancer Cell. 2011 Jun 14;19(6):701-14. doi: 10.1016/j.ccr.2011.04.017. PubMed

Mad2-induced chromosome instability leads to lung tumour relapse after oncogene withdrawal.
Sotillo, R., Schvartzman, J.M., Socci, N.D. & Benezra, R.
Nature. 2010 Mar 18;464(7287):436-40. Epub 2010 Feb 21. PubMed

Mitotic chromosomal instability and cancer: mouse modelling of the human disease.
Schvartzman, J.M., Sotillo, R. & Benezra, R.
Nat Rev Cancer. 2010 Feb;10(2):102-15. PubMed

Chromosomal Instability and Cancer: Mouse Modeling Through a Human Lens.
Schvartzman, J.M.*, Sotillo, R.*, Benezra, R. *equal contribution.
Nat Rev Cancer. 2010 Feb;10(2):102-15. Review.

Very CIN-ful: whole chromosome instability promotes tumor suppressor loss of heterozygosity.
Sotillo, R., Schvartzman, J.M. & Benezra, R.
Cancer Cell. 2009 Dec 8;16(6):451-2. PubMed

Hec1 overexpression hyperactivates the spindle assembly checkpoint and induces multiorgan tumor formation in vivo
Diaz-Rodriguez, E.*, Sotillo, R.*, Schvartzman, J.M., Benezra, R. *equal contribution
Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16719-24. Epub 2008 Oct 21

Hec1 overexpression hyperactivates the mitotic checkpoint and induces tumor formation in vivo.
Diaz-Rodriguez, E., Sotillo, R., Schvartzman, J.M. & Benezra, R.
Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16719-24. Epub 2008 Oct 21. PubMed

Mad2 overexpression promotes aneuploidy and tumorigenesis in mice.
Sotillo, R., Hernando, E., Diaz-Rodriguez, E., Teruya-Feldstein, J., Cordon-Cardo, C., Lowe, S.W. & Benezra, R.
Cancer Cell. 2007 Jan;11(1):9-23. Epub 2006 Dec 28. PubMed

Changing Mad2 levels affects chromosome segregation and spindle assembly checkpoint control in female mouse meiosis I.
Niault, T., Hached, K., Sotillo, R., Sorger, P.K., Maro, B., Benezra, R. & Wassmann, K.
PLoS One. 2007 Nov 28;2(11):e1165. PubMed

Autocrine PDGFR signaling promotes mammary cancer metastasis.
Jechlinger, M., Sommer, A., Moriggl, R., Seither, P., Kraut, N., Capodiecci, P., Donovan, M., Cordon-Cardo, C., Beug, H. & Grunert, S.
J Clin Invest. 2006 Jun;116(6):1561-70. PubMed

Cooperation between Cdk4 and p27kip1 in tumor development: a preclinical model to evaluate cell cycle inhibitors with therapeutic activity.
Sotillo, R., Renner, O., Dubus, P., Ruiz-Cabello, J., Martin-Caballero, J., Barbacid, M., Carnero, A. & Malumbres, M.
Cancer Res. 2005 May 1;65(9):3846-52. PubMed

Mammalian Cells Cycle without the D-Type Cyclin-Dependent Kinases Cdk4 and Cdk6
Malumbres, M., Sotillo, R., Santamaría, D., Galan, J., Cerezo, A., Ortega, S., Dubus, P., Barbacid, M.
Cell. 2004 Aug 20;118(4):493-504.

Cyclin-dependent kinase 2 is essential for meiosis but not for mitotic cell division in mice.
Ortega, S., Prieto, I., Odajima, J., Martin, A., Dubus, P., Sotillo, R., Barbero, J.L., Malumbres, M., Barbacid, M.
Nat Genet. 2003 Sep;35(1):25-31. Epub 2003 Aug 17.

Genetic rescue of Cdk4 null mice restores pancreatic beta-cell proliferation but not homeostatic cell number.
Martin, J., Hunt, S.L., Dubus, P., Sotillo, R., Nehme-Pelluard, F., Magnuson, M.A., Parlow, A.F., Malumbres, M., Ortega, S. & Barbacid, M.
Oncogene. 2003 Aug 14;22(34):5261-9. PubMed

Wide spectrum of tumors in knock-in mice carrying a Cdk4 protein insensitive to INK4 inhibitors.
Sotillo, R., Dubus, P., Martin, J., de la Cueva, E., Ortega, S., Malumbres, M. & Barbacid, M.
EMBO J. 2001 Dec 3;20(23):6637-47. PubMed

Invasive melanoma in Cdk4-targeted mice.
Sotillo, R., Garcia, J.F., Ortega, S., Martin, J., Dubus, P., Barbacid, M. & Malumbres, M.
Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):13312-7. Epub 2001 Oct 23. PubMed

Limited overlapping roles of P15(INK4b) and P18(INK4c) cell cycle inhibitors in proliferation and tumorigenesis.
Latres, E., Malumbres, M., Sotillo, R., Martin, J., Ortega, S., Martin-Caballero, J., Flores, J.M., Cordon-Cardo, C. & Barbacid, M.
EMBO J. 2000 Jul 3;19(13):3496-506. PubMed