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Toni Ortiz



858.597.3888 - phone
858.597.3804 - fax
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Dr. Ortiz's research interests have two main objectives: a) to understand at a molecular level the imbalance in signaling pathways that lead to a status of prolonged stress facilitating the initiation and maintenance of human disease and b) to discover novel therapies to prevent, treat and cure those pathologies.

A wide range of diseases share the burden of prolonged stress imposed by hostile environmental conditions as a common denominator. The Cellular Stress Response represents a key element on the fight against diseases ranging from cancer, to metabolic syndrome, neurodegeneration and others. Conditions such as ischemia in the heart and brain, hypoxia, hyperthermia, acidosis and nutrient deprivation within a tumor, accumulation of missfolded proteins during normal aging or overexpression of missfolding-prone mutant oncoproteins and a multitude of other stressors, induce the heat shock factor (HSF) family of transcription factors. HSF regulates the stress-inducible expression of heat shock proteins and a growing number of previously unknown genes to favor cellular adaptation and survival. The HSF family therefore represents a desirable target for pharmacological modulation both positively and negatively. HSF1 has been recently described as an enabler of malignant transformation. Hence, while inhibition of HSF1 activation could provide an effective anticancer strategy, it could also accelerate the progression of neurodegenerative diseases or impair the cellular response to infection. Therefore, a strong knowledge of the signaling pathways affected by HSF1 and its molecular targets will be instrumental to design novel screening tools to discover specific therapies to modulate its function.


  • 1985: Universidad Autonoma de Madrid, Spain, B.S. in Biology
  • 1992: Universidad Autonoma de Madrid, Spain, Ph.D in Biochemistry and Molecular Biology
  • 1983-1985: Centro de Biologia Molecular, Madrid, Spain. Undergraduate student.
  • 1985-1986: Montpellier High School, Biology teacher, Madrid, Spain.
  • 1985-1988: Ramon y Cajal Hospital, Madrid, Spain. Training in clinical virology.
  • 1988-1992: Centro de Investigaciones Biologicas, CSIC, Madrid, Spain. PhD student.
  • 1992-1997: The Burham Institute, LaJolla, California, USA. Postdoctoral Fellow.
  • 1997-1998: The Burham Institute, Senior Postdoctoral Associate.
  • 1998-present: Sidney Kimmel Cancer Center, San Diego. Senior Research Scientist.
  • February 2009-present: Torrey Pines Institute for Molecular Studies, San Diego, CA.  Assistant Member

Professional Affiliations

Honors & Awards

  • 1988-1991:      Predoctoral Fellowship from the Spanish Ministry of Education and Science.
  • 1992:               Predoctoral Fellowship “Caja de Ahorros y Monte de Piedad de Madrid”.
  • 1993:               Award “Caja de Ahorros y Monte de Piedad de Madrid” to the best Doctoral Thesis.
  • 1994-1996:      Postdoctoral Fellowship from the Spanish Ministry of Education and Science

Selected Publications (10 of 62)

  1. R. Apfel, D. Benbrook, E. Lernhardt, M. A. Ortiz, G. Salbert and M. Pfahl. A novel orphan receptor specific for a subset of TRE's and its interaction with the retinoid /thyroid hormone receptor subfamily. Molecular and Cellular Biology (1994), 14 (10): 7025-7035.
  2. M.A. Ortiz, F.J. Piedrafita, M. Pfahl and R. A. Maki. TOR: a new orphan receptor expressed in the thymus that can modulate the retinoid and thyroid hormone signals. Molecular Endocrinology (1995), 9 (12): 1679-1691.
  3. M.A. Ortiz, Light, J., Maki, R. A. and Assa-Munt, N. (1998). Mutation analysis of the Pip interaction domain reveals critical residues for protein-protein interactions. Proc. Natl. Acad. Sci., USA (1999), 96:2740-2745.
  4. M.A. Ortiz, F.J. Lopez-Hernandez, Y. Bayon, M. Pfahl, and F.J. Piedrafita. Retinoid-related Molecules Induce Cytochrome c Release and Apoptosis through Activation of c-Jun NH(2)-Terminal Kinase/p38 Mitogen-activated Protein Kinases.  Cancer Research, (2001), 61: 8504-8512.
  5. Y. Bayon, M.A. Ortiz, F.J. Lopez-Hernandez, F. Gao, M. Karin, M. Pfahl and F.J. Piedrafita. Inhibition of IκB kinase by a new class of retinoid related anticancer agents that induce apoptosis.  Mol. Cell. Biol., (2003), 23(3): 1061-1074.
  6. F.J. Lopez-Hernandez , M.A. Ortiz, Y. Bayon and F.J. Piedrafita.  Retinoid-related molecules require caspase 9-dependent release of Smac and the rapid induction of apoptosis.  Cell Death Diff., (2004), 11: 154-164.
  7. Y. Bayon, M.A. Ortiz, F.J. Lopez-Hernandez, P.H. Howe and F.J. Piedrafita. The retinoid antagonist MX781 induces clusterin expression in prostate cancer cells via HSF-1 and AP-1 transcription factors.  Cancer Res., (2004), 64: 5905-5912.
  8. C. Cavasotto, M.A. Ortiz, R.A. Abgayan and F.J. Piedrafita.  In silico identification of novel EGFR inhibitors with antiproliferative activity against cancer cells.  Bioorganic & Medicinal Chemistry Letters, (2006), 16: 1969-1974.
  9. P. Lorenzo, R. Alvarez, M.A. Ortiz, S. Alvarez, F.J. Piedrafita, and A.R. de Lera.  Inhibition of IkappaB kinase-β and anticancer activities of novel chalcone adamantyl arotinoids.  J. Med. Chem. (2008), 51: 5431-5440.
  10. S. Pérez-Rodríguez, M.A. Ortiz, J. García, R. Pereira, F. Rodríguez-Barrios, A.R. de Lera, and F.J. Piedrafita.  Highly Twisted Adamantyl Arotinoids. Synthesis, antiproliferative effects and RXR transactivation profiles.  Eur. J. Med. Chem. (2009), 44: 2434-2446.