Dr. Conejo-Garcia is Assistant Professor of the Departments of Microbiology and Immunology, and of Medicine at Dartmouth Medical School. He was interviewed on May 26, 2009, by OCRF’s Chief Executive Officer, Elizabeth Howard.
Elizabeth Howard: Dr. Conejo-Garcia, you are originally from Spain, where you grew up and studied medicine. How did you find your way to Dartmouth Medical School in New Hampshire?
Dr. Conejo-Garcia: It was quite convoluted. In 1998 I received a post-residency fellowship from the Spanish government to work on cancer biology in Switzerland. While working there, I was contacted by a German biotechnological company, which offered me a position to work on the identification of novel antimicrobial peptides. The peculiarities of the European academic system are difficult to explain to an honest mind, but, during my time in Germany I lost my contacts in Spain and I reached the end of my professional opportunities there. I was then lucky to find a position working on the immunobiology of ovarian cancer in Dr. George Coukos’ lab at the University of Pennsylvania. During the four years that I spent working with George – who is also an OCRF grantee – I participated in many of the revolutionary discoveries that his remarkable team accomplished. I finally accepted a tenure-track position to start my own laboratory at Dartmouth in 2005.
EH: When did you decide to focus on ovarian cancer? Isn’t it more difficult to find funding and support for your research?
JCG: While at the University of Pennsylvania I learned to view ovarian cancer as a fascinating biological system in which multiple cell types interact to generate a disease that is much more complicated than the mere expansion of tumor cells. I also discovered that ovarian cancer was a good fit for my research interests – it is the ideal tumor to change gene expression patterns in different types of cells, and to deliver nanoparticles to immune cells. We are currently working on these novel approaches.
In terms of funding, I have been lucky to get the support of OCRF and the National Institute of Health for my research. It is true that there is disproportionately more funding for other cancers, and the number of researchers focused on ovarian cancer is relatively small. We need more scientists and research dollars, and we especially need better translation of remarkable scientific advances into clinical settings where they can help ovarian cancer patients. Bringing together scientists and clinicians is key.
EH: You received a Liz Tilberis Scholar grant in 2005 for research on “vascular leukocytes as novel anti-tumor therapeutics.” Can you explain this to those of us who are not researchers?
JCG: Ovarian cancers cannot grow and disseminate in the absence of a microenvironment that is favorable. Different kinds of cells converge with tumor cells to create blood vessels which bring nutrients to the tumor, promote its growth and, unfortunately, paralyze the body’s natural immune response to the growth of cancer. We identified that dendritic cells – a type of immune cell – represent the most abundant kind of white blood cell in the microenvironment of ovarian cancers. This is remarkable because when we first identified them, these dendritic cells were viewed favorably, as the main orchestrators of the body’s protective immunity. However, we have since found that these cells are in fact recruited by ovarian cancer cells. When they are, they interfere with the capabilities of other cells to attack the tumor. Consequently, the elimination of this dendritic cell type may significantly increase survival of someone with aggressive ovarian cancer – we have found that this is the case in the animal models we’ve done in the lab.
We are currently working on changing these cells’ characteristics and biological capabilities through the delivery of something called “nanoparticles.” Our idea is that rather than merely eliminating these cells, we can be more efficient if we can promote their capacity to act as “Trojan Horses” against the tumor that they are infiltrating – seemingly harmless but in fact powerful against the tumor.
EH: I know that this kind of research takes time. What are the expected outcomes of your research?
JCG: Our goal is to transform non-tumor cell types in the ovarian cancer microenvironment from “bad cells” — accomplices in tumor growth and immunosuppression — to “good cells” that stimulate the body’s immune response and activate other immune cells to attack the tumor. Our final goal is to translate these strategies from the lab to the clinic and the patient, in order to complement existing ovarian cancer treatments.