Raj Batra

I am a translational physician-scientist who began studying lung cancer over 20 years ago, with the explicit goal of eradicating the disease. My commitment to that endeavor has not wavered. Based on translational expertise in gene and cell based therapy that was developed at UNC, I was recruited to UCLA in 1998 with a VA-Advanced Career Development Award to build a translational experimental therapeutics program for lung cancer. I was awarded my first NIH-RO1 in 1999 to study viral gene transfer into lung cancer cells, while jointly working as the Chief Architect of the UCLA Translational Gene and Cell Based Therapy program for treating lung cancer. That program led to UCLA being awarded a NCI Specialized Program of Research Excellence (SPORE) grant in Lung Cancer, the development of a clinical grade vector by NIH-Rapid Assistance to Intervention Development (RAID), and regulatory approvals by the NIH/OBA and FDA for a Phase 1 clinical trial in 2007. Unfortunately, the “academic credit” and accrued institutional resources from this work were withheld towards career development and independence for this physician-scientist by the administrative Principal Investigator, an appointed University vice-Chancellor. The “academic politics” were compounded by an administrative blockade of access to University Collaborative and Technical Infrastructure, as well as extramural funding mechanisms. In 2011, the basis for this blockade was attributed to an administrative (re)interpretation that I was “not a University employee.” Nevertheless, our important scientific mission and goals have persevered. In fact, key observations made in our pre-clinical studies on applications of viral gene therapy changed my entire frame of reference on lung cancer. I realized that gene therapy and Ad-virotherapy strategies can be quite effective if they are applied correctly for treating clinical disease. A key caveat that seemed to lead us astray in achieving translational potential was that our preclinical models were rather inadequate representations of disease in situ. By using inadequate models for proof-of-concept, we lost disease complexity, and consequently, predictability of effect. That realization prompted consideration that tumor heterogeneity confounded not only our gene therapy strategies, but possibly the effectiveness of all therapeutics. It made little sense to follow a status quo that we foresaw as unsuccessful; a different approach to study lung cancer needed to be developed. Our work since 2006 is a result of pursuing that novel idea. Our recent publications provide key pilot feasibility data, and a philosophical foundation on which we are challenging existing paradigms. We have developed a rational discovery paradigm for identifying the key molecular drivers of aggressive tumor cell behaviors. We are desirous of implementing this strategy to develop biomarker-signatures of aggressive disease phenotypes, and to jointly identify candidate combinatorial targets for treating aggressive disease. I and members of my team seek funding and strategic investment for advancing this strategy to clinical implementation. To that end, we bring an innovative (world-leading), scientifically sound approach, and comprehensive “bedside to bench to bedside” capabilities to the ongoing study and rationally-derived targeted treatment of lung cancer.