Dr. Rachana Garg is evident from her educational background and trainings, her research experience spans over 10 years in the field of molecular carcinogenesis, cancer chemoprevention, cancer signaling and biochemistry. During undergraduate studies, She worked closely with oral cancer patients and detected and typed the HPV prevalence in the clinical samples. A short but an inspiring experience had made her career goal clearer and allowed her to stay focused in cancer biology field thus far. Moving ahead with her research interest, her doctoral work specifically focused on delineating the mechanism of turmeric/curcumin mediated chemoprevention in vivo model systems (liver, lung, skin and oral tissues of mice and hamsters) and to identify surrogate end point biomarkers for drug effect measurements. During her Ph.D. research, she gained thorough experience in working with in vivo cancer models, broadly targeting the carcinogenic process by employing chemo preventive compounds. To extensively explore the essential mechanisms in cancer development and to enhance her acquired skills in the cancer biology field, she joined the renowned signal transduction laboratory of Dr. Kazanietz at UPenn, with the main interest in protein kinase C (PKC). she focused her postdoctoral studies largely on PKC, a kinase that is upregulated in many epithelial cancers. Of note, the mechanism by which this kinase contributes to the initiation and maintenance of the prostate cancer phenotype is largely unknown and remains uninvestigated thus far. Using cellular, biochemical, and molecular profiling approaches, she characterized the signaling markers and molecular signature of the prostate lesions driven by PKC epsilon overexpression and Pten loss. she generated organ-specific models for transgenic expression of PKC isozymes and determined the phenotypical consequences of crossing these mice with other models harboring oncogenic alterations such as Pten and K-Ras relevant to prostate, oral and lung cancer. Furthermore, by intercrossing lung-specific mutant Ras mice (LSL-K-rasG12D) with PKC KO mice, I demonstrated that deletion of the PKCgene (PRKCE) in mice impaired Ras-mediated lung tumorigenesis. Using human prostate cancer clinical samples, my study established correlation of oncogenic PKC epsilon overexpression with other common alterations (Pten loss, NF-kB hyperactivation, COX-2 and CXCl13 up-regulation) in prostate cancer. • Experienced in mammalian tissue culture, microarray and bioinformatics analysis, mouse biology, xenograft and transgenic mouse models. • Excellent communication and organizational skills. Strong interpersonal skills. Ability to work independently and in matrix settings. • Skilled in scientific writings, grant applications and oral presentations • Leadership/management and organizational role.
Dr. Rachana Garg's research experiences have launched a long-term interest in understanding the indepth mechanisms underlying carcinogenesis, with the ultimate goal of identifying targets for drug-based therapies and developing strategies for overcoming treatment-related resistance observed in most prevalent cancer including prostate, lung and oral squamous cell carcinoma.