Pancreatic ductal adenocarcinoma (PDAC) is the fourth leading cause of cancer death in the United States. In spite of recent therapeutic advances, long-term survival in PDAC is often limited to patients who have had surgery in the early stage of the disease. The biological aggressiveness of PDAC is due, in part, to the tumor's resistance to chemotherapy and to its propensity to metastasize even when the primary tumor is small. PDAC is also characterized by a high frequency of mutations in the Kras gene, as well as by the inactivation of several tumor suppressor genes such as p16Ink4a, p53 and Smad4. PDAC also displays abnormal upregulation of multiple mitogenic and angiogenic growth factors and their cognate high affinity receptors. Together, these alterations serve to enhance the biological aggressiveness of PDAC.
Dartmouth researchers have now found that stable expression of cyclin D1 shRNA by lentiviral vectors and sustained suppression of cyclin D1 expression in human pancreatic carcinoma cells results in attenuated growth of the tumor cells in anchorage-dependent and -independent conditions, as well as decreased invasiveness in vitro. Moreover, a single intra-tumoral injection of recombinant lentiviruses targeting cyclin D1 attenuate the growth of pre-existing tumors in a model system by decreasing cancer cell proliferation and angiogenesis. Therefore, this technology is useful in treating pancreatic cancer. The initial findings have been published in the journal Cancer Gene Therapy (Deharvengt et al. doi:10.1038/cgt.2009.75 (2009)).
This technology is claimed in the published PCT Application No. PCT/US2010/037716. We are seeking an industrial partner interested in its commercialization. (Ref: J530)
Last Updated: 7/24/12