Accession Number : ADA467585


Title :   Intra-Prostate Cancer Vaccine Inducer


Descriptive Note : Final rept. 26 Jan 2004-25 Jan 2007


Corporate Author : ANTIGEN EXPRESS INC WORCESTER MA


Personal Author(s) : Humphreys, Robert ; Xu, Minzhen ; von Hofe, Eric ; Lu, Xueqing ; Hillman, Gilda


Full Text : https://apps.dtic.mil/dtic/tr/fulltext/u2/a467585.pdf


Report Date : Jul 2006


Pagination or Media Count : 61


Abstract : Antigen Express has generated potent human Ii-RNAi constructs for use in prostate cancer therapy. We identified active Ii- RNAi sequences, selected the most active promoter (CMV) and demonstrated good suppression of Ii. The constructs also were used to enhance a gp120 DNA vaccine model, confirming that Ii suppression increases the potency of a tumor cell and DNA vaccine. We have shown that an anti-tumor immune response can be strongly induced by intratumoral induction of the MHC class 1+/11+/11- phenotype and effectively and specifically protects mice from re-challenge by the same tumor cells. The frequency and dose of plasmid injections have been optimized as well as the dose of IL-2 to induce a potent immune response following generation of the MHC class 1+/11+/11- phenotype. The duration of plasmid in cells in vitro and the in vivo have been evaluated and indicate that this immunotherapy should be safe. Finally, we have found that DU-145, PC-3, and LNcap prostate cell lines are heterogeneous for MHC class 11 and 11 expression and that PC-3 and LNcap cells are MHC class II-/Ii+. Overall, our results suggest that Ii suppression has the potential to be an elegant method for prostate cancer immunotherapy.


Descriptors :   *DEOXYRIBONUCLEIC ACIDS , *RIBONUCLEIC ACIDS , *VACCINES , *INJECTIONS(MEDICINE) , *ANTIGENS , *PROSTATE CANCER , INJECTION , IN VITRO ANALYSIS , DOSAGE , RESPONSE(BIOLOGY) , IMMUNITY , IMMUNOTHERAPY , PROSTATE GLAND , SUPPRESSION , CELLS(BIOLOGY) , IN VIVO ANALYSIS , MICE , THERAPY , PLASMIDS , NEOPLASMS


Subject Categories : Biochemistry
      Medicine and Medical Research


Distribution Statement : APPROVED FOR PUBLIC RELEASE