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Biotech / Medical : Gene therapy -- Ignore unavailable to you. Want to Upgrade?

To: scaram(o)uche who wrote (264)	12/4/2001 2:56:56 PM
From: tuck	Read Replies (1) \| Respond to of 319

>>Neil Goldstein is V.P. R&D at DGI Biotechnologies.<< Hmmm . . . these folks seem to be doing a lot of work together. If memory serves, INGN exclusively licensed the mda-7 gene from Corixa (would have to go back and dig a little), at least for gene therapy. Does Goldstein's c.v. mention a tour there? Has there been any mention before of an INGN/DGI connection? >>A combinatorial approach for selectively inducing programmed cell death in human pancreatic cancer cells. Proc Natl Acad Sci U S A 2001 Aug 28;98(18):10332-7 (ISSN: 0027-8424) Su Z; Lebedeva IV; Gopalkrishnan RV; Goldstein NI; Stein CA; Reed JC; Dent P; Fisher PB [Find other articles with these Authors] Department of Urology, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA. Pancreatic cancer is an extremely aggressive neoplasm whose incidence equals its death rate. Despite intensive analysis, the genetic changes that mediate pancreatic cancer development and effective therapies for diminishing the morbidity associated with this disease remain unresolved. Through subtraction hybridization, we have identified a gene associated with induction of irreversible growth arrest, cancer reversion, and terminal differentiation in human melanoma cells, melanoma differentiation associated gene-7 (mda-7). Ectopic expression of mda-7 when using a recombinant adenovirus, Ad.mda-7, results in growth suppression and apoptosis in a broad spectrum of human cancers with diverse genetic defects, without exerting deleterious effects in normal human epithelial or fibroblast cells. Despite the apparently ubiquitous antitumor effects of mda-7, pancreatic carcinoma cells are remarkably refractory to Ad.mda-7 induced growth suppression and apoptosis. In contrast, the combination of Ad.mda-7 with antisense phosphorothioate oligonucleotides, which target the K-ras oncogene (a gene that is mutated in 85 to 95% of pancreatic carcinomas), induces a dramatic suppression in growth and a decrease in cell viability by induction of apoptosis. In mutant K-ras pancreatic carcinoma cells, programmed cell death correlates with expression and an increase, respectively, in MDA-7 and BAX proteins and increases in the ratio of BAX to BCL-2 proteins. Moreover, transfection of mutant K-ras pancreatic carcinoma cells with an antisense K-ras expression vector and infection with Ad.mda-7 inhibits colony formation in vitro and tumorigenesis in vivo in nude mice. These intriguing observations demonstrate that a combinatorial approach, consisting of a cancer-specific apoptosis-inducing gene and an oncogene inactivation strategy, may provide the foundation for developing an effective therapy for pancreatic cancer.<< snip You see any overlap with DGI work? Cheers, Tuck