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Researchers at the National Cancer Institute (NCI) have developed orthotopic allograft models for pancreatic cancer that utilize low passage primary pancreatic adenocarcinoma cells or tumor fragments implanted into the cancer-free pancreata of recipient syngeneic immunocompetent mice. Tumor development in these models is more synchronized, latency is substantially shortened, and tumors develop only in one location, as pre-determined by the choice of a site for cells/tumor fragment implantation.

Neurofibromatosis type 1 (NF1) is a genetic disorder affecting 1 per 3000 individuals on average. Patients develop a variety of developmental benign and malignant pathologies. The most common tumors associated with NF1 are peripheral sheath tumors, including neurofibromas, optical gliomas, and malignant peripheral nerve sheath tumors.

The proto-oncogene c-Myc is deregulated and overexpressed in ~70% of all cancers. Thus, c-Myc is an attractive therapeutic target since disrupting c-Myc activity could be used as pan-chemotherapy. Beyond cancer, Myc is also a positive effector of tissue inflammation, and its function has been implicated in the pathophysiology of heart failure. Because c-Myc is a transcription factor, a rationally designed small molecule targeting c-Myc would be required to exhibit significant specificity.

RNA interference (RNAi) is a naturally occurring post-transcriptional gene regulation process that represses the expression of specific genes. Exploiting endogenous RNAi by externally-delivered small-interfering RNA (siRNA) is a promising therapeutic for the treatment of various diseases representing several major unmet medical needs. 

Ataxia telangiectasia mutated and Rad3 Related (ATR) protein kinase is essential for regulating DNA damage checkpoints during the cell cycle. ATR, is phosphorylated at threonine 1989 site (T1989) in response to DNA damage and ATR activation leads to activation of downstream substrates, signaling cascades and cell cycle arrest. ATR is a potential target for anticancer therapeutics to induce cancer cell death by inhibiting cell cycle arrest pathways in response to chemotherapeutics.

Diazeniumdiolates comprise a diverse class of NO-releasing compounds and materials that are known to exhibit sufficient stability to be useful as therapeutics.

The invention relates to novel lipid-based nanoparticles (liposomes) for use in targeted, on demand and on site drug delivery. The particles include a wall surrounding a cavity, wherein the wall is comprised of:

1. A lipid bilayer comprising 1,2-bis(tricosa-10,12-diynoyl)-sn-glycero-3-phosphocholine (DC_8,9PC), dipalmitoylphosphatidylcholine (DPPC), and 1,2-distearoyl-sn-glycero-3-

phosphoethanolamine-N-[methoxy(polyethylene glycol)-2000] (DSPE-PEG2000), and

This technology consists of highly specific rabbit monoclonal antibodies reactive with phosphorylated tyrosine located at amino acid 1235 in the human MET sequence. Binding to this pYl235 residue is independent of the phosphorylation of other tyrosines in the vicinity (1230 and 1234), does not cross-react with these nearby phosphotyrosine residues, and does not occur when Y1235 is unphosphorylated.

Most early work on CD133 was carried out using one of two monoclonal antibodies (mAbs), AC133 and AC141, which recognize an undefined glycosylated epitope of CD 133.

The invention listed below is owned by an agency of the U.S. Government and is available for licensing and/or co-development in the U.S. in accordance with 35 U.S.C. 209 and 37 CFR part 404 to achieve expeditious commercialization of results of federally-funded research and development.