The invention relates to improved culture methods for expanding epithelial stem cells and obtaining organoids, to culture media involved in said methods, and to uses of said organoids.

The invention relates to improved culture methods for expanding epithelial stem cells and obtaining organoids, to culture media involved in said methods, and to uses of said organoids.

The present invention relates to a method for producing extracellular vesicles (EV) in large quantities by using a peptide derived from Noxa protein that plays a key role in apoptosis and derivatives thereof, and the use of the peptide for promoting extracellular vesicle production and the method for producing extracellular vesicles by using the same of the present invention can efficiently and uniformly mass-produce extracellular vesicles, and can produce extracellular vesicles which load drugs passing poorly through cellular membranes as well as recombinant proteins or plasmid DNA.

The present invention is based, in part, on cancer vaccine compositions that comprise PTEN- and p53-deficient cancer cells with activated TGFβ-Smad/p63 signaling pathway, and methods for using same to prevent and/or treat cancer.

The invention provides for modified reovirus nucleic acid sequences and modified reovirus polypeptide sequences as well as reoviruses containing such modified nucleic acid or polypeptide sequences. The invention also provides for pharmaceutical compositions that include reoviruses having a modified sequence as well as methods of making and using such reoviruses.

The present invention provides a combination therapy which relies on a small molecule immune stimulator—cyclic-di-nucleotide (CDN)—that activates DCs via a recently discovered cytoplasmic receptor known as STING (Stimulator of Interferon Genes) formulated with allogeneic human tumor cell lines engineered to secrete high amounts of GM-CSF. This combination therapy can provide an ideal synergy of multiple tumor associated antigens, DC recruitment and proliferation, coupled with a potent DC activation stimulus.

The present invention provides a combination therapy which relies on a small molecule immune stimulator—cyclic-di-nucleotide (CDN)—that activates DCs via a recently discovered cytoplasmic receptor known as STING (Stimulator of Interferon Genes) formulated with allogeneic human tumor cell lines engineered to secrete high amounts of GM-CSF. This combination therapy can provide an ideal synergy of multiple tumor associated antigens, DC recruitment and proliferation, coupled with a potent DC activation stimulus.

Disclosed are lysine specific histone demethylase-1 (LSD1) inhibitors in methods and compositions for immune check-point inhibition. The invention also relates to proteinaceous molecules and their use in altering at least one of (i) formation, (ii) 5 N proliferation, (iii) maintenance, (iv) epithelial to mesenchymal cell transition (EMT), or (v) mesenchymal to epithelial cell transition (MET) of an LSD1 overexpressing cell.

Disclosed are combination therapies including administration of I-DASH inhibitors and PGE2 antagonists, and the use of such therapies in the treatment of cell proliferative diseases.

Disclosed are combination therapies including administration of I-DASH inhibitors and PGE2 antagonists, and the use of such therapies in the treatment of cell proliferative diseases.