The present invention provides a novel secretion reducing agent and novel secretion reducing method for reducing extracellular vesicle secretion from cells. The extracellular vesicle secretion reducing agent of the present invention is characterized in that it contains an inhibitor of a serine synthesis pathway. The cells are, for example, cancer cells such as colorectal cancer cells, lung cancer cells, melanoma cells, breast cancer cells, pancreas cancer cells, and multiple myeloma cells.

According to some aspects of the present disclosure, a platform and a set of consumables and reagents are provided to seamlessly integrate with and elegantly transform integrated Single Cell Next Generation Sequencing (SCNGS) platforms for dramatic improvements in efficiency and cost-effectiveness. Such aspects allow for the coupling of antibody polynucleotides, which have elements comprised of a universal sequence, a barcode sequence, and gene or nucleotide targeting sequences, together with individual cells into micron-sized vessels, as well as with beads containing primers which are separately barcoded. The process is performed in such a manner so to allow the primers contributed by the beads work with the primers contributed by the polynucleotide after it is digested with a restriction enzyme, to allow for the amplified DNA from that cell to be tagged for not only its cell identity but also for its sample identity. This allows cells to be multiplexed or pooled prior to encapsulation into the vessels, allowing numerous samples to be run through equipment and workflows that accomplish this encapsulation at the same time.

This invention concerns pathological angiogenesis and cancer, related treatment methods, and related compositions. Also disclosed are related diagnosis kits and methods.

The present application discloses roles for miR-93 in treating hypoxia and ischemia. Endothelial cells (HUVEC) and myocytes (C2C12) expressed miR-93 and up-regulated miR-93 in response to hypoxia and serum starvation. Over-expression of miR-93 in HUVECs promoted cell proliferation, prevented hypoxia-induced apoptosis, and enhanced endothelial cell tube formation. miR-93 knockdown in HUVECs resulted in increased hypoxia-induced apoptosis and decreased tube formation. Over-expression or knockdown of miR-93 in myocytes resulted in reduced or increased hypoxia-induced apoptosis, respectively. Down-regulation of miR-93 in C57BL/6 mice with antagomiR resulted in attenuated perfusion recovery (% non-ischemic leg at day-21: Scramble 85.22.9 vs. AntagomiR-93 67.96). Over-expression of miR-93 in BALB/C mice improved perfusion recovery (% non-ischemic leg at day 21: PremiR-93 757.5 vs. Scramble 59.62.5). The present invention encompasses the use of miR-93 and regulation of miR-93 to treat and prevent hypoxia, ischemia, and other injuries, diseases, disorders, and conditions associated with ischemia.

The present invention relates to a therapeutic compound comprising: an agent that inhibits the activity of at least one gene selected from the group consisting of HIC1, FOXS1, CREB5, IRF7, POU2F2, STAT4, TCF4, and/or an agent that enhances the activity of at least one gene selected from the group consisting of MAF, MEOX2, SIX2.

The disclosure is directed to compositions and methods that are useful for the treatment of a neoplasia. Specifically, methods for inducing cell death or reducing cell survival of a neoplastic cell (e.g., rhabomyosarcoma) and methods of treating a subject having a neoplasia characterized by a loss of VPS4 expression are disclosed.

Compositions and methods for treating FSHD and for identifying agents useful for the treatment of FSHD.

Described herein are molecules for editing a cell. The molecules described herein generally comprise the following covalently-linked components and a nucleic acid encoding a guide RNA (gRNA) sequence targeting a target region in a cell and a region homologous to the target region comprising a change in sequence relative to the target region.

The described invention provides a method of treating a patient with an epithelial cancer comprising administering a composition comprising a therapeutic amount of an inhibitor of a BTK protein and one or more chemotherapeutic agent(s) selected from the group consisting of an antimetabolite, a platinum coordination compound, an alkylating agent and a combination thereof, wherein the composition is effective to reduce one or more of tumor cell growth, tumor cell clonogenicity, tumor cell proliferation, tumor cell viability and tumor volume and the therapeutic amount of the inhibitor of a BTK protein and the one or more chemotherapeutic agent(s) exerts a synergistic effect. The described invention also provides methods of treating a chemotherapy drug-resistant cancer and sensitizing a cancer patient to chemotherapy.

This invention relates to the use of CRISPR nucleic acids to screen for essential and non-essential genes and expendable genomic islands in bacteria, archaea, algae and/or yeast, to kill bacteria, archaea, algae and/or yeast, to identify the phenotype of a gene or genes, and/or to screen for reduced genome size and/or a gene deletion in bacteria, archaea, algae and/or yeast.