Anti-angiogenic gene therapy with a combination of soluble Vascular Endothelial Growth Factors (sVEGFR) improves the efficacy of chemotherapy with paclitaxel for reducing ovarian cancer mean tumor volume (in cubic millimetres) as measured using magnetic resonance imaging. The study groups were: AdLacZ control, combination of AdsVEGFR-1, -2 and -3, combination of AdsVEGFR-1, -2, -3 and paclitaxel, bevacizumab monotherapy, paclitaxel monotherapy and carboplatin monotherapy. Effectiveness was assessed by survival time and surrogate measures such as sequential MRI, immunohistochemistry, microvessel density and tumor growth. Antiangiogenic gene therapy combined with paclitaxel significantly prolonged the mean survival compared to the controls and all other treatment groups (p=0.001). Tumors of the mice treated by gene therapy were significantly smaller than in the control group (p=0.021). The mean vascular density and total vascular area were also significantly smaller in the tumors of the gene therapy group (p=0.01).

The present application provides antibodies including antigen-binding fragment thereof that specifically recognizing Granulocyte-Macrophage Colony Stimulating Factor Receptor (GM-CSFRα). Also provided are methods of making and using these antibodies.

The present application provides antibodies including antigen-binding fragment thereof that specifically recognizing Granulocyte-Macrophage Colony Stimulating Factor Receptor (GM-CSFRα). Also provided are methods of making and using these antibodies.

The present invention relates to circular RNA platforms, their manufacturing processes from an engineered parental circular covalently closed synthetic plasmid DNA and, uses thereof. Novel engineered circular covalently closed plasmids comprising sequences capable of aiding in RNA circularization either autonomously or when processed with an engineered ligase are provided. The circular RNA platforms of the current invention have improved stability and increased half-life, display exceptional and stable protein production, while avoiding doublestranded intramolecular self-pairing RNA segments.

Microalgal mutant to produce high-value essential LCPUFA oils including eicosadienoic acid (EDA), dihomo-γ-linoleic acid (DGLA), arachidonic acid (ARA), and eicosapentaenoic acid (EPA) in various ratios in are provided.

The present disclosure relates to the fields of biotechnology, molecular biology and genetic engineering. In particular, the present disclosure relates to a genetically modified alga comprising a recombinant cytochrome c6 gene, methods of producing the same and applications thereof. The present disclosure also relates to a codon optimised nucleic acid sequence encoding a cytochrome c6 polypeptide, expression cassette, vectors and host cell thereof. In an embodiment, the present disclosure also relates to a method of increasing biomass and photosynthetic efficiency of algae.

The present disclosure relates to the fields of biotechnology, molecular biology and genetic engineering. In particular, the present disclosure relates to a genetically modified alga comprising a recombinant cytochrome c6 gene, methods of producing the same and applications thereof. The present disclosure also relates to a codon optimised nucleic acid sequence encoding a cytochrome c6 polypeptide, expression cassette, vectors and host cell thereof. In an embodiment, the present disclosure also relates to a method of increasing biomass and photosynthetic efficiency of algae.

Disclosed are means of suppressing production of the inflammatory cytokine TNF-alpha through contact-dependent and contact-independent means by fibroblast populations and products and/or derivatives of fibroblast populations. In one embodiment, fibroblasts are cultured under conditions allowing proliferation of said fibroblasts, wherein said proliferative status of fibroblasts correlates with the ability to directly suppress TNF-alpha production, and/or to release one or more factors capable of suppressing TNF-alpha production. In one embodiment, fibroblasts are used for treatment of inflammatory diseases by their ability to suppress TNF-alpha production. In other embodiments, conditioned media and/or exosomes of said fibroblasts are utilized to treat inflammatory diseases by their ability to suppress TNF-alpha production.

Disclosed are means of suppressing production of the inflammatory cytokine TNF-alpha through contact-dependent and contact-independent means by fibroblast populations and products and/or derivatives of fibroblast populations. In one embodiment, fibroblasts are cultured under conditions allowing proliferation of said fibroblasts, wherein said proliferative status of fibroblasts correlates with the ability to directly suppress TNF-alpha production, and/or to release one or more factors capable of suppressing TNF-alpha production. In one embodiment, fibroblasts are used for treatment of inflammatory diseases by their ability to suppress TNF-alpha production. In other embodiments, conditioned media and/or exosomes of said fibroblasts are utilized to treat inflammatory diseases by their ability to suppress TNF-alpha production.

Provided are use of an Echovirus 25 (ECHO25) or a modified form thereof, or a nucleic acid molecule comprising a genomic sequence or cDNA sequence of the ECHO25 or a modified form thereof, or a complementary sequence of the genomic sequence or cDNA sequence, in treatment of a tumor in a subject, and in the manufacture of a medicament for treatment a tumor in a subject.