Abstract: The presently disclosed subject matter provides antibodies or antigen-binding fragments thereof that bind to uPAR and methods of using such antibodies or antigen-binding fragments thereof same.

Abstract: The present disclosure provides methods for treating Covid-related lung fibrosis or rectal cancer in a subject. Also disclosed herein are methods for delaying or mitigating the effects of aging in a subject in need thereof. The methods of the present technology comprise administering to the subject an effective amount of engineered immune cells that express a uPAR-specific chimeric antigen receptor.

Abstract: The presently disclosed subject matter provides for antigen-recognizing receptors that specifically target uPAR and cells comprising such uPAR-targeted antigen-recognizing receptors. The presently disclosed subject matter further provides uses of the uPAR-targeted antigen-recognizing receptors for treatment.

Abstract: The presently disclosed subject matter provides for antigen-recognizing receptors that specifically target uPAR and cells comprising such uPAR-targeted antigen-recognizing receptors. The presently disclosed subject matter further provides uses of the uPAR-targeted antigen-recognizing receptors for treatment.

Abstract: The presently disclosed subject matter provides antibodies or antigen-binding fragments thereof that bind to uPAR and methods of using such antibodies or antigen-binding fragments thereof same.

Abstract: The present technology provides methods for treating and/or preventing pancreatic cancer using inhibitors of Type 2 cytokine signaling. Also disclosed herein are methods for selecting a pancreatic cancer patient for treatment with an inhibitor of Type 2 cytokine signaling. Kits for use in practicing the methods are also provided.

Abstract: The use of mitogen activated kinase inhibition therapy in combination with receptor tyrosine kinase therapy for the treatment of cancer is described.

Abstract: The invention provides compositions, methods, and kits for the treatment of acute myeloid leukemia in a subject.

Abstract: The present invention encompasses the recognition that epigenetic dependencies in sarcoma can be therapeutic targets. The present invention encompasses a method of treating sarcoma comprising the step of administering a PRC1.1 inhibitory agent to a subject suffering from or susceptible to sarcoma. In some embodiments, the PRC1.1 inhibitory agent is a KDM2B inhibitory agent, a BCOR inhibitory agent, and/or a PCGF1 inhibitory agent. In some embodiments, the PRC1.1 inhibitory agent reduces interaction of the SS18-SSX fusion protein with a polycomb repressive complex. In some embodiments, administration of the PRC1.1 inhibitory agent results in differentiation of synovial sarcoma cells into a more mesenchymal like state, comprising increased expression of COL1A1, SERPINE1 (PAI-1), ACTA2 (a-SMA), CDKN1A and/or CDKN2B.

Abstract: The invention provides compositions, methods, and kits for the treatment of acute myeloid leukemia in a subject.

Abstract: The use of mitogen activated kinase inhibition therapy in combination with receptor tyrosine kinase therapy for the treatment of cancer is described.

Abstract: The invention provides compositions, methods, and kits for the treatment of acute myeloid leukemia in a subject.

Abstract: PDGFRb inhibitors and the use of such inhibitors to treat mutant p53-expressing tumors are described. The present disclosure encompasses the discovery that mutant p53-induced upregulation of the platelet-derived growth factor receptor b (PDGFRb) contributes to invasion and/or metastasis of tumors expressing mutant p53. Specifically, the present disclosure encompasses the discovery that mutant p53 can disrupt a p73/NF-Y complex (which can repress PDGFRB transcription), leading to transcription of PDGFRb. The present disclosure therefore provides, at least in part, PDGFRb modulators (e.g., activators or inhibitors) for use in medicine, and specifically in diagnosis, treatment and/or prevention (e.g., delay of onset) of certain disorders, e.g., cancer.

Abstract: Provided is a mosaic mouse model for use in determining the potency of an shRNA in vivo for reducing survival of cancer cells of chemotherapy-resistant leukemia. The syngeneic mouse recipient is transplanted with tet-on competent leukemia cells carrying a bicistronic nucleic acid construct comprising a promoter operably linked to a fusion gene associated with chemotherapy-resistant leukemia, and a sequence encoding a reverse tet-transactivator protein, such that both coding sequences are co-expressed from the promoter. Also provided are methods of treating soft tissue cancers.

Abstract: Provided is a single construct combining a sequence encoding an RNAi molecule, a sequence encoding a reporter, and a target sequence specific for the RNAi molecule. The construct can be used to determine the potency of the encoded RNAi molecule in a direct and unbiased way. These results can be used to inform the design of potent RNAi molecules of various types and can be extended to several other applications, including: (1) generation of tiled libraries comprising every possible RNAi molecule-encoding sequence for a given gene target; (2) large-scale parallel validation of RNAi molecules targeting many genes to generate validated RNAi molecule-encoding libraries; (3) experimental comparison of design algorithms and strategies; and (4) investigation of RNAi biology in target site mutagenesis assays by screening pools containing single nucleotide changes in target sites and/or in the RNAi molecule to identify the most relevant sequence characteristics of potent RNAi-target site predictions.

Abstract: Provided is a single construct combining a sequence encoding an RNAi molecule, a sequence encoding a reporter, and a target sequence specific for the RNAi molecule. The construct can be used to determine the potency of the encoded RNAi molecule in a direct and unbiased way. These results can be used to inform the design of potent RNAi molecules of various types and can be extended to several other applications, including: (1) generation of tiled libraries comprising every possible RNAi molecule-encoding sequence for a given gene target; (2) large-scale parallel validation of RNAi molecules targeting many genes to generate validated RNAi molecule-encoding libraries; (3) experimental comparison of design algorithms and strategies; and (4) investigation of RNAi biology in target site mutagenesis assays by screening pools containing single nucleotide changes in target sites and/or in the RNAi molecule to identify the most relevant sequence characteristics of potent RNAi-target site predictions.

Abstract: Provided is a mosaic mouse model for use in determining the potency of an shRNA in vivo for reducing survival of cancer cells of chemotherapy-resistant leukemia. The syngeneic mouse recipient is transplanted with tet-on competent leukemia cells carrying a bicistronic nucleic acid construct comprising a promoter operably linked to a fusion gene associated with chemotherapy-resistant leukemia, and a sequence encoding a reverse tet-transactivator protein, such that both coding sequences are co-expressed from the promoter. Also provided are methods of treating soft tissue cancers.

Abstract: The invention relates to recombinant vectors for inducible and/or tissue specific expression of double-stranded RNA molecules that interfere with the expression of a target gene. In certain embodiments, the invention relates to the use of Tet (tetracycline)-responsive RNA Polymerase II (Pol II) promoters (e.g., TetON or TetOFF) to direct inducible knockdown in certain cells of an integrated or an endogenous gene, such as p53. The invention also relates to a method for producing transgenic animals (e.g., mice) expressing inducible (such as tetracycline-regulated), reversible, and/or tissue-specific double-stranded RNA molecules that interfere with the expression of a target gene.

Abstract: In one aspect, the invention generally relates to use of miR-34 as a biomarker to estimate TP53 function in a cell. In another aspect, the invention generally relates to multiple uses of miR-34 and siRNAs functionally and structurally related to miR-34 for the treatment of cancer.

Abstract: Provided is a mosaic mouse model for use in determining the potency of an shRNA in vivo for reducing survival of cancer cells of chemotherapy-resistant leukemia. The syngeneic mouse recipient is transplanted with tet-on competent leukemia cells carrying a bicistronic nucleic acid construct comprising a promoter operably linked to a fusion gene associated with chemotherapy-resistant leukemia, and a sequence encoding a reverse tet-transactivator protein, such that both coding sequences are co-expressed from the promoter. Also provided are methods of treating soft tissue cancers.