Abstract: Disclosed herein are triazine compounds (e.g., triazines and pyrazole triazines) and methods of treating diseases and/or conditions (e.g., inflammation) with the triazine compounds disclosed herein. In several embodiments, the disclosed triazine compounds are used for the inhibition of Jumonji domain-containing protein D3 (JMJD3) and/or the treatment of JMJD3 related disease states.

Abstract: Disclosed herein are compounds (e.g., pyrrole compounds, carboxy pyrroles, etc.), including pharmaceutical compositions that include one or more of such compounds (e.g., carboxy pyrroles). Also disclosed are methods of making carboxy pyrrole compounds. Also disclosed herein are methods of treating diseases and/or conditions (e.g., inflammation and/or cancer) with the carboxy pyrrole compounds disclosed herein.

Abstract: Disclosed herein are quinazolinyl compounds, compositions, and methods of use thereof. The compounds may be used in the treatment of kinase-related disorders (including cancer, autoimmune disease, and Duchenne muscular dystrophy).

Abstract: The present disclosure provides compounds and compositions capable of treating cancer or an autoimmune disease, such as Crohn's disease, and methods of use thereof.

Abstract: Disclosed herein are quinazolinyl compounds, compositions, and methods of use thereof. The compounds may be used in the treatment of autoimmune disorders or cancer.

Abstract: Disclosed herein are quinazolinyl compounds, compositions, and methods of use thereof. The compounds may be used in the treatment of autoimmune disorders or cancer.

Abstract: Disclosed herein are quinazolinyl compounds, compositions, and methods of use thereof. The compounds may be used in the treatment of autoimmune disorders or cancer.

Abstract: The present disclosure provides compounds and compositions capable of treating cancer or an autoimmune disease, such as Crohn's disease, and methods of use thereof.

Abstract: The present embodiments provide for compositions and methods that regulate microRNA-binding protein-mediated miRNA biogensis; for example Lin28-mediated biogenesis of let-7; and in particular Lin28A-recruited 3? terminal uridylyl transferase (TUTase) uridylation of pre-let-7. A particular embodiment provide compositions and methods for screening for agents that inhibit TUTase-dependent Lin28A-mediated repression of let-7 miRNA.

Abstract: The present embodiments provide for compositions and methods that regulate microRNA-binding protein-mediated miRNA biogensis; for example Lin28-mediated biogenesis of let-7; and in particular Lin28A-recruited 3? terminal uridylyl transferase (TUTase) uridylation of pre-let-7. A particular embodiment provide compositions and methods for screening for agents that inhibit TUTase-dependent Lin28A-mediated repression of let-7 miRNA.

Abstract: This application discloses methods of treating, preventing, and diagnosing colorectal cancer and IBD in a subject comprising administering an effective dose of antisense miR-133? or AFTPH to the subject or detecting expression levels of miR-133? and AFTPH.

Abstract: The present embodiments provide for compositions and methods that regulate microRNA-binding protein-mediated miRNA biogensis; for example Lin28-mediated biogenesis of let-7; and in particular Lin28A-recruited 3? terminal uridylyl transferase (TUTase) uridylation of pre-let-7. A particular embodiment provide compositions and methods for screening for agents that inhibit TUTase-dependent Lin28A-mediated repression of let-7 miRNA.

Abstract: The present embodiments provide for compositions and methods that regulate microRNA-binding protein-mediated miRNA biogenesis; for example Lin28-mediated biogenesis of let-7; and in particular Lin28A-recruited 3? terminal uridylyl transferase (TUTase) uridylation of pre-let-7. A particular embodiment provide compositions and methods for screening for agents that inhibit TUTase-dependent Lin28A-mediated repression of let-7 miRNA.

Abstract: The present embodiments provide for compositions and methods that regulate microRNA-binding protein-mediated miRNA biogensis; for example Lin28-mediated biogenesis of let-7; and in particular Lin28A-recruited 3? terminal uridylyl transferase (TUTase) uridylation of pre-let-7. A particular embodiment provide compositions and methods for screening for agents that inhibit TUTase-dependent Lin28A-mediated repression of let-7 miRNA.

Abstract: MicroRNA (miRNA) profiling of cells showed unique miRNA signatures for each of three Akt isoforms. Among differentially regulated miRNA species, the miR-200 family was downregulated in Akt2-expressing cells. Akt1 knockdown inhibited expression of miR-200 and promoted TGF?-induced epithelial-mesenchymal-transition (EMT) and a stem cell like phenotype. Carcinomas developing in MMTV-cErb2/Akt1?/? mice exhibited increased invasiveness because of EMT induced by miR-200 downregulation. EMT was found to be controlled by miRNA species that are regulated by the balance between Akt1 and Akt2, rather than overall Akt levels.

Abstract: Disclosed herein is a method for treating a tumor in a subject in need thereof comprising administering an enhancing amount of metformin and a reduced amount of one or more chemotherapeutic agents. One example of an enhancing amount of metformin is about 250 mg/day. Also disclosed is a Untreated method for preventing cancer or delaying the recurrence of cancer in a subject comprising administering an effective amount of metformin to the subject. In one example of such a method, the amount of metformin is about 75 mg/day. Also disclosed is a composition comprising an enhancing amount of metformin, and a reduced amount of one or more chemotherapeutic agents and a pharmaceutically acceptable carrier. Kits comprising metformin and one or more chemotherapeutic agents are also disclosed.

Abstract: MicroRNA (miRNA) profiling of cells showed unique miRNA signatures for each of three Akt isoforms. Among differentially regulated miRNA species, the miR-200 family was downregulated in Akt2-expressing cells. Akt1 knockdown inhibited expression of miR-200 and promoted TGF?-induced epithelial-mesenchymal-transition (EMT) and a stem cell like phenotype. Carcinomas developing in MMTV-cErb2/Akt1?/? mice exhibited increased invasiveness because of EMT induced by miR-200 downregulation. EMT was found to be controlled by miRNA species that are regulated by the balance between Akt1 and Akt2, rather than overall Akt levels.