Abstract: The disclosure includes compositions comprising synthetic zinc finger degrons, and their use with non-naturally occurring or engineered programmable nucleases. Compositions specifically targeting the engineered programmable nucleases for control of gene editing outcomes, and compositions, systems and method of use are further detailed.

Abstract: The present invention features methods for increasing sensitivity and/or reversing resistance to chemotherapy, methods for treating or preventing a cancer in a subject, methods for treating clonal hematopoiesis of indeterminate potential in a subject, and methods of identifying resistance or sensitivity to chemotherapy in a subject. In some embodiments, the methods contain the step of administering an agent that inhibits the expression or activity of a Protein phosphatase 1D (PPM1D) polypeptide or polynucleotide. The present invention also features compositions for increasing sensitivity and/or reversing resistance to chemotherapy.

Abstract: The invention features methods for characterizing a cancer as sensitive or resistant to Bcl6 therapies, as well as compositions and methods for inducing the degradation or polymerization of a polypeptide of interest.

Abstract: The methods described herein include methods for the treatment of subjects who have Clonal Hematopoiesis of Indeterminate Potential (CHIP) or a Philadelphia-negative myeloproliferative neoplasm (MPN), e.g., polycythaemia vera (PV) or essential thrombocythaemia (ET), using inhibitors of JAK-STAT signaling.

Abstract: The present invention features methods for increasing sensitivity and/or reversing resistance to chemotherapy, methods for treating or preventing a cancer in a subject, methods for treating clonal hematopoiesis of indeterminate potential in a subject, and methods of identifying resistance or sensitivity to chemotherapy in a subject. In some embodiments, the methods contain the step of administering an agent that inhibits the expression or activity of a Protein phosphatase 1D (PPM1D) polypeptide or polynucleotide. The present invention also features compositions for increasing sensitivity and/or reversing resistance to chemotherapy.

Abstract: Disclosed are methods for predicting a response of a subject with myelodysplastic syndrome to treatment with a hypomethylating agent, for example using a sample obtained from the subject. The methods can be used to select a subject for treatment with a hypomethylating agent, and/or measure a subject's response to therapy and/or disease progression/regression. The methods include detecting, in a nucleic acid sample obtained from a subject, one or more mutations of any one or more genes selected from Table 3a.

Abstract: The present invention features methods for increasing sensitivity and/or reversing resistance to chemotherapy, methods for treating or preventing a cancer in a subject, methods for treating clonal hematopoiesis of indeterminate potential in a subject, and methods of identifying resistance or sensitivity to chemotherapy in a subject. In some embodiments, the methods contain the step of administering an agent that inhibits the expression or activity of a Protein phosphatase 1D (PPM1D) polypeptide or polynucleotide. The present invention also features compositions for increasing sensitivity and/or reversing resistance to chemotherapy.

Abstract: The present disclosure relates to therapeutic methods and clinically useful molecular switches, for which activity or degradation of a switch-presenting polypeptide can be precisely induced via administration or withdrawal of an FDA-approved drug. Certain aspects of the disclosure relate to an engineered drug-inducible heterodimeric system including a first polypeptide presenting a CRBN polypeptide disrupted for or lacking a DDB1-interacting domain and a second polypeptide presenting a CRBN polypeptide substrate, where binding between the CRBN polypeptide and the CRBN polypeptide substrate are inducible via administration of an FDA-approved thalidomide analog immunomodulatory drug (IMiD). Another aspect of the disclosure relates to a chimeric antigen receptor (CAR) that presents a minimal fragment of the CRBN polypeptide substrate IKZF3 capable of triggering proteasomal degradation of CAR upon administration of an FDA-approved IMiD.

Abstract: The application presently discloses a method of treating atherosclerosis in a human subject comprising administering an effective amount of an IL-8 inhibitor, an IL-6 inhibitor, and/or an IL-1? inhibitor, wherein the subject has a TET2 and/or DNMT3A mutation thereby treating atherosclerosis. It also discloses a method for treating atherosclerosis in a human subject comprising sequencing at least a part of a genome comprising TET2 and/or DNMT3A of one or more cells in a blood sample of the subject; determining from the sequencing whether the subject has one or more mutations in TET2 and/or DNMT3A, if it is determined that the subject has at least one TET2 and/or DNMT3A mutation, administering an IL-8 inhibitor, an IL-6 inhibitor, and/or an IL-1? inhibitor to a subject to the subject thereby treating atherosclerosis.

Abstract: The methods described herein include methods for the treatment of subjects who have Clonal Hematopoiesis of Indeterminate Potential (CHIP) or a Philadelphia-negative myeloproliferative neoplasm (MPN), e.g., polycythaemia vera (PV) or essential thrombocythaemia (ET), using inhibitors of JAK-STAT signaling.

Abstract: Disclosed are methods for predicting a response of a subject with myelodysplastic syndrome to treatment with a hypomethylating agent, for example using a sample obtained from the subject. The methods can be used to select a subject for treatment with a hypomethylating agent, and/or measure a subject's response to therapy and/or disease progression/regression. The methods include detecting, in a nucleic acid sample obtained from a subject, one or more mutations of any one or more genes selected from Table 3a.

Abstract: The invention relates to expression profiles of HIV-specific T-cells and their methods of use, including but not limited to treatment of HIV, increasing T-cell function and/or survival in HIV infected subjects, monitoring HIV disease progression and classifying HIV infected subjects as controllers or chronic progressors.

Abstract: The invention provides methods of treating certain blood related disorders, in particular, thrombocytopenia and anemia comprising increasing miR-150 expression or inhibiting miR-150 in progenitor cells respectively.

Abstract: The invention provides methods of treating certain blood related disorders, in particular, thrombocytopenia and anemia comprising increasing miR-150 expression or inhibiting miR-150 in progenitor cells respectively.

Abstract: The invention provides methods of treating certain blood related disorders, in particular, thrombocytopenia and anemia comprising increasing miR-150 expression or inhibiting miR-150 in progenitor cells respectively.

Abstract: The invention provides methods of treating certain blood related disorders, in particular, thrombocytopenia and anemia comprising increasing miR-150 expression or inhibiting miR-150 in progenitor cells respectively.

Abstract: The invention relates to expression profiles of HIV-specific T-cells and their methods of use, including but not limited to treatment of HIV, increasing T-cell function and/or survival in HIV infected subjects, monitoring HIV disease progression and classifying HIV infected subjects as controllers or chronic progressors.

Abstract: The invention provides methods of treating certain blood related disorders, in particular, thrombocytopenia and anemia comprising increasing miR-150 expression or inhibiting miR-150 in progenitor cells respectively.