The present disclosure is directed to compositions and methods of treating Triple Negative Breast Cancer (TNBC) in a human subject. A method of treating TNBC in a human subject includes administering a therapeutically effective amount of a neoantigen vaccine composition comprising a fusion protein comprising at least one TNBC-associated neoantigen epitope joined to a mutant ubiquitin protein, or a nucleic acid molecule encoding such a protein.

A method of treating cancer in a subject, including: providing a subject having a plurality of cancer cells; and administering to the subject, a therapeutically effective amount of a composition including: an HDM-2 binding component; and a membrane resident component, the membrane resident component bound to the HDM-2 binding component. Also provided are a method of selectively necrosing cancer cells, a method of causing membranolysis in cancer cells, and a cancer treatment composition.

Stable, liquid formulations of anti-cancer peptides where the formulation contains about 1-75 mg/ml of anti-cancer peptides, about 5-30 mM acetate buffer, about 10-80 mg/ml mannitol, and about 0-30% sucrose, where the formulation has a pH of about 4.0-6.0, and wherein the anti-cancer peptides include an HDM-2 binding component and a membrane resident component.

Provided is a method for biosynthesis of a protein heterocatenane. The basic structure of a protein precursor sequence of the protein heterocatenane comprises form an N-terminal to a C-terminal: L.sub.1-1-X-L.sub.1-2-(in situ enzyme cutting site)-L.sub.2-1-X-L.sub.2-2, wherein the Xs represent entangled motifs for forming dimers, the two Xs can be the same or different, L.sub.1-1/L.sub.1-2 and L.sub.2-1/L.sub.2-2 represent two pairs of cyclization motifs that undergo an orthogonal coupling reaction in cellulo, and the two pairs of cyclization motifs can be two orthogonal peptide-protein reactive pairs, or combinations of peptide-protein reactive pairs and split inteins, or two orthogonal split inteins. When the peptide-protein reactive pair and the split intein are combined for use, biosynthesis of branched protein heterocatenanes can be achieved; and when the two orthogonal split inteins are combined for use, the protein heterocatenane having a completely cyclized main chain can be obtained.

Embodiments of the disclosure include methods and compositions for in situ cardiac cell regeneration, including transdifferentiation of cardiac cells to cardiomyocytes. In particular embodiments, in situ cardiac cell regeneration encompasses delivery of p63 shRNA and one or both of Hand2 and myocardin, and in specific embodiments further includes one or more of Gata4, Mef2c, and Tbx5. In specific aspects of the disclosure, adult cardiac fibroblasts are reprogrammed into cardiomyocytes using viral vectors that harbor p63 shRNA and one or both of the transcription factors Hand2 and myocardin.

The invention is a novel reporter system for measuring protein-protein interactions. The system uses a pair of functionalized coiled coil subunits that spontaneously form two separate homo-oligomers when expressed in cells. The coiled coil subunits are functionalized with fluorescent proteins and complementary interacting proteins. Upon an activation stimulus which promotes the protein-protein interaction, the interacting proteins drive the formation of multivalent aggregates of the homo-oligomers in phase-shifted droplets. The highly concentrated fluorescent proteins in these structures provide high brightness over background fluorescence and a readily observed, quantitative and dynamic indicator of the protein-protein interaction. The reporters and assay methods are amenable to cells and whole organisms.

A new system for identification and treatment against cancer, specifically the mutation or deletion of an antioncogene. An ideal candidate is a patient with family history for hereditary mutations in a known antioncogene. The first method of this system identifies the mutation of a patient's at-risk antioncogene by causing a natural fluorescence only when the specific at-risk antioncogene has mutated or deleted. The second method of this system utilizes a virus to attack and dissolve cancer cells with special markers to avoid the damage to normal cells, thereby achieving the purpose of treating cancer.

Provided herein is a method of treating medulloblastoma or glioblastoma in a subject by administering to the subject a PI3K activator (e.g., thymosin β-4 or a derivative thereof) and one or more chemotherapeutic agents and/or radiation. The combination therapy is effective in the treatment of medulloblastoma or glioblastoma characterized by cells with elevated p53 levels.

Provided are compositions and methods for used in solubilizing, stabilizing and expressing proteins. The proteins are fusion proteins that contain a protein of interest. The fusion proteins contain segments of Ribose Binding Protein (RBP) or Maltose Binding Protein (MBP). The fusion proteins can have the RBP or MBP segments flanking the target protein, and the RBP or MBP segments can be in the fusion protein in the same orientation as they normally occur (except for being interrupted by the target protein) or the segments can be permuted. Novel segments of the RBP and MBP are provided and result in improved expression and/or solubility of the proteins. Some examples include one or a combination of two complete or partial Histidine tags. Some examples allow for the target protein to be separated from all or a part of the fusion protein such as by enzymatic or non-enzymatic cleavage.

An isolated peptide is provided. The peptide comprises an amino acid sequence arranged in a space and configuration that allow interaction of the peptide with the DNA Binding Domain (DBD) of p53 through at least one residue of the DBD by which pCAP 250 (SEQ ID NO: 1) binds the DBD, wherein the peptide at least partially reactivates a mutant p53 protein, with the proviso that the peptide is not SEQ ID NO: 59-382.