Lipid particles for nucleic acid delivery and clinical applications of same are provided. Accordingly there is provided a lipid particle comprising a cationic lipid encapsulating a nucleic acid sequence, wherein said nucleic acid sequence encodes a protein having a length of at least 500 amino acids, the cationic lipid being represented by Formula I, as defined in the specification.

Provided is a method comprising determining polo-like kinase 1 (PLK1) activity in a cancer in a patient by measuring phosphorylation of a PLK1 target (a) prior to treatment of (i) the patient or (ii) a cancer sample from the patient with a PLK1 inhibitor, and (b) after the treatment.

Also provided is a method comprising determining polo-like kinase 1 (PLK1) activity in a cancer in a patient by measuring phosphorylation of a PLK1 target without treatment with a PLK1 inhibitor.

Presented herein are cancer peptide agents and uses thereof for treating cancer and/or inhibiting metastasis. Also presented herein are methods of treating cancer, or inhibiting metastasis of cancer in a subject, comprising administering a therapeutically effective amount of a composition comprising one or more cancer peptide agents to the subject. Also presented herein is a method of treating a cancer in a subject, or inhibiting metastasis of a cancer in a subject that comprises administering a therapeutically effective amount of a composition comprising one or more cancer peptide agents, and administering a chemotherapy or chemotherapeutic agent.

The present invention relates to a HLA-A2 subtype-specific PLK1-derived epitope inducing an antigen-specific T cell immune response to a PLK1 protein. More specifically, a HLA-A2 subtype-specific PLK-1-derived epitope inducing an antigen-specific T cell immune response to a PLK1 protein according to the present invention can provide a CD8+ T cell immune response specific for tumor cells.

Presented herein are cancer peptide agents and uses thereof for treating cancer and/or inhibiting metastasis. Also presented herein are methods of treating cancer, or inhibiting metastasis of cancer in a subject, comprising administering a therapeutically effective amount of a composition comprising one or more cancer peptide agents to the subject. Also presented herein is a method of treating a cancer in a subject, or inhibiting metastasis of a cancer in a subject that comprises administering a therapeutically effective amount of a composition comprising one or more cancer peptide agents, and administering a chemotherapy or chemotherapeutic agent.

An object of the present invention is to provide an approach of removing non-endocrine unintended cells coexisting with insulin-secreting cells obtained by the differentiation. The present invention relates to a method for producing an insulin-producing cell population, comprising the step of treating an insulin-producing cell population obtained by the differentiation from pluripotent stem cells with a PLK inhibitor.

Novel compounds are provided that bind to polo-like kinases through the polo-box domain. In certain embodiments, the novel compounds are PEGylated peptides. The PEGylated peptides in accordance with the invention demonstrate high PBD-binding affinity. In certain embodiments, the PEGylated peptides have also achieved activities in whole cell systems. The invention also provides compounds that bind polo-like kinases through the polo-box domain and possess reduced anionic charge. Further provided are methods of design and/or synthesis of the PEGylated peptides and methods of use thereof. The invention provides methods of use of the compounds and methods of synthesis of the compounds.

The present invention relates to a HLA-A2 subtype-specific PLK1-derived epitope inducing an antigen-specific T cell immune response to a PLK1 protein. More specifically, a HLA-A2 subtype-specific PLK-1-derived epitope inducing an antigen-specific T cell immune response to a PLK1 protein according to the present invention can provide a CD8+ T cell immune response specific for tumor cells.

Presented herein are cancer peptide agents and uses thereof for treating cancer and/or inhibiting metastasis. Also presented herein are methods of treating cancer, or inhibiting metastasis of cancer in a subject, comprising administering a therapeutically effective amount of a composition comprising one or more cancer peptide agents to the subject. Also presented herein is a method of treating a cancer in a subject, or inhibiting metastasis of a cancer in a subject that comprises administering a therapeutically effective amount of a composition comprising one or more cancer peptide agents, and administering a chemotherapy or chemotherapeutic agent.

Methods for developing non-peptidic inhibitors that target the polo-box domain of PLK1 proteins are described. Methods include developing structure activity relationships for peptidic inhibitors followed by development of non-peptide fragment alternatives for portions of the peptide inhibitors. The non-peptide fragment can provide similar structure activity relationship as the replaced peptide. Fragment alternatives to key binding determinants are identified in an iterative computational and synthetic process facilitated through understanding of the peptide structure-activity relationships. The approach is informed by peptide structure-activity data obtained through synthesis and testing of truncated and mutated analogs of known PBD binding motifs.