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.

The present invention is in the field of oncology, and more particularly of cancer stem cells. It relates to a method for producing cancer stem cells based on overexpression of Δ133p53β isoform, Δ133p53γ isoform, or both Δ133p53β and Δ133p53γ isoforms; a method for predicting the risk that treatment with a chemotherapeutic anti-cancer agent induces cancer stem cells in a subject suffering from cancer from a cancer sample of said subject, based on detection of an increase in Δ133p53β isoform, Δ133p53γ isoform, or both Δ133p53β and Δ133p53γ isoforms following chemotherapeutic anti-cancer treatment; to therapeutic uses of a combination of chemotherapeutic anti-cancer agent and an agent reducing Δ133p53β isoform, Δ133p53γ isoform, or both Δ133p53β and Δ133p53γ isoforms expression; and also to screening methods for anti-cancer stem cells agents.

A method is disclosed for treating small cell lung cancer (SCLC) in a subject that involves administering to the subject a therapeutically effective amount of dendritic cells engineered to overexpress p53. In some embodiments, the method further involves administering to the subject a therapeutically effective amount of all-trans-retinoic acid (ATRA). The method can also involve administering to the subject a therapeutically effective amount of an immune checkpoint inhibitor.

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.

Mitochondria modified by a targeting protein, according to one embodiment of the present invention, can be effectively delivered to a target. In addition, when a protein of interest bound to the modified mitochondria is delivered into a cell, various activities can be exhibited. The modified mitochondria can effectively cause cancer tissue death, and thus can also be used as an anticancer agent. Furthermore, various activities are exhibited according to a protein of interest loaded on modified mitochondria, and thus the modified mitochondria can be applied in the treatment of various diseases. Additionally, a fusion protein comprising a protein of interest and a fusion protein comprising a targeting protein, according to one embodiment of the present invention, can be used in order to modify mitochondria. Moreover, mitochondria modified with the fusion proteins exhibits various effects in a target cell.

The present disclosure describes the synthesis of peptidomimetic macrocycles and methods of using peptidomimetic macrocycles to treat a condition. The present disclosure also describes methods of using peptidomimetic macrocycles in combination with at least one additional pharmaceutically-active agent for the treatment of a condition, for example, cancer.

Disclosed herein is a novel p53 complex and a collection of compounds that can tightly associate with p53 to efficiently rescue wildtype p53 structure and function, and the methods of making and using the complex and the compounds, including for diagnosis, prognosis, and treatment of p53 related disorders such as cancer and aging.

The present application discloses a lentiviral transfer system which includes: (i) a self-inactivating transfer vector comprising: multiple gene units, wherein each gene unit includes a heterologous nucleic acid sequence operably linked to a regulatory nucleic acid sequence; and (ii) a helper construct which lacks a 5′ LTR, wherein the 5′ LTR has been replaced with a heterologous promoter, in which the helper construct further comprises: a lentiviral env nucleic acid sequence containing a deletion, wherein the deleted env nucleic acid sequence does not produce functional env protein; and a packaging signal contains a deletion, wherein the deleted packaging signal is nonfunctional.

The present invention provides novel peptidomimetic macrocycles and methods of using such macrocycles for the treatment of disease.

The disclosure provides for a multimodal cancer therapy comprising chimeric viral/nonviral nanoparticles and anticancer agents and uses thereof to treat a subject with cancer or suspected of having a cancer.