The present disclosure provides compositions and methods for selectively killing senescent cells, wherein the composition comprises piperlongumine derivative thereof. The selective killing of senescent cells may delay aging and/or treat age-related disorders.
Mutant Myxoma viruses are provided herein and methods of using these viruses to treat cancer or elicit an interferon response in a subject are also provided. The mutant Myxoma virus is modified to reduce or eliminate the activity or expression of Myxoma virus protein M62 as compared to a control virus. The mutant virus is capable of stimulating an interferon response in subjects after administration and can also lead to inhibition, reduction or elimination of the CD14+ tumor associated macrophage inhibition of CD4+ T cells in a subject having cancer and lead to a change in the tumor microenvironment to treat the cancer or work in combination with other cancer therapeutics to treat the cancer as described herein.
The present disclosure provides compositions and methods for selectively killing cancer cells, wherein the composition comprises a compound of Formula (I). The selective killing of cancer cells occurs with an improved potency and safety profile compared to similar compounds. In particular, the compositions and methods of the invention show reduced platelet toxicity and retained or improved toxicity in cancer cells.
The present disclosure provides SL and SL derivatives comprising a polar substituent adjacent to the lactone ring. Additionally, the present disclosure provides methods of using the SL and SL derivatives to inhibit the growth of leukemic cancer cells.
The present inventors have developed antigen-binding reagents and antigen-binding conjugates that recognize a cancer-specific glycan (carbohydrate) modification on the human Periostin protein. Various in vitro and in vivo diagnostic and/or therapeutic methods using these compositions are also disclosed herein specifically for treating cancers that have amplification of the Mgat3 gene.
The invention provides, inter alia, methods of prognosing a subject with, or suspected of having, multiple myeloma. In certain embodiments, the methods entail testing the gene expression levels of enolase 1 (ENO1), fatty acid binding protein 5 (FABP5), thyroid hormone receptor interactor 13 (TRIP13), transgelin 2 (TAGLN2), and replication factor C (activator 1) 4 (RFC4) in a biological sample isolated from the subject. The invention also provides methods of treatment for multiple myeloma, as well as kits, oligonucleotides, and systems for performing the methods provided by the invention.
Gene expression profiling in multiple myeloma patients identifies genes that distinguish between patients with subsequent early death or long survival after treatment. Poor survival is linked to over-expression of genes such as ASPM, OPN3 and CKS1B which are located in chromosome 1q. Given the frequent amplification of 1q in many cancers, it is possible that these genes can be used as powerful prognostic markers and therapeutic targets for multiple myeloma and other cancer.
The present disclosure provides compositions and methods for selectively killing senescent cells, wherein the composition comprises piperlongumine (PL) or derivative thereof. The selective killing of senescent cells may delay aging and/or treat age-related disorders.
Gene expression profiling is a powerful tool that has varied utility. It enables classification of multiple myeloma into subtypes and identifying genes directly involved in disease pathogenesis and clinical manifestation. The present invention used gene expression profiling in large uniformly treated population of patients with myeloma to identify genes associated with poor prognosis. It also demonstrated that over-expression of CKS1B gene, mainly due to gene amplification that was determined by Fluorescent in-situ hybridization to impart a poor prognosis in multiple myeloma. It is further contemplated that therapeutic strategies that directly target CKS1B or related pathways may represent novel, and more specific means of treating high risk myeloma and may prevent its secondary evolution.
The present disclosure relates to methods and compositions for detecting mitochondrial dysfunction. In particular, the disclosure relates to reporter molecules that are cleavable by the zinc metalloprotease Metalloendopeptidase OMA1 (OMA1). In each embodiment, the reporter molecules of the invention are particularly useful for drug discovery and detection of diseases associated with mitochondrial dysfunction.
