Author: Bioventures Team

Use of gene expression profiling to predict survival in cancer patient

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.

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Diagnosis, prognosis and identification of potential therapeutic targets of multiple myeloma based on gene expression profiling

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.

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OMA1 activity assay

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.

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Electrode for peripheral nerve stimulation

Devices and methods for peripheral nerve stimulation with an electrode assembly having a lead body with a tapered transition, at least one anchor, and at least one distal lead configured to connect to the lead body are disclosed.

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Methods of protecting against neurodegeneration

The disclosure provides a method of preventing or reducing protein aggregates using combretastatin-A4 (CA4) or an analog thereof. The disclosure also provides methods of reducing the risk, delaying the onset, delaying or slowing the progression, or reversing the signs or symptoms of a neurodegenerative (or other age-progressive) disease using a combretastatin-A4 (CA4) or an analog thereof. The combretastatin-A4 (CA4) or an analog thereof may bind glial fibrillary acidic protein (GFAP). The combretastatin-A4 (CA4) or an analog thereof is described by compounds of Formula (I).

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