Abstract: In certain embodiments, methods of activating the mitochondrial unfolded protein response (UPRmt) and inducing mitohormesis in the brain and/or central nervous system of a mammal are provided where the methods can involve administering to the mammal an effective amount of N-proparglyglycine (N-PPG). In certain embodiments, the mammal is a mammal with a neurodegenerative disease and the method provides for the treatment or prophylaxis of the neurodegenerative disease.

Abstract: In various embodiments a cancer treatment method is provided based on inhibition of proline catabolism. When combined with p53 restoration therapy and/or inhibition of glutaminase, the inhibition of proline catabolism results in a “synthetic lethal” and synergistic anticancer response. Novel suicide inhibitors that induce the degradation of proline dehydrogenase (PRODH) are also provided. Also provided is a method of assaying PRODH to identify responders/non-responders to inhibition of proline catabolism and/or glutaminase.

Abstract: In various embodiments a cancer treatment method is provided based on inhibition of proline catabolism. When combined with p53 restoration therapy and/or inhibition of glutaminase, the inhibition of proline catabolism results in a “synthetic lethal” and synergistic anticancer response. Novel suicide inhibitors that induce the degradation of proline dehydrogenase (PRODH) are also provided. Also provided is a method of assaying PRODH to identify responders/non-responders to inhibition of proline catabolism and/or glutaminase.

Abstract: Provided herein are compositions of histone deacetylase (HDAC) inhibitors for the treatment of cancers overexpressing the large ribosomal subunit protein 24 (RPL24) in a subject in need thereof. Provided herein are methods for treating RPL24-overexpressing cancers in a subject in need thereof, comprising administering to the subject an effective amount of an HDAC inhibitor. Also provided herein are methods for inhibiting the viability of an RPL24-overexpressing cancer cell with an HDAC inhibitor. Also provided herein are methods for assessing the efficacy of an HDAC inhibitor against a cancer.

Abstract: This invention provides for a cDNA that is a coding region of a previously unknown member of the ETS transcription regulator family. The gene described herein (designated ESX) is located at chromosome 1q32 a region amplified in 50% of early breast cancers. The ESX gene of this invention is associated with the etiology of various cancers including breast cancers. Detection of the ESX gene or gene product is thus of diagnostic and/or prognostic value.

Abstract: An injection method for feeding a particulate material to a process vessel, including a valve with at least one cavity adapted for receipt of a predetermined volume of particulate and a sweep stream source for providing a sweep stream having flow in a direction generally toward the valve to remove substantially all of the particulate from the cavity of the valve.

Abstract: An injection system and method for feeding a particulate material to a process vessel, including a valve with at least one cavity adapted for receipt of a predetermined volume of particulate and a sweep stream source for providing a sweep stream having flow in a direction generally toward the valve to remove substantially all of the particulate from the cavity of the valve.

Abstract: A method and assay for determination of functionality of steroid receptors present in breast or other tumors. The method is useful for determination of cancer responsiveness to hormonal therapy by establishing a correlation between functioning estrogen receptors and those which are dysfunctional or nonfunctional. The assay is useful for determination whether the cancer, particularly the breast cancer, will respond to anti-estrogen hormonal therapy.