This technology is a therapeutic target and diagnostic marker for cachexia, a metastatic cancer-induced muscle wasting disorder.
Cachexia is a phenomenon in which tumor-secreted factors induce extensive muscle damage and weakness in cancer patients. This condition can render patients too weak to tolerate standard doses of cancer treatments and can cause premature death due to wasting of heart and diaphragm muscles. Despite the devastating ubiquity of this condition, the cellular mechanisms of cachexia are not fully understood. As such, there are currently no approved pharmaceutical treatments to alleviate this condition.
This technology identifies the zinc transporting protein ZIP14 as a primary mediator of muscle atrophy in cachexia. ZIP14 has been found to be upregulated in cachectic tissue, where it facilitates aberrant accumulation of zinc in muscle tissue, leading to muscle wasting. As a result, this technology identifies a crucial role for ZIP14 in skeletal muscle as a mediator of cancer-induced muscle atrophy, which could provide a basis for designing anti-cachexia therapies and diagnostic markers of cachectic tissue in metastatic cancers.
This technology has been validated in metastatic mouse models.
IR CU18030
Licensing Contact: Ron Katz