Minerva announces breakthrough in cancer therapy

Minerva used its proprietary nanoparticle technology to elucidate a key molecular mechanism that is involved in cancer cell growth and metastasis. The study focused on a cell surface receptor, called MUC1, which according to scientific literature is aberrantly expressed on 75% of all human solid tumors – 96% of breast cancers, 47% of prostate cancers, as well as high percentages of ovarian, colorectal, non-small cell lung, and pancreatic cancers.

Using its unique nanoparticle research platform, Minerva has shown that MUC1 is actually cleaved to a new form, called MUC1*. Once cleaved, MUC1* dimerizes with itself and other growth factor receptors through binding of a newly discovered ligand for MUC1*, called NM23. Binding and dimerization then acts to activate the tumor to unregulated cell growth, invasion and metastasis. Blocking MUC1* dimerization and NM23 binding leads to cancer cell death. Minerva has identified both antibody-based and small molecule therapeutics that disable the receptor and block cancer cell growth.

In collaboration with a diagnostic reference lab in California, Minerva has also shown that MUC1* is expressed to much higher levels than MUC1 in a variety of human tumor tissues, and in the future could provide both diagnostic and prognostic information on tumor development.