Volastra’s research into genomic instability is distinguished by an experienced interdisciplinary team. Our team is poised to address the underlying cell biology of CIN through cellular analyses, computational approaches, state-of-the-art animal modeling, and a collection of unique, patient-derived organoids.³ Our goal is to develop therapeutic strategies to tackle metastasis and therapeutic resistance driven by CIN.

Background

Doctors Cantley, Bakhoum, and Elemento identified a unique mechanism that drives the formation and migration of metastatic cancer cells. They discovered that high levels of CIN within cancer cells enable cell migration and alter key immunologic processes to evade immune system detection. These chromosomally unstable cells migrate from the primary tumor and invade distant tissues, which produces metastatic colonies resistant to a wide array of therapies.

Therapeutically targeting CIN

It has long been assumed that CIN could not be targeted directly. Volastra harnesses unique druggable pathways that inhibit genomic instability and the underlying disease process. By targeting altered biologic pathways in cells with high levels of CIN, we hope to halt and potentially prevent metastasis in difficult-to-treat solid tumors for which there are limited therapeutic options. Our approach also aims to render aggressive tumors sensitive to immunotherapy.

To accelerate the drug development and enhance its precision, we will utilize a library of patient-derived, metastatic tumor organoids. This platform will be used to validate our compounds, discover novel targets, and perform high-throughput single-agent and combination drug screens. The library will support patient selection and stratification in combination with advanced analytics.