A novel target for the treatment of cancer
For more than three decades, scientists have known that blocking calcium entry into a cell will stop the cell from dividing. However, the channel responsible for calcium entry was a mystery.
Tau discovered that the T-type calcium channel Cav3 is the predominant influx mechanism by which extracellular calcium enters in most solid cancers. Virtually all growth factor receptors converge at this pathway making it a “choke” point for proliferation.
Inhibition of calcium entry, through the use of a T-type calcium channel blocker, halts cell cycle progression just prior to the G1/S boundary or checkpoint. This action results in accumulation of cancer cells at this restriction point as individual, asynchronously dividing cells arrive at the checkpoint and are inhibited from entering S phase, the phase in which many cancer cells are susceptible to chemotherapy.
In in vitro and in vivo models, Tau has found that inhibitors of Cav3 both hold cancer cells at the G1/S checkpoint and prevent their proliferation, successfully achieving cell cycle arrest. As an independent treatment modality in animal models, T-type calcium channel inhibitors markedly slowed the growth of several tumors and thereby reduced tumor burden over time. This novel use of T-type calcium channel blockers may usher in the potential to treat cancer as a chronic disease – one that is simply managed by taking a daily T-type calcium channel blocker to control the growth of cancer cells. In the near term, this cell cycle arrest could potentiate the effectiveness of conventional cytotoxic chemotherapies. Tau has named this latter approach Interlaced Therapy™.