Cancer is many things, so one tool or technique cannot be used against all, but even so, it is good news every time a new tool has been discovered that can help fight some cancers.

From ScienceDaily: Light switch wakes sleeping cancer cells and makes them vulnerable again

Some cancer cells evade treatment by entering a dormant state triggered by stress hormones. ETH Zurich scientists have created a light-controlled molecular switch that selectively destroys the receptors responsible for this survival mode. In laboratory lung cancer cells, the approach woke sleeping tumor cells and could help make future cancer therapies more effective while minimizing damage to healthy tissue.

It sounds counterintuitive that you want the cancer cells to be active, but the ScienceDaily article explains it:

In certain forms of cancer, including some types of lung cancer, stress hormones can trigger this response. Specialized proteins called glucocorticoid receptors detect those hormones inside tumor cells. Once activated, the receptors can push the cells into a dormant state where cell division slows dramatically. As a result, many therapies become far less effective.

So, in other words, we can only fight them effectively when they are active.

The ScienceDaily article is based upon the paper Light-controlled disruption of cancer cell dormancy via photoswitchable stress hormone receptor degraders by Karina M. Freitag et al in PNAS.

I will freely admit that the actual paper is a bit above my biochemistry level, but the “significance” section is fairly understandable, especially combined with the ScienceDaily writeup

Stress hormone signaling through the glucocorticoid receptor (GR) induces a reversible, drug-tolerant dormancy state in cancer cells. However, systemic GR depletion is not viable due to its essential roles in non-pathological physiology. In this study, we developed light-responsive Proteolysis Targeting Chimeras (photoPROTACs) that enable reversible, wavelength-specific control of GR degradation. PhotoPROTACs featuring arylazopyrazole photoswitches showed potent, isomer-dependent GR degradation and high target specificity at nanomolar concentrations. In addition, transcriptomic profiling in lung cancer cells revealed that only the active isomer disrupts dormancy-associated gene networks, highlighting the potential of photoPROTACs to target GR-driven dormancy exclusively in cancerous tissue.