Know your enemy, know yourself. It's a centuries-old strategy. But even in the present-day war against cancer, achieving it remains elusive. In many cases, cancer cells blend in with healthy ones. They bear no unique molecular markers or targets that we can aim clinical defenses at. That means any deadly strike on enemy cancer cells could result in casualties among healthy ones as well. The untenable toxicity of this artless warfare has led some researchers to rethink the ancient script—and flip it: know yourself, know your enemy.
In a set of clever and highly technical tricks, researchers are working on ways to precisely mark and shield healthy cells from chemical weapons, abandoning the effort to pick out enemy cancer cells specifically. By exploiting molecular markers common among many types of cells, researchers can safeguard healthy cells, leaving only the cancer cells in harm's way.
A drug or therapy that targets common markers would normally lay waste to cancerous and healthy cells alike. But that's not the case in this radical approach, which is first being used to treat blood cancers. For the strategy, researchers collect healthy blood stem cells and genetically engineer tiny, benign changes to a common molecular marker on them. Those tiny changes make the healthy cells essentially invisible to killer treatments. After the engineered cells are transplanted into a patient, clinicians can deploy the treatments. The cancerous cells that lack the genetic tweak are now easily killed by the drug or therapy, while the healthy engineered cells are left untouched.
The utility of the tactic doesn't end there. While cloaking healthy cells means researchers no longer need to know their specific enemy from healthy cells with precision, that imprecision opens vast possibilities. For one, it has the potential to create a virtually universal treatment for blood cancers. Whatever specific type of cancer is present, targeting a ubiquitous marker on blood cells and cloaking healthy cells will eradicate whatever strain of cancer is lurking among them.
I'm alive because of a similar medication that came out in 2001. I have PH+ CML (the chronic version of AML referenced in the article). Prior to the discovery of Gleevec, most folks lived about 3 years. I'm alive 16 years later thanks to these Tyrosine Kinase Inhibitors (currently on Sprycel).
They are highly targeted medications that MOSTLY leaves healthy cells in tact. I take one pill per day and have minimal residual disease.
I live a mostly full life and hope these new developments can bring the same (or better) quality of life I've been afford thanks to these novel therapies and incredible scientists.