Switch Off Cancer Genes!

If you or a loved one has one or more known cancer gene(s), then wouldn’t it be great to be able to just turn them off?

With this new epigenetic therapy, that may now be possible.

First, for anyone wondering…

What is epigenetics? In few words and put simply, it’s the study of “around genetics”, i.e. the things that are not the genes themselves, but modulate how (and indeed, whether or not) genes are expressed.

Cancer’s off switch?

Most of us have slightly higher or slightly lower genetic risk for various diseases, including various specific cancers.

Some of us have a greatly higher risk of certain diseases, including specific cancers.

See for example: Knowledge Is Power! What You Don’t Know Can Kill You

If you don’t know what your genetic profile is like in that regard, you might want to check out: Genetic Testing: Health Benefits & Methods

Now, for those who have such risks, there are well-known lifestyle-based methods to manage those risks.

We wrote about some of them, here: 5 Ways To Beat Cancer (And Other Diseases)

More recently, researchers (Dr. Vita Levina et al.) discovered how to switch off some of those unfortunate genes, using targetted gene therapy drugs—this is very different from what is generally called chemotherapy; chemo is a matter of “we’re going to poison the cancer cells while trying to poison as few of your healthy cells as possible in the process”. With gene therapy drugs, in contrast, it doesn’t really affect much (or sometimes, anything) else.

To give a light example, here’s a less ground-breaking pop-science article from mid-2025: Aggressive blood cancer: A key protein could pave the way for targeted therapies

You might be wondering: “does this mean it’s changing our genes?”

And the answer is: no, epigenetic drugs reset abnormal gene on/off states caused by cancer mutations, rather than altering DNA itself, targeting gene-control machinery that got hijacked.

So, what’s the big discovery?

❝Menin inhibition induces PRC1.1-dependent deposition of H2AK119ub to silence a subset of MLL-FP targets, whereas DOT1L inhibition results in a genome-wide increase in H2AK119ub. We show that enhanced PRC1.1 activity arises specifically from the progressive loss of DOT1L-mediated H3K79 methylation, independent of MLL-FP displacement or transcriptional repression. This regulatory crosstalk is conserved across cell types and is driven by direct biochemical antagonism between H3K79 methylation and PRC1 activity.❞

Translating that from sciencese: the drug inhibits an epigenetic protein that causes cells to go wrong, by leveraging one of them to erase the epigenetic memory of the other, leaving it with no memory of the errant “ignore cancer cells” instruction, so that even after treatment, the cells (and cells that replace them) return to their normal cancer-killing default.

You can read the paper in full, here: DOT1L provides transcriptional memory through PRC1.1 antagonism

Of course, the drugs are not hitting prescription pads just yet; there is more testing to do, especially to establish its safety—which latter does seem certain, but science doesn’t run on what “seems to be”, it runs on careful tests, so more rounds of tests will be done.

So, in the meantime, if you want to improve your chances, you might consider: The Lifestyle Factors That Matter >8 Times More Than Genes

Want to learn more?

For a much deeper dive into epigenetics, check out:

Identically Different – by Dr. Tim Spector ← this is about epigenetics in twin studies

Or if you want to really understand epigenetics, we highly recommend:

The Epigenetics Revolution – by Dr. Nessa Carey

Enjoy!