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Medical treatments have come a long way in the last couple of centuries.
We now have all sorts of options,
from carefully formulated capsules to treatments that harness x-rays.
But for all our progress, modern medicine still has a ways to go.
Especially when it comes to cancer treatments.
That’s because cancer drugs often target any rapidly dividing cells,
which include but are not limited to a patient’s cancer.
that can lead to some not-so-nice side effects like nausea or hair loss.
But researchers might have found a way to treat tumors –
and only tumors –
by exploiting their love for iron.
And they published their findings this week
in the Journal of Experimental Medicine.
Researchers were interested in a particularly nasty kind of pancreatic cancer
called pancreatic ductal adenocarcinoma, or PDA.
Treatments for PDA aren’t that effective right now,
partly because tumors start out microscopic in size, making it hard to get drugs to go
there.
So having a targeted treatment option would be really helpful.
One way to target cancer cells may be to go after o
ne or several of the mutations that make it different to the body’s regular cells.
And that’s what researchers in this study were looking at –
a mutation in the KRAS protein.
In healthy cells, this protein acts as an important onoff switch for cell growth,
where it sends signals to the cell telling it to divide.
Mutated KRAS is stuck in the on position, meaning cells grow out of control,
which leads to cancer.
But these researchers noticed something else about cells with KRAS mutations.
They loved iron.
In particular, a relatively reactive form of iron
called ferrous iron.
Researchers noticed that genes that controlled iron intake
and metabolism were really active in PDA tumors.
And that meant that those tumors ended up with lots of iron stored up inside them.
The tumors were so chock-full of iron,
that researchers described these tumors as having an “addiction” to the stuff.
Researchers thought they could use the tumor’s addiction
against them to deliver anti-cancer drugs directly into tumor cells.
They started with a drug called an FeADC –
short for ferrous iron-activatable drug conjugate.
This is a mouthful, but these do exactly what it says on the tin.
They’re inactive until they come in contact with ferrous iron, and then they switch on
and release the drug.
By linking one of these FeADCs to an already-existing cancer drug
called cobimetinib, researchers created a drug
that was activated only inside human PDA tumor cells full of iron,
and not healthy skin or eye cells.
See, healthy eyes, skin, and gut tissue
are often the unassuming victims of these kinds of anti-cancer drugs,
so researchers were particularly interested
to see if this new drug avoided them.
By adding the FeADC to the cancer drug,
the drug was essentially switched off until it came in contact with ferrous iron in the
tumor.
They called the drug combo TRX-COBI.
Next, researchers tested TRX-COBI on different mouse models
that had different kinds of KRAS-driven cancers,
including PDA but also a kind of lung cancer.
And again, the drug slowed down tumor growth,
d to when they tried cobimetinib on its own,
which affected regular and cancer cells.
Plus, the drug did not go after organs that naturally have iron stored up in them,
like the liver.
That might be because the iron stored there is in an inactive form
and so it can’t activate the drug in the same way as the ferrous form.
In short, this new drug worked as well as an existing cancer drug
but without all the toxicity.
As a final test, researchers tried TRX-COBI together with other anti-cancer drugs.
Because, if the drug wasn’t harming regular cells,
then maybe patients could handle a more intense burst of therapy
to really knock out their tumor.
And these combination therapies worked even better
at limiting tumor growth in those mouse models,
with few side effects on normal tissue.
And the researchers think this iron switch
could be used with other anticancer drugs too.
Of course, this study was done in the lab and in mice,
so it’s not up to human testing quite yet.
But hopefully, with more work, it could lead
to more effective cancer treatments
with fewer side effects down the line.
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