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Chemotherapy sucks.
By all accounts, it’s basically poison.
It interferes with stuff in your own cells
in hopes that it’ll kill cancer before cancer kills you.
While it works – and it definitely works – doctors generally are not fond
of putting patients through its gauntlet of side effects.
And they’re making steady progress towards not doing that.
So here’s a look at why we use chemo, some new options we can use instead,
and how cancer treatment is getting better and smarter all the time.
[♪ INTRO]
To be absolutely clear: chemotherapy works.
That’s why we use it so much.
At its most basic, chemotherapy, or “chemo” for short,
is just using drugs to treat cancer.
And between 2013 and 2020, about one in five cancerous tumors in England,
that is, more than half a million of the suckers,
got treated with some form of chemotherapy.
One thing that’s important to keep in mind is that
chemo comes in many shapes and sizes.
There are hundreds of different cancer drugs out there, and patients will get one
or a combination of different drugs depending on their circumstances.
Sometimes the idea is to make their cancer go away completely, while other times
the chemo helps to make other treatments like surgery more effective.
And sometimes the goal is to simply manage symptoms when a cure isn’t possible.
But cures do happen.
Newly diagnosed Hodgkin lymphoma, testicular cancer,
and acute lymphocytic leukemia can all be treated with chemotherapy
with the expectation that in most patients, the cancer goes away — for good.
If you want an example that I am intimately familiar with, one common drug
is called doxorubicin, which is sometimes combined with three other drugs
with similarly difficult-to-pronounce-names into a cocktail called ABVD.
Without going too deep into it, doxorubicin is good at killing dividing cells
because normally, the nucleus is a tangled mess of DNA, and it uses
an enzyme called topoisomerase as like a molecular detangling spray.
The cell needs to detangle its DNA
in order to shrink down those neat little chromosomes and divide,
which it can’t do without its detangling spray, which doxorubicin blocks.
So that’s why doxorubicin targets mostly cancer cells
but also can affect other cells that like to divide.
This is a common problem with chemo drugs.
We want to target the cancer cells, but the cancer cells,
on a molecular level, look very similar to the rest of you.
But one thing almost all cancers have in common
is that they grow and divide quickly.
So a lot of chemo drugs target various growth and division mechanisms.
Unfortunately, that means that they can do a fair amount of collateral damage,
especially to cells that have to replicate a lot for their normal jobs,
like growing hair, replacing the stomach lining, or creating immune cells.
So while I can tell you from personal experience that chemotherapy is miserable,
it also has done amazing things for me, personally,
and I’m extremely grateful for all of the different drugs in ABVD.
But if we can do better, we like doing better!
There are at least two important avenues of research
for better, less regular-cell-death-inducing treatments:
targeted and personalized therapies.
Right now, most chemo drugs go in your arm
or into your stomach and then everywhere in the body.
Which is how they get to your stomach lining and hair follicles, et cetera.
But targeted therapies are designed to more specifically
go after the cancer, leaving the non-cancerous cells alone.
Some of these are so-called small-molecule drugs
that target different parts of a tumor’s growth cycle.
The term refers to small molecules that you would recognize
as similar to traditional drugs like aspirin or penicillin.
By interfering with molecular processes that only cancer cells have,
they can spare a patient some of the harmful side effects of regular chemotherapy.
One of the earliest success stories in this space is a drug called imatinib,
which is used for some leukemias.
These leukemias have a ridiculously specific mutation known as BCR-ABL.
It happens when two different chromosomes get stuck together in one exact place,
sending levels of a certain cellular growth signal into the stratosphere,
and that mutation is only in the cancer, not in the patient’s healthy cells.
Imatinib shuts that growth signal back down.
This method of stopping messages that are specific to a cancer is promising.
In fact, a 2018 review estimated about 150 drugs in the same vein
as imatinib were in clinical trials, plus countless others that work in other ways.
But good small-molecule drugs are hard to make because you need to know
a lot about the molecular processes of cancer that you are trying to treat,
and then once you’ve got something that works for one cancer,
there’s no guarantee it will work for even a slightly different disease.
Luckily biology gives us an even better tool for targeting a specific thing.
Monoclonal antibodies are another major category of targeted therapy.
You may have noticed that a lot of newer cancer drugs have a fancy “-mab” suffix,
like trastuzumab, pembrolizumab, and rituximab.
These are all monoclonal antibodies.
They come to us courtesy of our own immune system.
They are those Y-shaped molecules that normally
stick to viruses and other invaders.
But with a little science,
we can convince them to stick to pretty much anything we'd like.
The “monoclonal” bit on the antibody just means all of the ones in a given batch
are the same, and stick to the same thing.
In general, monoclonal antibodies do one of three things in cancer treatment:
they block cancer cells from growing, or flag the cells to the immune system
as baddies, or they deliver harmful chemicals into the cell.
Trastuzumab, for example, attaches to a protein
found on some cancers called HER2.
When cancers have these proteins, they have a lot of them,
and they help the cancer grow and divide.
So by blocking them, trastuzumab stops this growth.
On the other hand, pembrolizumab is designed to attach to proteins
on your immune cells and super-charge them
to better identify and eliminate cancer cells.
Since this strategy recruits your immune system,
it’s also known as immunotherapy.
Now, another big area of research right now is in personalized therapy.
That’s because no two cancers are exactly alike,
and no two people have the exact same genetic background.
If you have a mutated version of the genes called BRCA1 or BRCA2,
you are significantly more likely to develop breast cancer in your life.
It’s now way easier and cheaper than ever before to do a test early on to find out
if you’re at risk because of your genetics, and then do something about it,
either by just being more aware and then screening more often,
or by choosing pre-emptive therapy.
More than that, knowing if you have these genes can also impact
the best treatment for you if you do develop cancer.
For example, a big cancer drug trial published in the
New England Journal of Medicine in 2021 found that cancers with BRCA1
or BRCA2 mutations are more susceptible to a type of drug called a PARP inhibitor.
And that’s not all we can do to individualize treatment.
In fact, we don’t even need to move beyond breast cancer for another example.
Some breast cancers have receptors for estrogen, and some don’t.
Those with estrogen receptors respond to drugs that block them, like tamoxifen.
But those drugs won’t work if your cancer
doesn’t have those receptors to begin with.
The same thing happens with receptors for progesterone, and also for HER2.
We have drugs to target any of the three.
A “triple-negative” breast cancer doesn’t have any of those three receptors,
and tends to be the hardest to treat.
On the flip side, though, we can do tests to find that out,
and that can help doctors develop the patient’s treatment plan.
Forewarned is forearmed.
If we can better understand — at a molecular level — not only the cancer,
but also the person it’s growing in,
we can use exactly the right drug in exactly the right place.
Chemotherapy is not going anywhere in the next five, ten, or twenty years.
In fact, some targeted therapies just deliver the exact same old chemo drugs
right to the tumor, like a little side-effect-avoiding Uber driver.
But we’re developing more, better arrows to have in our quiver,
to keep people not only alive but feeling better.
And that’s something to feel good about.
Chemotherapy is always going to be a balance,
but it’s a system we currently have in place and understand pretty well.
And making new systems work can be a challenge,
whether they’re systems to fight cancer or solve mathematical problems.
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[♪ OUTRO]