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subscription at Brilliant.org/SciShow. 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. That’s why Brilliant has
made a course to help make Systems of Equations a little more approachable. Brilliant is an online learning platform
with thousands of lessons in science, computer science, and math. And this particular Brilliant
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not just tell you about them. And you can try it out at Brilliant.org/SciShow or in the link in the description down below. That link also gives you a
free 30-day trial and 20% off an annual premium Brilliant subscription. Thanks to Brilliant for
supporting this SciShow video! [♪ OUTRO]
