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As a SciShow viewer, you can keep  building your STEM skills with a 30-day free trial and 20% off an annual premium  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  course walks you through everything from linear systems to systems with quadratics. With Brilliant, you’ll learn in a new way. This interactive course uses visual  models and interactive graphing to show you how systems work,  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]