According to the American Cancer Society, between one third and one half of the people
in the United States will develop some form of cancer in their lifetimes.
So scientists, doctors, and the many organizations that fund their research, are what you’d
call “motivated” to find a cure.
But... they haven’t found one, if you hadn’t heard.
Plenty of drugs and treatments have been tested, but they often don’t seem to work.
One person can take a cancer drug and get better, but another person -- with the same
type of cancer -- can take the same drug and not get better.
So, after billions of dollars and decades of research, why haven’t we cured cancer?
Well, a better question is why do we keep talking about “THE cure for cancer"?
If every tumor worked the same, we would probably by now have that magic bullet that we need.
The trouble is, cancers may look the same on the outside, but each one develops differently
in their own way, and can originate in any type of tissue.
So we haven’t found a cure for cancer, because it’s not a single disease.
If we’re going to beat them, we’re going to have to take on all of the cancers, one
at a time.
So the challenges start with the basics here: first we’ve got to figure out what cancer
actually is.
We tend to think of cancer as one thing because we have one word for it. But the word “cancer”
really refers to lots of different conditions that have a few similarities.
The main thing cancers have in common is uncontrolled cell division. And that uncontrolled growth
usually starts from a sudden change within a small set of your genes.
No matter what triggers it, you get the same result: a mass of cells growing out of control
and invading other tissues, which is very bad for the body.
But under the hood, each cancer works differently. It’s practically a different disease every
time, and not every cancer will progress in the same order.
Mostly, that’s because every cancer is caused by a different set of genetic mutations.
Genes consist of a sequence of DNA, and each sequence is a set of chemical bases called
nucleotides that are arranged in a very specific order. Together, they tell the cell how to
manufacture proteins, and we are mostly just made up of proteins - so that’s how we build
ourselves.
Mutations change those instructions, and that’s where things start to go wrong.
Now, we know by this point that cancers usually come from mutations of two kinds of genes,
called oncogenes and tumor suppressors.
An oncogene starts out as just a normal gene that codes for proteins that signal the cell
to grow.
And normally, they just spend a lot of their time dormant, because growth is generally
good, but cells shouldn’t always be growing.
But just one mutation in one of these genes is often enough to throw it into high gear,
and it can’t be turned off.
That’s when it becomes an oncogene, telling the cell to keep growing and dividing over
and over, even when it shouldn’t. That’s also when it gets dangerous.
Some of the most well-known oncogenes -- the usual suspects, if you will -- are RAS and
MYC. They’re especially powerful growth genes that show up in many kinds of cancer.
A lot of the time, it’s the RAS gene that somehow gets mutated, which changes the shape
of the protein that it makes. The altered protein gets stuck in a position that always
sends a signal for the cell to grow, whether it’s supposed to or not.
And with its new shape, other proteins -- ones that usually deactivate the RAS protein before
things can get out of hand -- can’t recognize what they’re supposed to be targeting and
switch it off.
So the cell never stops getting the signal to grow and divide, and it starts forming
a tumor.
Then there are tumor suppressors, another type of cancer-causing gene -- and they’re
actually the opposite of oncogenes.
As you might guess from their name, tumor suppressors stop a cell from growing, unless
conditions are just right.
As with all of your genes, every cell in your body has two copies of the tumor suppressor,
so they’re harder to put out of commission: Even when one copy is mutated, the other one
still works.
But of course, cancer has a tendency to find its way around all kinds of safeguards.
Often, a tumor suppressor might be mutated on one chromosome to the point of not working
at all. Then, the cell just happens to lose the chunk of DNA containing the other copy.
With one copy mutated and the other deleted, there’s no tumor suppressor left to restrain
the cell’s growth.
And those mutations can happen in any number of ways. With so many possible combinations,
we can’t just create a drug to keep tumor suppressors from mutating.
Which is where things start to get even more complicated. Because just one mutated gene
isn’t usually enough to cause cancer -- it really takes at least five or six genetic
changes before normal human cells become truly cancerous.
Then, as tumors get bigger, more and more genes tend to mutate. Some of those mutations
make the cancer nastier and more aggressive.
How quickly this happens varies a lot, with different rates being associated with certain
kinds of cancer.
But there can be thousands of possible combinations of mutations going on in a cell -- which is
partly why a drug might not work for some patients, even if it’s proven effective
for that type of cancer.
So every single tumor will follow a different genetic path, which makes it hard for doctors
and drug-makers to know what to target.
So how do you kill a tumor cell, when you don’t know which of the potentially dozens
of problematic genes are making it grow?
The most obvious way to treat a tumor is to get a knife and cut it out of the body. That’s
called resecting it. But it’s not always possible, and even when it is, sometimes they
grow back.
So typically, you go to Plan B: Use a blunt instrument to smash the cancer, and hope for
the best.
For a long time, the best cancer therapy we’ve had is to send in a treatment so toxic it
attacks all rapidly dividing cells in the human body, instead of just the cancer.
Those treatments are chemotherapy and radiation.
The kind of radiation that’s useful in cancer treatment is ionizing radiation -- the kind
whose energy can ionize atoms, and the kind that most people mean when they talk about
“radiation.” And it works simply because it can tear DNA to shreds. Once the cancer
cell’s DNA is mangled beyond recognition, it can no longer make copies and divide.
But of course, it damages the DNA of nearby, healthy cells too. So doctors try to aim it
right at the tumor, to expose as little healthy tissue to the radiation as possible.
And then there’s the group of drugs we refer to collectively as chemotherapy.
These drugs work in a few different ways, but because they circulate through the bloodstream,
they tend to affect the whole body.
Some types of chemo imitate one of the building blocks of DNA, so that cells try to incorporate
them into their chromosomes without realizing they’re useless. Other kinds target the
cell’s cytoskeleton -- its internal framework -- so that it can’t pull itself apart when
it divides.
These kinds of chemo can stop a cancer cell from dividing -- but again, there are a lot
of healthy cells in your body that need to divide, as well.
Hair follicles need to go on producing hair, and the lining of your gut needs to constantly
renew itself against harsh stomach acids. That’s why chemo causes hair loss and digestive
symptoms, along with a whole bunch of other nasty side effects.
It can work, but it isn’t pretty.
Fortunately, there are new alternatives.
One of the newest weapons in the battle against cancer is one that biologists have been refining
for decades: Genome sequencing.
It’s faster and cheaper than anyone dreamed possible even ten years ago, and it’s finally
ready to directly help patients.
Within a matter of days, scientists can now sequence lots of different types of cancer
cells, and figure out exactly where and how their genes were mutated.
Using that information, they can predict what drugs will be effective against those cancers.
So, instead of using a blunt instrument that kills pretty much everything it touches, we
can develop much more refined ways to treat a certain cancer, in a certain person, through
personalized medicine.
Two major projects have taken the lead on this new approach -- one’s called the Cancer
Genome Project and the other, the Cancer Cell Line Encyclopedia. They’ve tested many kinds
of cancer cells and drugs on a large scale.
In both cases, researchers confirmed that certain drugs are more effective against particular
types of cancer. Some drugs, for instance, work better for brain cancer than stomach
cancer.
They also found that they could predict the effectiveness of a drug based on the mutations
that they find in a particular set of cancer cells.
So choosing drugs for cancer treatment doesn’t have to be a shot in the dark anymore -- at
least, in theory.
There’s a serious problem, though.
One study compared the results of the Cancer Genome Project and the Cancer Cell Line Encyclopedia,
and it found that they came to different conclusions alarmingly often.
When the two different groups of researchers treated the same cancer cells with the same
drugs in a lab, they got different results.
Even though the cells they used were more or less identical, they would sometimes respond
differently to the exact same drugs.
And even when the two projects agreed that a drug could treat a certain kind of cancer,
they disagreed about what dose was needed to be effective.
So, we won’t be able to count on personalized medicine to work until scientists come up
with more effective ways to test these drugs, and figure out how to use them in people.
So there are still some glitches to work out, but it’s probably the most promising lead
we have in the fight against cancer.
So it’s true: We haven’t found one cure for cancer yet, but that’s kind of a question
wrongly asked; there is no cancer to cure -- there are lots of cancers we need to cure.
Advances in things like DNA sequencing mean that, even though there are as many cancers
as there are cancer patients, soon there may be as many cancer treatments as there are
cancers.
And that’s pretty good news.
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