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[MUSIC]
GRAY: Cancer is one of the most complex diseases that mankind has to face.
We used to think that cancers were more or less similar as long as you stayed within one
anatomic site, like breast cancers tended to be similar to one another and colon cancers
tended to be similar to one another. What we now know is that’s not at all true.
HAYES: If you look at lung cancer, the number one cancer killer in the world by a mile,
the number one variant of this tumor is called non-small cell lung cancer. If you think about that
for a second, that means “we don’t know what it is, but it’s not small-cell.” That’s the diagnosis that most
people in the world carry today when they’re diagnosed with the number one cancer killer.
So, it’s a disease, which is not further classified in most cases and I will acknowledge that there
have been some very interesting developments over the last five years. For most patients, those
developments still are not part of the treatment paradigm. So, I’m looking for rethinking
the number one cancer killer in the world.
LEVINE: If we can figure out what type of genomic defects exist in a given tumor for an individual person,
we can then try to tailor this therapy towards that individual person.
HAYES: In glioblastoma we were able to generate an amazing data set of integrated data with gene
expression and copy number mutation. One of the things that we noticed was groups of patients with
glioblastoma who had very different patterns of disease. We called these subtypes and this type of subtype
discoveries something we do a lot in cancer research. One of the important things is that the subtypes look
like they differed by one of our most exciting therapeutic targets and that’s the epidermal growth factor receptor.
LEVINE: In the past, many targeted trials have failed because they’ve taken one drug to treat
a whole population of patients. But if you can identify the best population to match a given
drug with, you’re more likely to achieve success, and even great success, in a smaller fraction of
patients who have this disease.
CHIN: That type of success example is driving the effort to count in parallel characterize the
changes as we’re doing in TCGA, but in parallel, also influencing a shift in clinical practice, where
more and more physicians and more and more hospitals are beginning to think about how they
can profile their patients coming in so that they have the information and match them up to the right therapy.
LINEHAN: I can see a day not too far from now, when physicians like me would be doing that
routinely and that would then let us pick a directed therapy, a personalized therapy for that patient’s cancer.
We set out nearly thirty years ago to identify the genes that cause cancer of the kidney. It took us ten years to
find our first gene. Now, we’re very happy about that. We can use that gene to make the diagnosis earlier in
a whole lot of families and in patients with this disorder, with this cancer. But also, now the FDA has approved six
drugs, six drugs for patients with advanced cancer based on that first cancer gene.
What it took us ten years to do with the Cancer Genome Atlas, we could probably now do in six months.
It’s just so much faster. Even though we’ve come a long way, we have a long way to go.
[MUSIC]