The Cancer Genome Atlas: Molecular Characterizations of Cancer

Uploaded by NCIresearchfunding on 28.01.2011

GRAY: What we lack right now is a comprehensive understanding of how variable
the cancers are, one to the next, and what common features there are between the cancers
so that we can begin to focus on those common features as possible sites of therapeutic attack
or as possible markers that would allow us to predict how a cancer is going to behave clinically.
LAIRD: TCGA is really important because until now we’ve been studying cancer as snippets,
really little pieces, bit by bit. I always like to use the analogy of the
elephant with the blind men feeling the elephant and one blind man feels one of the legs and thinks
an elephant looks like a tree. Another one grabs the trunk and thinks that it looks like a snake.
That’s really how we’ve been approaching cancer research and what TCGA is really set up to do is
to really get a complete picture of the whole elephant, to investigate all parts.
SANDER: We have to use all these different measurements that they’re doing in high tech
laboratories with lots of new technology and try to combine them in order to get a picture,
an image, a description of what’s happening in this tumor, what’s happening in the cells.
GABRIEL: The point of what we’re trying to do is really define the whole spectrum of mutations.
There’s every reason to believe that knowing about the entire spectrum of mutations within
a cancer will point you to a pathway you might never have thought about before.
CHIN: I think the other way to think about that is we’re trying to make a long list of
all the things that goes into making a cancer. It’s almost like the parts list for a car.
The mechanic needs it, but then the next step is the mechanic has to put all these bits and
pieces together to make a car. We’re trying to reverse engineer and figure out what makes a cancer.
SPELLMAN: Tumors evolve in sort of a random process. If we only looked at a handful of tumors, we wouldn’t
be able to tell the things that were randomly happening from things that are responsible for
the underlying process of tumor evolution.
LAIRD: We would not have been able to find out that this mutation in IDH1 occurred in
exactly the same tumors as our epigenetic profile if these had been done in separate studies.
Actually, the IDH1 mutation had been identified in a separate study and they had not identified
the epigenetic profile that goes with it because they didn’t have this comprehensive approach on
exactly the same samples.
SPELLMAN: A lot of studies might look at fifty or one hundred or even a few hundred tumors using
one assay and for Atlas, that’s not good enough. We need to know how changes in a gene expression
relate to changes in the DNA sequence and whether or not those changes in the DNA sequence are at the
level of single-based mutations that cause little changes in proteins, or at the level of duplications
or deletion events. All those coordinated analyses are what makes TCGA special.
GABRIEL: What the Cancer Genome Atlas will allow us to drive forward is taking a common set of samples
and understanding them completely.