Efforts under way at these two cancer centers are creating some of the first
ripples in what many scientists predict
will be a growing wave of genetic testing
of tumors. Traditionally doctors order
tests to see if just one of a small handful
of genes is broken, and such tests have
been used widely for the treatment of
only breast cancer and a few other cancer types. But that piecemeal approach
is giving way to more comprehensive
probes of cancer’s molecular workings.
Big cancer centers and clinical labs at
university-affiliated hospitals around
the country are now adopting tumor-testing programs similar to those in
Massachusetts and Oregon. Even though
the wave has yet to swell outside of academic centers to smaller community
hospitals and doctors’ offices, some clinicians are already finding troublemaker
genes and drugs that can counteract
them. Scientists are taking the process
many steps further in the lab, deciphering a tumor’s complete genetic instruction book. Having such information, at
least in the case of one man with a rare
cancer, has helped uncover unexpected
cancer drivers and tailor patient care.
Such comprehensive testing is begin-
ning to change the way many doctors and
researchers think about cancer. Soon
tumors may be diagnosed and treated
much like an infectious disease. Just as
identifying the bacteria or virus respon-
sible for an infection helps doctors pre-
scribe the right medication, finding the
mutations behind a tumor could lead to
treatments that target and knock out
cancer cells while sparing healthy ones.
Live (longer) with it
Pharmaceutical companies have a couple of success stories that suggest Ryan’s
vision may not be far-fetched. A drug
called Gleevec has extended by years the
lives of people with one form of leukemia.
That drug stops the cancer-promoting
action of specific proteins that help tell
a cell when to grow and divide.
Some cancer-causing mutations
switch these proteins, known as tyrosine
kinases, to a permanent “on” position,
like the accelerator pedal in a car getting
stuck to the floor. Gleevec helps pull back
on the throttle, slowing or stopping the
cancer’s growth. Other drugs (erlotinib,
gefitinib, cetuximab) block the action of
a tyrosine kinase called the epidermal
growth factor receptor or EGFR, which
turns on cell growth programs. Genetic
mutations that keep the protein permanently active or that cause too much of it
to be produced can lead to lung cancer.
Despite these signs that targeting
specific genes and their products can
help fight cancer, only about 5 percent
of all cancer patients have benefited
from genetic testing thus far, estimates
Daniel Haber, a cancer geneticist at Mass
General who counts the development
of erlotinib as the happiest experience
of his research career. Yet the number of
beneficiaries may be about to grow.
Tumor testing dreams though some patients do benefit from drugs that target specific cancer-causing mutations, in most cases a tumor’s
underlying mutations are unknown. Someday, researchers hope, comprehensive genetic tumor testing (steps depicted below) will become cheap
and fast enough to influence patient care, providing every cancer sufferer with personalized treatment.
E. FEliciano
Extract genetic information from multiple
cells in a tumor, as
well as healthy cells
in the same patient
for comparison.
Decipher the genetic
blueprint, identifying
mutations and sites
where genes are
lost, inserted, duplicated or otherwise
modified.
Using online databases of known
cancer-related genes,
catalog the modifications and try to
pinpoint the troublemakers.
Deliver a cocktail of
drugs that target the
potentially troublesome genes and
protein products.
assess the patient’s
health. Switch up
the drug cocktail as
needed, or get new
genetic information
as the tumor cells
change over time.
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September 24, 2011 | SCIENCE NEWS | 19
