Everyone responds differently
to medicines. The dose of a
drug that cures one person can
be ineffective-or even
toxic-in someone else.
Although many non-genetic
factors play a role in how an
individual patient responds to
a particular drug treatment,
many differences in drug
response come from genetic
variation. Individual
more

Everyone responds differently
to medicines. The dose of a
drug that cures one person can
be ineffective-or even
toxic-in someone else.
Although many non-genetic
factors play a role in how an
individual patient responds to
a particular drug treatment,
many differences in drug
response come from genetic
variation. Individualizing a
drug's dose based on
pharmacogenomic information
can help a patient get the
most benefit from a drug while
minimizing side effects. Take
the example of treating
colorectal cancer with a
chemotherapy regimen that
includes Camptosar
(irinotecan). A gene, called
UGT1A1, produces an enzyme
that metabolizes Camptosar.
Variations in this gene can
influence a patient's ability
to break down the drug. About
10 percent of the North
American population has a
variation of the UGT1A1 gene
that reduces their ability to
metabolize Camptosar, leading
to high blood levels of the
drug and a higher risk of
toxic side effects. If these
patients are given standard
doses of Camptosar, about half
will develop severe
neutropenia, which can be
fatal. A test, called the
Invader UGT1A1 Molecular
Assay, can identify whether a
patient has the genetic
variant affecting the
metabolism of Camptosar and
thus would be at higher risk
for developing severe
neutropenia. The drug label
says to consider lowering the
starting dose of the Camptosar
for those patients found to be
high risk.FDA Patient Safety
News: June 2007For more
information, please see our
website:http://www.accessdata.
fda.gov/scripts...

Category News & Politics

Tags camptosar, irinotecan, pharmacogenomics, colon, cancer, toxicity, chemotherapy, genetics