PHOTO COURTESY OF ZHENKUN LOU
Zhenkun Lou, lead researcher at the Mayo Clinic (seated), and colleague Huadong Pei.
small fraction of the 200 cancer genes, they account for many of
the most common forms of cancer.
Two years ago, Massachusetts General built the country’s
first hospital lab for genetic profiling. Researchers initially examined only lung, colorectal, and brain tumors. As targeted drugs
expanded to treat a wider variety of cancers, so did testing. Borger’s lab now offers profiling for every cancer patient at the Boston
hospital, and similar labs are now cropping up in cancer centers
across the country.
In the new version of the profiling process, after a pathologist
examines cells collected during a biopsy, his or her analysis is sent
to Borger’s lab, where DNA, RNA, and microRNA are extracted and
then multiplied to create enough for analysis. Technicians heat
the DNA to separate the double helix into two single strands and
add an enzyme to initiate a polymerase chain reaction (
sometimes called DNA cloning), which in turn builds two new DNA
strands. Each new DNA molecule now consists of one original and
one copied strand. With more heat and the addition of a Taq polymerase enzyme, the new molecules multiply again to create four
molecules, then eight, sixteen, and so on. In just a few hours, one
DNA molecule can grow to more than a billion, providing Borger
and his team with enough material to determine whether the
tumor’s mutation matches any of the growing arsenal of targeted
Attacking on many fronts
Like the roots of cancer, targeted drugs are varied. Herceptin is one
of several signal transduction inhibitors that block enzymes and
growth factor receptors that promote uncontrolled growth. Herceptin also belongs to another class of targeted drugs called mono-clonal antibodies, synthetic molecules that mimic natural antibodies and stimulate the immune system to attack cancer cells.
Still other targeted drugs block angiogenesis, or the formation
of blood vessels. These drugs, including the widely used Avastin,
stem from research started half a century ago, when Judah Folkman speculated that a cancer tumor produces a substance that
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sparks the development of blood vessels and that without this
blood supply the tumor would be destroyed.
Folkman worked on his theory in relative obscurity for more
than 20 years before discovering natural proteins that inhibit
angiogenesis. This discovery, in turn, led to the development of
drugs that mimic that inhibition.
Conventional chemotherapy or radiation also is commonly
prescribed along with targeted therapy. Targeted drugs work
to stop tumor growth, while the other treatments destroy the
tumor. As the Cancer Genome Project uncovers more cancer
genes and mutations, Borger and other scientists will be able to
identify them in biopsied cancer cells. His hope is that therapies
that target those mutations will keep pace.
“When we profile lung cancer or colorectal cancer, we can
identify mutations in 60 to 70 percent of the cases,” he says. “We
want to tell every patient we can pair their cancer with therapy.
But at present, the question is, ‘Is there a drug available?’”
Cynthia Washam is a freelance writer based in southern