AARP The Magazine - April/May 2012

used to think of cancer by organ. Now we must think
about it as molecules in order to target the treatment
specific to that person’s cancer.”
Most cancers have yet another means of confounding
doctors: metastasis, which is when cancer cells enter
lymphatic and blood vessels and then travel and invade
other parts of the body. Just when you think you have
nailed them, cancer cells ensconce themselves in some
other organ, where they may remain dormant for years
before resurrecting old habits.
Metastasis is a killer: It’s “responsible for more than 90
percent of the morbidity and mortality associated with
cancer,” according to the AACR’s 2011 Progress Report,
and it has baffled the medical community for years. Why
do many cancers resist confinement? Why do some cancer
cells travel to, say, the liver and others to the brain? And
why do the same types of cancer metastasize differently in
one patient than in another?
Cancer presents one more significant hurdle: The
mutated cells adapt, particularly under the stress of treat-
ment, and they often adapt differently in any two people.
Despite these challenges, most researchers would agree
that their understanding of cancer improved significantly
in the years following the National Cancer Act. “It’s an
explosion of knowledge,” says Garber.
A case in point is the drug that Stutman takes—Gleevec—
which has transformed gastrointestinal stromal tumors
(GIST) and another form of cancer—chronic myelogenous
leukemia (CML)—from fatal illnesses into chronic ones.
The first breakthrough came in 1973, when Janet Rowley,
M.D., at the University of Chicago, showed that in those with
CML, chromosome 22 attaches to chromosome 9. It would
be another 10 years before Dutch and American research-
ers discovered the full significance: The 22-9 attachment
had prompted two genes to fuse. The resulting “oncogene”
triggered the uncontrolled cell division of CML.
All of this was great for the textbooks. What made a
difference to CML and GIST sufferers was the discovery
by Brian Druker, M.D., of the Oregon Health and Science
University in Portland, of a molecule that would block
a protein produced by the gene, and turn off its replica-
tion switch. The cancer community had its long-sought-
after magic bullet. Gleevec, the drug that emanated from
Druker’s research, attacked the root of the problem but left
the healthy cells alone—a type of chemotherapy with far
fewer side effects.

So where does that leave us today? Are we close to find-
ing a cure for cancer?
Not quite. Cancer remains a disease too diverse and too
canny to be eradicated anytime soon. But researchers are
working on multiple fronts not only to discover additional
drugs like Gleevec but to reduce the incidence of most
forms of cancer and to improve the treatments.
Just last year the FDA approved vemurafenib, which has
proven successful in the treatment of melanoma.
Some 150 “chemoprevention” clinical trials are under
way across the country, testing drugs that will reduce the
incidence of cancer in high-risk populations. Tamoxifen and

1972
1971
The development
of computed tomog-
raphy (CT) revolu-
tionizes radiology.
FDA approves
the first vaccine
against hepati-
tis B, one of the
primary causes
of liver cancer.

1981

Early
1990s

For the first time,
overall cancer
death rates
begin to fall.

Cancer
survivors reach
12 million,
a four-fold
increase since
1971 and a
20 percent
increase
since 2001.

2012
President
Nixon signs the
National
Cancer Act.

2001

1964
A U. S. Surgeon
General’s report
establishes an
undeniable link
between smoking
and cancer.
1973
1973
Janet Rowley, M.D.,
shows chromosome
abnormalities in
those with cancer.

The FDA approves Gleevec,
the first drug to target a
specific gene mutation.

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