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SCIENCE
NEWS
This Week
gaps, such as the exclusion of data from the
charter-boat fishing in the Southeast.
Coleman and her colleagues worked out
ways to fill in the gaps. Their new estimate
for the annual recreational landings for
all species, not just the troubled ones,
comes to 4 percent. In all the calculations,
bycatch, discards, and catch-and-release
fish are omitted.
The team removed from its analysis menhaden and pollack, the two species with the
largest commercial catch. These fish are neither flagged for concern nor much targeted
for sport. For the remaining 907 saltwater
species, sportfishing accounted for 10 percent of landings.
The researchers then focused on fish
that the National Marine Fisheries Service
has assessed as either overfished or
experiencing overfishing. Coleman and
her colleagues determined, for example,
that recreation accounts for 59 percent of
red snapper landings in the Gulf of Mexico and 93 percent of red drum landings
in the southern U.S. Atlantic.
The researchers also calculated the share
of recreation landings by region for the
troubled species: 12 percent in the Northeast, 38 percent in the southern Atlantic,
and 59 percent off the Pacific Coast.
The data may suggest a need for new limits on recreational fishing for some species,
say Coleman and her colleagues. Often,
anglers are permitted to catch only a limited number of fish of a given species, but
regulators rarely limit the number of people who may fish.
Michael Sissenwine, chief science advisor at the National Marine Fisheries Service

in Silver Spring, Md., responds that the

impacts of recreational fishing have always
been recognized by fisheries managers.
According to Andrew Rosenberg of the
University of New Hampshire in Durham,
a former deputy director of the National
Marine Fisheries Service, the role of
sportfishing hasnt always been appropriately factored into management plans,
but often for political reasons, not lack of
knowledge.
Marine ecologist Jane Lubchenco of Oregon State University in Corvallis welcomes
the new report because, although some scientists worried about the impact of recreational fishing, nobody had the numbers,
she says. S. MILIUS

Keeping Cells
under Control
Enzyme suppression
inhibits cancer spread
Shutting down an enzyme can slow the

spread of cancer in mice, scientists in Israel

report. The finding suggests that further
study of this enzyme, called heparanase,
might lead to a treatment for cancer
patients.
Normally, heparanase facilitates cell
migration in the body. This enables immune
cells, for example, to travel to sites of infection. To provide this service, heparanase
cleaves a carbohydrate called heparan sulfate, one of the components of tough organic
sheets located throughout the body.
These sheets, called basement membranes, typically serve as scaffolding for
cells making up an organ. If those cells
become cancerous, the membrane provides an added benefit: It keeps the tumor
cells in place.
Unfortunately, excess heparanase can

FISH COUNT Once targeted by both recreational and commercial fishing boats, the
economically important lingcod is one of many species being overfished.
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VOL. 166

weaken the membrane and permit metastasis, the spread of malignant cells to
other organs.
Scientists have been building a case
against heparanase for years. Theyve noted
that tumor cells often contain excess
heparanase and that a high concentration
of heparanase in the urine of cancer
patients correlates with aggressive cancers.
Even more incriminating is evidence
that when heparanase degrades heparan
sulfate, the reaction releases growth factors. These include proteins that may stimulate growth of blood vessels that nourish
tumor growth (SN: 7/24/99, p. 53).
In the new study, Israel Vlodavsky and his
colleagues at the Israel Institute of Technology in Haifa short-circuited production
of heparanase to clarify its role in cancer.
In laboratory-dish experiments, they
compared the number of breast cancer
cellssome with heparanase and some
genetically engineered to lack itthat broke
through a sheet resembling a basement
membrane. Three times as many breast
cancer cells producing heparanase penetrated the membrane as did those lacking
the enzyme. The team got similar results
when it used brain cancer cells.
Next, the researchers implanted lymphoma cellssome making heparanase
and some notunder the skin of mice. The
animals survived significantly longer before
succumbing to the cancer when the lymphomas lacked the enzyme, the researchers report in the Aug. 18 Journal of the
National Cancer Institute.
Autopsies revealed that, after the lymphomas metastasized to the liver, the
tumors devoid of heparanase showed
poor-quality blood vessel growth. Without heparanase, growth factors dont seem
to escape the clutches of heparan sulfate
to stimulate the vessel growth that
strengthens the tumors, Vlodavsky and his
colleagues assert.
Finally, Vlodavsky and his colleagues
injected mice with melanoma cells with or
without heparanase-making capability.
Nine times as much metastasis occurred in
the lungs of animals receiving melanoma
with heparanase as in the others.
This is an important study showing a
necessary role for [heparanase] to drive
cancer invasion, angiogenesis, and metastasisthe lethal aspects of cancer, says
Lance A. Liotta, a pathologist at the
National Cancer Institute in Bethesda, Md.
Heparanase constitutes a potential therapeutic target for cancer therapy.
While an anti-heparanase strategy
holds promise, its unlikely that inhibiting
this enzyme alone will do the job, says
Douglas D. Boyd, a molecular biologist at
M.D. Anderson Cancer Center in Houston. Id be far more optimistic about multiple combinations [of enzyme inhibitors]
being successful, he says. N. SEPPA
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