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Health Briefs
April
19, 2002
by Robert A. Wascher, M.D., F.A.C.S.
ANTI-INFLAMMATORY RXs MAY REDUCE
GROWTH OF BREAST CANCER CELLS
I have previously reported on intriguing research that may help to explain
why some cancers appear to be less common in people who regularly take
certain anti-inflammatory medications (e.g., aspirin, ibuprofen, naproxen,
Vioxx, Celebrex, etc.).
In the current issue of the journal
Cancer Research, new research shows that the growth of at least
some types of breast cancer cells can be inhibited by exposure to Celebrex
and related anti-inflammatory drugs. These drugs inhibit a class of
enzymes referred to as COX enzymes (cyclooxygenase).
When exposed to Celebrex in this study,
breast cancer cells that normally produce COX not only grew at a significantly
slower rate, but when implanted into mice, Celebrex appeared to also
significantly reduce the number of these tumor cells that spread to
distant sites (metastasized).
Several different types of cancers have
already been shown to synthesize COX enzymes, including many breast,
prostate and colorectal cancers. However, it is currently unknown whether
all-or even most-types of cancer are responsive to these drugs, although
a great deal of research is currently underway to answer this question
(there are already several research studies that have shown an apparent
reduction in the risk of developing colon polyps in people who take
anti-inflammatory COX-inhibitors).
This is a very exciting area of cancer
research, as there are many anti-inflammatory drugs already approved
for human use. Of course, all of these medications can have potentially
serious side effects, and none of them are approved as "anti-cancer"
drugs at this time. However, I predict that this area of cancer research
is going to produce some significant breakthroughs in terms of cancer
prevention and, possibly, cancer treatment.
CHANGE YOUR SEX BY DRINKING WATER?
From the Proceedings of the National Academy of Science (PNAS)
comes a rather disturbing finding. Biologists have been studying an
apparently rising incidence of deformities in frogs throughout the United
States over the past decade or so. Missing or deformed limbs and abnormal
sex organs are two of the most commonly seen deformities in these amphibians.
The study in PNAS exposed African clawed
frogs to a pesticide called atrazine, which is in widespread use throughout
the US. Indeed, so prevalent is atrazine in the water supply, the FDA
sets allowable concentration limits for its presence in public drinking
water.
After exposing frog larvae in the laboratory
to concentrations of atrazine that were comparable to levels measured
in the wild, the University of California (Berkeley) researchers found
that male frogs became "demasculinized."
Worse still, many of the frogs went
on to develop microscopic evidence of hermaphroditism (the presence
of sexual organs from both sexes in one individual). A ten-fold decrease
in testosterone levels was also noted in the male frogs exposed to atrazine.
Scientists around the world have previously
linked, at least theoretically, the observed decline in human sperm
counts with the pervasive presence of certain pesticides in the environment.
Many of these compounds are so chemically stable that it may take many
decades for them to be broken down into less toxic substance. While
humans may or may not react to atrazine in the same manner as amphibians,
the results of this study are nonetheless worrisome, as frogs and humans
share amazing similarities when it comes to reproductive physiology.
RADIATION TREATMENT REDUCES REPEAT
NARROWING OF BYPASS GRAFTS
In coronary artery bypass patients who must subsequently undergo angioplasty
and placement of coronary artery stents (tiny expandable tubes that
help to keep the narrowed coronary artery open) because the arterial
bypass graft has become narrowed, repeated episodes of graft artery
narrowing can occur at the site of the stent. When this occurs, the
angioplasty must be repeated (using a tiny inflatable sausage-shaped
balloon) to allow blood to flow through the artery, and to the heart
muscle, once again. Drugs and radiation treatment are, therefore, routinely
used to reduce the risk of restenosis, or narrowing, in bypass grafts
taken from the arteries (internal mammary arteries) that run alongside
the breastbone (sternum). However,
the effectiveness of radiation treatments to heart bypass grafts taken
from leg veins has not been well studied. In almost all patients who
require multiple coronary artery bypasses, at least some of the bypass
grafts are created using the greater saphenous vein(s) from one or both
legs.
In this week's New England Journal
of Medicine is a report on the use of radiation treatment following
restenosis of previously stented saphenous vein bypass grafts. These
study patients had all undergone coronary artery bypass with saphenous
veins, and had subsequently required angioplasty and stenting of these
vein grafts due to stenosis. When the patients presented again with
recurrent stenosis in the stented segment of the bypass grafts, they
were treated, once again, with angioplasty.
A total of 60 patients then underwent
radiation treatment of the reopened vein bypass grafts and 60 patients
received only a "placebo treatment" (no radiation). The restenosis rate
in the irradiated group of patients was 21% after six months of observation,
as compared to a 44% restenosis rate in the placebo group. Likewise,
at 12 months, the irradiated group had required significantly fewer
(17% versus 57%) additional procedures to reopen a clogged bypass graft
than did the placebo group. Finally, 32% of the irradiated group experienced
a recurrent heart attack or death due to heart attack, while 63% of
the placebo group experienced such adverse events after 12 months of
observation.
Bottom line: in coronary artery bypass
patients who have required angioplasty and stenting of saphenous vein
bypass grafts because of bypass graft stenosis, irradiation of the stented
grafts should probably be considered.
Dr. Robert A. Wascher
Dr. Robert A. Wascher
is a senior research fellow in molecular & surgical oncology at the John
Wayne Cancer Institute in Santa Monica, CA
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