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Antibody
By Shahida Nisar
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A new, more
targeted approach to treating autoimmune disorders
may stop Type 1 Diabetes
There are plenty of reasons
not to tell you about an experimental
new treatment for Type 1 diabetes, a particularly devastating
form of diabetes in which the body’s immune system
attacks the insulin-producing cells of the pancreas.
Experimental therapies often fail, and even
when the treatments
work, widespread availability is usually years
away. But study in the new England Journal of Medicine
last
month offers such intriguing insights into the future
of treatment, not
just for Type 1 diabetes but also for a number of auto-immune
disorders, that it’s hard to resist. Just keep
in mind that these are preliminary results.
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First a little background: no one
knows why the immune system goes haywire and starts triggering
auto-immune disorders, but at least one culprit is a particular
kind of immune cell called a T cell. In Type 1 diabetes (which
used to be known as juvenile-onset diabetes), T cells destroy
the cells of the pancreas. In multiple sclerosis, they cross
the bio-molecular barrier that protects the brain and attack
the outer covering of nerve cells. If you could deactivate the
right T cells, you might be able to slow down the degenerative
process, and may be halt it altogether.
That’s exactly what seems to have happened in the NEJM
study. Researchers cloned anti-bodies known to target T cells
and for two weeks gave them to 12 patients who had just had
Type 1 diabetes diagnoses. Another dozen patients received standard
medical care. A year later, doctors examined their subjects
and discovered that the disease had been halted in nine of the
patients who received the antibodies. The still had to take
insulin because the damage that had already occurred could not
be undone. Most of the control group, by contrast, seemed to
have got worse and had to take more insulin.
The most exciting thing about these results, say Jeffrey Bluestone,
an immunology expert at the University of California, San Francisco,
who developed the treatment, is that is show “you can fundamentally
change the immune system without the need for long-term therapy.”
In other words, the immune system can be retrained.
There are side effects, some patients developed fevers, rashes
and anemia. There’s also a theoretical possibility, says
Dr. Kevan Herold, principal investigator at Columbia University’s
medical school, that the treatment will increase the risk of
developing cancer. But for now, researchers are sufficiently
encouraged to launch another trial that will test whether repeating
the two-week treatments every 6 or 12 month makes a difference.
There are also plans to try the antibody treatment on a kind
of autoimmune arthritis that develops in people with psoriasis
(The treatment is not expected to work on Type 2 diabetes, which
has different causes.)
Doctors still have a lot to learn in their efforts to restore
the wayward defenses of patients with autoimmune disorders.
These new results suggest, however, that they are well on their
way. |
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French
Fries & Cancer
The
evidence is thin. But there are plenty of other reasons you
should go easy on the fries.As if the galore count on a supersize
serving of McDonald’s French fries weren’t scary
enough, one of the big health stories last month was a report
suggesting that eating any fried or baked starch could increase
your risk of getting cancer. According to Swedish
researchers, frying potatoes or other starchy foods triggers
the formation of an organic molecules called acrylamide, which
has been shown to cause cancer in lab rats.
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know what to do with a report like this. The evidence
is so preliminary. There’s no scientific paper to
read, no clinical-trial results to analyze, just a press
release and some figures on an Internet site. Even the
scientists from the University to Stockholm and the National
Food Association of Sweden, who scheduled a press conference
to announce their findings, are not calling for any special
action, just further study. They acknowledge that most
of the problems associated with acrylamides stem from
breathing them, not eating them. And if the Swedish results
holdup, there still may not be any cause for alarm. “Just
because you can detect something doesn’t mean it’s
significant,” says Mary |
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Ellen Camire, professor of food
science and nutrition at the University of Maine in Orono. Our
tools for detecting the presence of minute quantities of contaminants,
she points out, are far more refined than our understanding
of how the body deals with them.
No that frying is such a great thing, health-wise. Food scientists
have long known that our cooking processes create wide variety
of carcinogens. Grilling or broiling a nice marbled steak, for
example, dramatically increases the concentration of heterocyclic
amines-compounds that under laboratory conditions cause the
kind of genetic damage that leads to cancer. No one has proved,
however, that eating grilled steaks increases your chances of
getting cancer. (Nor is anyone likely to try; the endeavor would
be too difficult.) You would expect that after millions of years
of eating meat, our bodies might have evolved a few mechanisms
for getting rid of the carcinogens in burned flesh. But if you’re
worried about carcinogens, you can reduce your consumption by
marinating meat before grilling it. Don’t get me wrong.
I’m not defending deep-frying. The last thing we need is
to burden our hearts, not to mention our waistlines, with more
of the artery-clogging fat found in any fried food. But there
are already plenty of things you can do to reduce your risk
of cancer, starting with a vow to quit (or not start) smoking.
“You get more acrylamide from smoking than you do from
food,” says Lois Gold, director of the Carcinogenic Potency
Project at the University of California, Berkeley. You should
also eat at least five servings of fruits and vegetables a day,
go easy on red meat and exercise regularly. Taking these steps
can’t guarantee that you will never develop cancer, but
they may tip the odds in your favour. |
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Prevent
Before....!
As
cancer specialists from around the world gathered last month
in Orlando, Florida,
for the annual meeting of the American Society of Clinical
Oncology, a new sense of optimism
was in the air. It’s not that cancer has been cured there
are too many different types of malignancies to hope for a
universal treatment. Rather, it’s that doctors are beginning
to piece together new strategies for keeping cancer from recurring
and, in some cases, preventing if from taking
root in the first place. As ASCO president Dr. Larry Norton
puts it, “Cancer is not a bolt
of lightning. It’s more like a thunderstorm. We have
plenty of time to close the
windows if we know what to do.”
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One of those windows opens up right after a patient’s
initial treatment. It’s becoming clear that whatever form
that treatment takes, surgery, chemotherapy, radiation, medication,
what doctors and patients do in the weeks afterward may determine
whether a cancer comes back.
Breast cancer is a prime example. For more than two decades,
women with early stage, estrogen-sensitive breast cancers have
been treated with surgery followed by a combination of tamoxifen
and chemotherapy. Adding tamoxifen seemed to makes sense, since
it blocks estrogen’s cancer-promoting effects. It turns
out, however, that tamoxifen may act as spoiler, preventing
the chemotherapy agents from entering cancer cells and doing
their job. In a paper presented at the conference, researchers
reported on a finding that should change the way doctors threat
patients from now, on: after eight years of follow-up exams
women who waited until their chemotherapy was complete before
taking tamoxifen were 18% more likely to survive without a recurrence
than women who took them together.
In another study, women with early-stage breast cancer that
had spread to several lymph nodes significantly cut the risk
of recurrence simply by replacing one of the standard chemotherapy
agents with a drug called docetaxel (Taxotere). By blocking
cancer cell’s division and growth process, docetaxel reduces
the risk of tumour recurrence 50%.
And in a preliminary but promising finding in lung cancer, doctors
discovered that a special form of vitamin A might reverse some
of the changes in lung tissue caused by smoking. In a small
study, former smokers who took the vitamin A derivative produced
higher levels of a protein thought to be important in suppressing
tumour growth than ex-smokers who took a placebo.
Because cancer research is moving quickly, it pays for cancer
survivors, and their loved ones, to be vigilant. Think of cancer
as a chronic condition, one you will have to stay on top of
for the rest of your life. (This is also true for people at
high risk for cancer who have been lucky enough to escape it
so far.) Ask for your doctor regularly if you’re doing
everything you can to keep the tumours at bay. The latest studies
suggest that prevention really is the best medicine. |
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Smallpox Immunity
Just because you were vaccinated against
smallpox as a child doesn’t mean you would
be protected in the event of a bio-terrorism attack
now. That’s the conclusion of a study in which
researchers re-vaccinated more than 300 microbiologists
whose work put them at risk of infection. It turns out
that 0 out of 10 of the microbiologists developed swelling,
blisters and scabs at the new
inoculation site, all telltale signs that their prior
immunity had disappeared.
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