This is a breakthrough using a failed protocol and a possible game
changer for brain tumors in particular.
I wonder how it may work with a baking soda protocol happening as
well to block the ability of the cancer to respond to a direct attack
like this. These are simple ideas but we surely need the data and it
is safe enough to push that envelop.
We continue to see a wide range of new therapeutic approaches coming
on board and what is becoming badly needed is way more direct
involvement with patients and their doctors to produce a far larger
empirical database to support this work.
Small-molecule drug
drives cancer cells to suicide
Studies in mice show
therapy is effective even in hard-to-treat brain tumours.
07 February 2013
Cancer researchers
have pinned down a molecule that can kick-start the body’s own
tumour-destroying systems, triggering cell death in cancerous but not
healthy tissue in mice.
The molecule, TIC10,
activates the gene for a protein called TRAIL
(tumour-necrosis-factor-related apoptosis-inducing ligand), which has
long been a target for cancer researchers looking for drugs that
would avoid the debilitating effects of conventional therapies.
“TRAIL
is a part of our immune system: all of us with functional immune
systems use this molecule to keep tumours from forming or spreading,
so boosting this will not be as toxic as chemotherapy,” says Wafik
El-Deiry, an oncologist at Pennsylvania State University in Hershey
and lead author of the study, which is published today in Science
Translational Medicine1.
Experiments
showed that TIC10 had potent effects against a variety of
tumours, including breast, lymphatic, colon and lung cancer. It was
especially effective at triggering cell suicide in glioblastoma, a
kind of brain tumour that is notoriously difficult to treat2. Mice
with glioblastomas that were treated with TIC10 in combination with
bevacizumab — a drug used against diseases including brain tumours,
and sold under the name Avastin — survived three times as long as
untreated mice. Even mice treated with TIC-10 alone still had better
survival rates (6% longer) than those treated with bevacizumab alone.
Quick and
collaborative
El-Deiry says that
TIC10 is so effective because it is much smaller than proteins that
have previously been tested as TRAIL-based drugs. The molecule is so
compact that it can cross the blood–brain barrier, which separates
the main circulatory system from the brain. This barrier normally
acts to prevent hazardous agents such as microbes from infecting the
brain, but can also thwart anti-cancer drugs by keeping them out. “We
didn’t actually anticipate that this molecule would be able to
treat brain tumours — that was a pleasant surprise,” says
El-Deiry.
Furthermore, it seems
that TIC10 activates the TRAIL gene not only in cancerous cells, but
also in healthy ones. This gives it enormous potential to create a
'bystander effect', in which apoptosis — or cell death — is
induced in cancer cells immediately next to healthy ones. Healthy
cells are also stimulated to increase the amount of TRAIL receptors
on their cell surface. These receptors can then bind to the adjacent
cancerous cells, triggering their demise. “It’s almost like
TRAIL-plus — it does so much more,” says El-Deiry.
Tough TRAIL
This is by no means
the only mechanism thought to trigger cell death in cancer. In
particular, cancer researchers have been developing a number of
drugs, including TRAIL-based therapeutics, that work by activating
the cellular messenger tumour protein 53 (p53). But p53-based methods
are not always effective, says El-Deiry. "Most tumours have
dysfunctional p53, so in order to develop new therapeutics for
cancer, one needs them to be effective in tumours with mutated p53,”
he explains. His team's approach bypasses p53 entirely.
Although the study was
limited to mice, the team is confident that a similar approach would
work in humans. Other researchers are sceptical, in part because
TRAIL-based strategies have not lived up to past hype.
The potential for TRAIL to usher in a new age in cancer therapy
was first identified in the mid-1990s3. However, although early
clinical trials for TRAIL-based therapies showed little toxicity,
they were not very successful at treating cancer, says Andrew
Thorburn, an oncologist at the University of Colorado Denver, who
co-authored a review on the subject last year4. “All the large
clinical trials found no significant survival benefit to adding
TRAIL-based therapeutics to standard treatments,” he ads. Many
large biomedical research groups have shelved their TRAIL-based
drugs.
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