This is a breakthrough using a failed protocol and a possible gamechanger for brain tumors in particular.
I wonder how it may work with a baking soda protocol happening aswell to block the ability of the cancer to respond to a direct attacklike this. These are simple ideas but we surely need the data and itis safe enough to push that envelop.
We continue to see a wide range of new therapeutic approaches comingon board and what is becoming badly needed is way more directinvolvement with patients and their doctors to produce a far largerempirical database to support this work.
Small-molecule drugdrives cancer cells to suicide
Studies in mice showtherapy is effective even in hard-to-treat brain tumours.
Zoe Cormier
07 February 2013
http://www.nature.com/news/small-molecule-drug-drives-cancer-cells-to-suicide-1.12385
Cancer researchershave pinned down a molecule that can kick-start the body’s owntumour-destroying systems, triggering cell death in cancerous but nothealthy tissue in mice.
The molecule, TIC10,activates the gene for a protein called TRAIL(tumour-necrosis-factor-related apoptosis-inducing ligand), which haslong been a target for cancer researchers looking for drugs thatwould avoid the debilitating effects of conventional therapies.
“TRAILis a part of our immune system: all of us with functional immunesystems use this molecule to keep tumours from forming or spreading,so boosting this will not be as toxic as chemotherapy,” says WafikEl-Deiry, an oncologist at Pennsylvania State University in Hersheyand lead author of the study, which is published today in ScienceTranslational Medicine1.
Experimentsshowed that TIC10 had potent effects against a variety oftumours, including breast, lymphatic, colon and lung cancer. It wasespecially effective at triggering cell suicide in glioblastoma, akind of brain tumour that is notoriously difficult to treat2. Micewith glioblastomas that were treated with TIC10 in combination withbevacizumab — a drug used against diseases including brain tumours,and sold under the name Avastin — survived three times as long asuntreated mice. Even mice treated with TIC-10 alone still had bettersurvival rates (6% longer) than those treated with bevacizumab alone.
Quick andcollaborative
El-Deiry says thatTIC10 is so effective because it is much smaller than proteins thathave previously been tested as TRAIL-based drugs. The molecule is socompact that it can cross the blood–brain barrier, which separatesthe main circulatory system from the brain. This barrier normallyacts to prevent hazardous agents such as microbes from infecting thebrain, but can also thwart anti-cancer drugs by keeping them out. “Wedidn’t actually anticipate that this molecule would be able totreat brain tumours — that was a pleasant surprise,” saysEl-Deiry.
Furthermore, it seemsthat TIC10 activates the TRAIL gene not only in cancerous cells, butalso in healthy ones. This gives it enormous potential to create a'bystander effect', in which apoptosis — or cell death — isinduced in cancer cells immediately next to healthy ones. Healthycells are also stimulated to increase the amount of TRAIL receptorson their cell surface. These receptors can then bind to the adjacentcancerous cells, triggering their demise. “It’s almost likeTRAIL-plus — it does so much more,” says El-Deiry.
Tough TRAIL
This is by no meansthe only mechanism thought to trigger cell death in cancer. Inparticular, cancer researchers have been developing a number ofdrugs, including TRAIL-based therapeutics, that work by activatingthe cellular messenger tumour protein 53 (p53). But p53-based methodsare not always effective, says El-Deiry. "Most tumours havedysfunctional p53, so in order to develop new therapeutics forcancer, one needs them to be effective in tumours with mutated p53,”he explains. His team's approach bypasses p53 entirely.
Although the study waslimited to mice, the team is confident that a similar approach wouldwork in humans. Other researchers are sceptical, in part becauseTRAIL-based strategies have not lived up to past hype.
The potential for TRAIL to usher in a new age in cancer therapywas first identified in the mid-1990s3. However, although earlyclinical trials for TRAIL-based therapies showed little toxicity,they were not very successful at treating cancer, says AndrewThorburn, an oncologist at the University of Colorado Denver, whoco-authored a review on the subject last year4. “All the largeclinical trials found no significant survival benefit to addingTRAIL-based therapeutics to standard treatments,” he ads. Manylarge biomedical research groups have shelved their TRAIL-baseddrugs.
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