Another treatment to be bought out and shelved.
Article is here http://cancerres.aacrjournals.org/content/73/16/5169 in pdf format.A BREAKTHROUGH treatment that prompts cancer cells to kill themselves is set to revolutionise treatment and could be available within five years.
The medical breakthrough by scientists at the University of NSW came from research into the devastating and deadly childhood cancer neuroblastoma.
However it has also been proven to destroy melanoma cancer cells and is expected to be effective in treating most cancers.
The journal Cancer Research reports today that the compound TR100 targets the protein tropomyosin, which is one of the building blocks of cancer cells. "It is much like what happens when you see a building collapse on the TV news," researcher Professor Peter Gunning, from UNSW Medicine said.
"Our drug causes the structure of the cancer cell to collapse - and it happens relatively quickly."
Read more: http://www.news.com.au/lifestyle/hea...#ixzz2cA69s2vi
Another treatment to be bought out and shelved.
So what are these other treatments?
Those other treatments you may have heard likely didn't even get past Phase 1. TR100 is promising in its specificity for targeted tropomyosin proteins in various cancer cells. Hopefuliy it gets through all the trialing and becomes part of the chemotherapy process.
Tropomyosin is also present in large quan ies in muscle cells and is critical in muscular contraction.
It will be interesting to see how specific these compounds are. The magic bullet has always been a tough nut to crack.
I remember interferon...
wow I hadn't heard/seen interferon in years.
It was the hyped anti cancer cure all.
I remember, just hadn't heard the term in some time.
Five candidate drugs made from the compound are currently being tested on animals in the United States to determine whether they cause any toxicity.It will be used in conjunction with other chemotherapies.
Researchers hope to test the drug on a dozen Australian children with high-risk neuroblastoma in 2015 but need $1 million to get the trial under way.
I was only able to read the abstract of this, but testing has been mostly in vitro so far from what I've read. Interesting concept and it makes sense, but I'll get excited when there are successful clinical trials on actual CA pts.
In an equally impressive breakthrough, did you read the (paraphrased) "10 crazy things celebrities do to stay hot" article advertised in the OP's link:
The puts doodoo on her faceVictoria Beckham (Posh e) apparently loves using a mask of rice bran and water mixed with powdered nightingale droppings – the beauty treatment that was behind the flawless complexions of Japanese geishas. “The urea in the droppings has whitening enzymes,”![]()
Naive times when interferon hit the world. Looking back it was apparent we thought Cancer was going to be easy.
I am skeptical of the OP. They are targeting a ubiquitous protein in muscles. Side effect potential is huge imo based solely on the abstract. There is obviously more to this.
From article:
Of the two isoform categories under which tropomyosin falls under, muscle and nonmuscle, TR100 targets the nonmuscle type (the one that's required in cellular interactions and the regulation of the cell's cytoskeleton).We have developed a novel class of anti-tropomyosin (an m) compounds, which preferentially target cytoskeletal (nonmuscle) tropomyosin-containing filaments in cancer cells.
So add at the end of your quote, cellular interactions and the regulation of the cell's cytoskeleton only in cancer cells?
Don't understand where you're going with this but I'll try. The study shows that TR100 targets isoforms of tropomyosin that are upregulated in various cancer cell lines.
When cells divide, the cell signaling is relayed by the following proteins in sequence: Ras → BRaf → MEK → ERK. Keep in mind that a lot happens in throughout the cell signaling (upregulating and downregulating of pathways). In various cancer cell lines, one of these is usually mutated, which leads to the common (common as in being common among various cancer cells) upregulation of integral components such as the cytoskeletal tropomyosin isoform in question, cytoskeletal Tm5NM1/2 containing actin filaments (the tropomyosin isoform that's targeted by TR100). I believe the aforementioned regarding common upregulations among different types of cancer cells is a primary reason why the article emphasizes this new development of anti-actin compounds as being a viable treatment for a variety of cancers.
All said in the first sentence.
I am not going anywhere. Just skeptical as I have seen so many of these compounds before that later are found to have side effects because they are not as specific as first thought, illicit an immune response, etc... But it's cool.
Cool. I was kinda confused as to what you were actually asking. That said, it'd be better if you were a bit more specific regarding your concerns. Judging from the concerns addressed in your first couple of posts, I thought you would go the route of elaborating on the part where the article talks about TR100's lack of absolute specificity for the targeted isoform.
Do you have a copy of the entire article?
I was gonna shoot Brody the link to the article so he could see dem in vivo studies, tbh
Thanks. Just skimmed over it briefly, but will read the whole thing at work tomorrow. For the poster who was questioning the side effects, there's a section en led: "TR100 has minimal impact on differentiated cells." Like I said earlier, this is pretty cool stuff but I'll be more interested once they've started clinical trials on CA patients (assuming they already haven't).
they were just animals, right?![]()
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