Drug Turns Immune System Against All Tumor Types 330
sciencehabit writes, quoting an article in Science: "A single drug can shrink or cure human breast, ovary, colon, bladder, brain, liver, and prostate tumors that have been transplanted into mice, researchers have found. The treatment, an antibody that blocks a 'do not eat' signal normally displayed on tumor cells, coaxes the immune system to destroy the cancer cells."
The abstract and full paper are freely available. It seems fairly promising: "In mice given human bladder cancer tumors, for example, 10 of 10 untreated mice had cancer that spread to their lymph nodes. Only one of 10 mice treated with anti-CD47 had a lymph node with signs of cancer. Moreover, the implanted tumor often got smaller after treatment — colon cancers transplanted into the mice shrank to less than one-third of their original size, on average. And in five mice with breast cancer tumors, anti-CD47 eliminated all signs of the cancer cells, and the animals remained cancer-free 4 months after the treatment stopped."
Re:Mouse != Human (Score:5, Informative)
While, you have a point
that mice and humans are different enough that most cures don't translate 1:1 to humans.
at least it has been tested on
human breast, ovary, colon, bladder, brain, liver, and prostate tumors that have been transplanted into mice
, rather than just on mice anatomy.
Re:But... (Score:5, Informative)
Yeah this seems to be the problem with all chemotherapy drugs. They target fast growing tissue, including the immune system. Being treated for these conditions can make you wish you were dead.
Re:Optimisim (Score:2, Informative)
So does not curing them, because THEY DIE.
Your conspiracy falls short around every turn and faceplants into a wall every time.
Re:But... (Score:5, Informative)
The authors share your concern. From the paper [pnas.org]:
A concern in translating this therapy to human application is the potential for toxicity. CD47 is highly expressed on tumor cells, but also at varying levels on normal (nontumor) cells. However, here we demonstrate that blockade of CD47 in immune competent mice produces an effective antitumor response without unacceptable toxicity, albeit with a temporary anemia.
Re:But... (Score:5, Informative)
What about non-tumor cells, which also display this cell determinant?
They will die. But, from TFA: "CD47 is overexpressed on cancer cells". Cancer treatment is about destroying much more cancer cells than healthy ones.
Re:How long it will take to turn it into medicamen (Score:5, Informative)
I'm no expert in these things, but AFAIK the process goes something like this:
Each of these steps can take months. Some of it's political and administrative wrangling, some of it's just that the test itself will take some time before you can be sure of the results. A drug can fail at any one of these stages and it's back to the drawing board (or maybe the test tube).
The whole process takes years. Yet newspapers often start reporting about "miracle cure" drugs that have only just completed the first round of live animal trials. Which is why you hear about all sorts of miracle cures that never see the light of day.
I'll hazard a guess. (Score:4, Informative)
What is the normal function of the "do not eat" signal? Just what normal function is going to get messed up when you turn this off?
I'm not sure which "do not eat" signal they're talking about. But one that I do know a little about is the one that prevents rejection of a placenta and multiple sclerosis.
The immune system apparently recognizes and avoids attacking its own body primarily by:
- Editing the sections of DNA coding for antibodies to produce a bunch of small clones of proto-antibody-producing cells that randomly react to all sorts of stuff.
- Shortly after birth (when most of mommy's random cellular components have been purged from baby's body) letting these clones take a grand tour of baby's body - and anybody who recognizes anything dies off.
- Then the survivors (who don't recognize any tissue in baby) turn themselves on and get ready to do a growth spurt if they recognize a target at the same time they're getting an "I'm being damaged" signal (i.e. histamine).
Result: A no-autoimmune immune system. Well, almost.
A significant problem is that there are a few tissues that aren't deployed yet when the baby is just born. One such tissue is the myelin sheaths of the nerves. Another, of course, is placental tissue from a pregnancy. (Unlike tribbles, humans aren't born pregnant.) If nothing were done about this, the immune system tissues would be a time-bomb, ready to go into attack mode if it happens to see a damage signal near a nerve or a placenta. This would result in multiple sclerosis or spontaneous abortion - both very big negative scores in the evolutionary game. So the immune system has a patch.
The main myelin protein has a short sequence that tells the immune system that this is a late-blooming tissue, so leave it alone. (I'm guessing this may be the "do not eat" signal they're talking about.) Placental tissue has the same sequence. There are lots of opportunities for failure, of course. (Defects in the signal molecules, disease organisms mimicing it, etc.) But when this patch is working right the nerves and a new baby are protected without significantly degrading the immune system's response to diseases.
This, by the way, is the reason nursing on cow's milk is a risk factor for MS. Milk has a protein related to the myelin sheath protein, but with the "do not eat" signal slightly different. As a result a baby may develop an allergy to that component of cow's milk - and thus to the common stretch of the myelin protein. Result: Autoimmune reaction to the myelin sheaths.
Re:Sounds like Burzynski therapy (Score:5, Informative)
Probably because he's a fraud:
https://en.wikipedia.org/wiki/Stanislaw_Burzynski [wikipedia.org]
Miraculous claims require miraculous proofs. And doctors aren't just sitting on the sidelines waiting to be paid more to kill more people, despite what you might think.
Re:But... (Score:4, Informative)
The article states that it also weakens the defenses of blood cells, but that the mice's bodies produced enough replacement blood cells to compensate.
Re:But... (Score:4, Informative)
Although macrophages also attacked blood cells expressing CD47 when mice were given the antibody, the researchers found that the decrease in blood cells was short-lived; the animals turned up production of new blood cells to replace those they lost from the treatment...
Re:But... (Score:5, Informative)
Re:But... (Score:4, Informative)
Sadly anemia is a horrible symptom in itself. Best case is lightheadedness, extreme tiredness and complete inability to sustain even mild exercise ("look ma, the docter said I can't run and look !" <wham> patient lies unconscious on the floor, usually with a few bruises and a suspicious spreading discoloration in his/her face). Worst case it causes you to choke to death while your lungs are operating fine.
Re:Optimisim (Score:4, Informative)
Re:How long it will take to turn it into medicamen (Score:3, Informative)
Re:But... (Score:5, Informative)
That's the nature of drug testing. You test it out in several animals of varying levels of similarity to humans before you start testing in humans. Mice are a common starting point because they're inexpensive and small, and you can run trials with thousands of mice. Also, mice sort of self-destruct if things start going badly in them, they are fairly fragile. So they make good canaries because when things are going badly, the signs are not often subtle.
Plenty of compounds show promising results in mice that prove to have reduced results in later trials with more complex animals or in humans, or show side effects only later in the drug study regime. Conversely it's almost certain that there are compounds out there which would provide amazing results in humans, but which failed early stage drug studies in animals. It's just not a great idea to be testing drugs for the first time in humans without some idea as to what the outcome would be; the fatality rate in animals is pretty high, and you can purposely infect them to treat for a specific disease. There are drugs that even with this prep work still fail in clinical (human) trials, either because of efficacy problems or because of unexpected or more-severe side effects, or some combination (if it's effective but with bad side effects in animals, then not very effective and with horrible side effects in humans, it will be rejected).
The study in this article is the very earliest stage. Usually they do tiny studies like this as the very first trial. Many, many drugs produce interesting results at this stage, and fail the very next set of studies (statistically large populations, which 10 mice is not, even with extremely promising results such as this). The chances of such a drug making it to clinical trials is vanishingly small, almost all compounds fail, only a few ever make it.