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First Anti-Cancer Nanoparticle Trial On Humans a Success
An anonymous reader writes "Nanoparticles have been able to disable cancerous cells in living human bodies for the first time. The results are perfect so far, killing tumors with no side effects whatsoever. Mark Davis, project leader at CalTech, says that 'it sneaks in, evades the immune system, delivers the siRNA, and the disassembled components exit out.' Truly amazing."
... to start smoking ....
They have RNA that attaches to cancerous and only cancerous cells. Of course, there are types of cancer that wont "bind" with this thingies, but supposedly, if I remeber correctly, they are the rarest.
NO SIG
Well, what's meaningful is that they all didn't up and die, and that a bigger round of testing is to go forward.
Non impediti ratione cogitationus.
The point of the study is to make sure that people don't explode when the procedure is performed, or for something similarly unpleasant to happen--it's a Phase I study, not a real effectiveness trial.
From comments on TFA, "The Lab" writes: "a science editor would be more capable of pointing out what is really exciting here, which is the ability to stop cells from producing a given protein."
I think the cancer aspect is great (if it works) but this has potential for curing a whole host of diseases.
Now we just need to figure out how to change people's DNA on the fly.
Not to mention there are now at least 15 extremely happy people out there :)
...
Well I can finally go to California, everything is known to cause cancer in California,
Or "its known to the State of California to cause cancer".
I could never figure it out, so I just stay away from California.
As long as the subjects have the same distribution as the population, this sample can be considered representative of the population. This means that they didn't pick 15 terminal patients and didn't pick 15 100%-survival-rate patients. You can achieve quite a lot when your sample is well selected.
The nanoparticles have a component that attaches to the transferrin receptor on the surface of a cancer cell. Transferrin receptors are highly abundant on cancer cells because iron (what transferrin carries) is needed for cell division processes. Coincidentally, this is a fact I learned the first time this story was posted a few days ago.
"FDA staff reviewers expressed concern about the number of patients who were left out of the study because they died."
How about Nature?
1. Start smoking, paying $$$ for cigs
2. Get cancer
3. Pay $$$ for an operation to remove cancer cells
4. ???
5. Profit ?!?
It's a phase-I trial, it only confirms safety already established in animal models and kinetics. Phase-II and phase-III trials, much larger in scale, assess efficacy and optimum dosing. That will tell us if this can be more effective than traditional chemotherapy (possible) and monoclonal chemotherapy (much more difficult to predict).
Incorrect. There are significant physiological and genetic differences between cancerous cells and normal cells. It would be entirely possible to target the RNA sequence to only bind to malignant cells and ignore normal ones.
Camel Lights, now with siRNA Nanoparticles!
Gizmodo? Call me when a reputable publication reports on this.
You came to Slashdot because Gizmodo isn't a reputable publication? Hehehe.
"I like to lick butts!" by MobileTatsu-NJG (#32700246) (Score:5, Informative)
What, those hippies? I want something Fair and Balanced!
All that will accomplish is to fill the world with beautiful, bisexual nympho women who still aren't interested in you...
I cannot see anything meaningful coming from such a small sample size. It has potential but obviously much more research is needed.
You can't just jump from rats to tens of thousands of humans. That's why the sample size is 15. That's why it's a Phase I trial. There are four phases of clinical pharmaceutical testing that follow preclinical (animals, in vitro, etc.) testing. Phase I normally tests a treatment in healthy humans in order to see the negative effects of the treatment (this is not necessarily the case in cancer treatments because all cancer treatments have significant negative effects). Phase I trials are only a couple dozen people, max. Successful Phase I trials allow for Phase II trials. These usually have one or two hundred people with the disease the therapy is intended to treat. In Phase II, they are mainly gathering pharmacokinetic data (half life, metabolism, volume of distribution, etc.). Phase III is where you start to see the trials you're clamoring for. These are typically done in several thousand patients, all with the disease in question. These trials are placebo-controlled, randomized, double-blind studies (the hallmark of research). Statistical analysis then allows you to determine if the therapy was effective in improving outcomes. If so, the drug goes to the FDA. 30 days later, it is officially on the market. Phase IV studies begin here, and continue perpetually. They are called post-marketing surveillance, and they study long-term effects (because previous trials are not long enough to do this), as well as very rare adverse effects (where the sample size in previous trials may have been too small to correctly detect the progressive multifocal leukoencephalopathy that occurs in 0.1% of patients treated).
So don't claim the study size wasn't big enough - it wasn't supposed to be. Phase III trials are what you want. Phase I and II trials are of no interest to anyone outside of health professions, really.
Please stop pluralizing words with an apostrophe. That is not what it is there for.
How else would you define targeting in this context other than to mean only binding to cancerous cells? It seems you are implying that targeting can only refer to conscious 'aiming', but that is only a subset of things that can be considered targeted.
Targeted can mean 'select as an object of attention or attack'. That is what they are doing when the design a drug.. selecting cancer cells for attack, and then designing the drug so it will only effect those cells. Check out http://en.wikipedia.org/wiki/Drug_design
Targeted drugs DO mean something specific in pharmacology.
Of course they do: ENHANCE!
If God forks the Universe every time you roll a die, he'd better have a damned good memory.
Great post. But please, can we stop using effect as a verb?
No. We only need to effect such a change such that people stop using the verb "to effect" incorrectly.
Let q be a radix > 1. I am in ur base-q, killing 10 d00ds.
> everything is known to cause cancer in California... I could never figure it out, so I just stay away from California.
Everything says it causes cancer because of Proposition 65. Basically, if something in California is known to cause cancer (even only if ingested by the ton), you have to label it, or lawyers can sue you under a "private attorney general" law. In theory it might be a good idea, but it was implemented so that the defendant has the burden of showing that it's basically impossible to the nth degree that the thing could cause cancer in the quantities you're talking about.
This resulted in a lot of litigation where basically lawyers went around everywhere and said "Oh! You have flame-retardant furniture! Did you know it can cause cancer if you lick it?" "You're a dentist! You use drugs that can cause cancer if you administer them for a week and you didn't post a notice!"
This resulted in a plethora of notices to prevent lawsuits--notices which the public ignores because they're on everything. So in the cases where the warning is actually important, it gets ignored because there are so many.
IIRC, there have been some efforts by the AG (and some courts) to limit abuse.
-- IANAL, this isn't legal advice, and definitely isn't legal advice for you. Also, Squee!
Any technology which is distinguishable from magic is insufficiently advanced.
Well, the summary says that the results have been perfect so far, so that's a real good sign. Frankly something like this sounds too good to be true, but every once and a while breakthroughs do happen, so we can hope!
We hope your rules and wisdom choke you / Now we are one in everlasting peace
Why is this the first example of the concentration of nanoparticles showing a correlation with the initial dose? To me it seems obvious that this would happen, so I'm curious as to what normally prevents this.
The dose-response characteristics of a substance carries important information about its pharmacokinetics, such as how rapidly it is metabolized and excreted. It is NOT obvious that increasing dose always results in increased concentration in the targeted tissue(s), just as it is the case in chemical reactions in which increasing the proportion of one reagent may not necessarily increase the yield. For example, increasing dosage may also increase hepatic clearance. What the researchers demonstrated basically boils down to this: the nanoparticles' activity is highly specific to the tumor cells and does not get "broken down" or excreted proportionally higher as the dose increases. Such characteristics are highly desirable.
It would be entirely possible to target the RNA sequence to only bind to malignant cells and ignore normal ones.
Yeah but chemotherapy and radiotherapy work the same way. The problem is that the characteristic of cancerous cells they bind to is the fact that they grow fast.
No they don't work the same way. Radiotherapy, and most current gen chemotheraputics, work against all dividing cells. It sounds like these nanoparticles use a specific protein (NOT rna) to bind to the cancer cell, then once inside they cause RNAi (this is where the RNA comes in) to knock down a specific gene transcript.
I obviously don't know the specifics, but if you make a nanoparticle that binds to and is taken up by cells expressing a specific growth factor, that's -not- going to be taken up by all cells. There are a lot of growth factors, and often in cancers, growth factor receptors are expressed far more than they normally are. So the targets are found only on some cell types, and there are hundreds more on the cancer cells than the healthy cells.
Furthermore, you could target individual genes to be knocked down by the RNAi effect, potentially genes that aren't even expressed by the normal cells which are expressing the receptor you're targeting. I'd guess for maximal efficiency, you'd be targeting housekeeping genes that all cells needed, but in principle you could make it a gene that cancer specifically needed.
Both levels of specificity, even if they're not used, are a far cry from "damage every dividing cell and hope you kill the cancer before you kill the dividing tissues the patient needs to survive." And they don't actually use RNA to bind to the cell, they use protein to target the cell and RNA once inside the cell to target the specific gene. ... by the way, I am not a molecular cancer biologist.