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Drug made from toxic weed kills cancer
- johndavidback 14y agoIf this drug also kills cells in near proximity to the cancer, would it be effective treatment for brain tumors?
- drharris 14y agoIt sounds like it wouldn't be perfect (some good brain cells would die), but it'd likely be a heck of a lot more selective than existing methods of dealing with brain tumors. And certainly better than an alternative of letting the tumor grow any more. It sounds like this could work on cancerous tissue in its infancy, which is probably the most promising thing. Imagine a potential vaccine for cancer, just enough dosage to kill that first bad group of cells.
- warfangle 14y agoThe bigger problem with brain cancer is crossing the blood-brain barrier, no? I don't think this molecule can do that.
- robbiep 14y agoBrain cancers mostly disrupt the blood brain barrier, Which is an organised tissue structure that exists to preserve the microenvironment of the brain against normal fluctuations and insults. Cancer is disorganised tissue that doesn't know how to produce nice neat blood brain barrier tissue organisation
- bedris 14y agoCorrect. This tumor-mediated disorganization of the blood-brain barrier (BBB) is what enables cytotoxic drugs to reach larger cancerous brain lesions, which explains why these growths often show a clinical response. Under normal circumstances, many cytotoxic drugs cannot cross the BBB.
- cwjacklin 14y agoif you are looking for treatment options for brain cancer, please see http://pubmedly.com/demo http://pubmedly.com/demo there's the standard temodar and then there's the other options that may have better outcomes, like novocure
- wkdown 14y agoClinicalTrials.gov link [1] Johns Hopkins link [2] [1] http://clinicaltrials.gov/ct2/show/NCT01056029 http://clinicaltrials.gov/ct2/show/NCT01056029 [2] http://www.hopkinsmedicine.org/kimmel_cancer_center/research_clinical_trials/clinical_trials/search_results/J09113 http://www.hopkinsmedicine.org/kimmel_cancer_center/research...
- rorrr 14y ago"This study is currently recruiting participants." Well, get back to us when they find out all the side effects.
- jmj42 14y agoMiserable, but not dead? I'll take it.
- abduhl 14y agoYou would be surprised how much you might come to regret that choice. Especially when you realize you've only slowed the cancer's growth rate and allowed it to metastasize throughout your body. If you are lucky you will die before you lose major cognitive functions. If you aren't you will slowly lose a grip on everything as you become dependant on others just to survive. There are things much worse than death, especially for the ones you leave behind.
- carbocation 14y agoThat's like reading the announcement of new software and saying, get back to us when they discover all the bugs. Naturally, there will be adverse events due to toxicity. But unless you have some particular insight into why this should be much worse in this case than for other drugs, merely mentioning that there will be toxicities doesn't really advance the discussion. At least, not as written.
- rorrr 14y agoDo you realize that only 9% of drugs pass from Phase I of clinical trials to the FDA approval? Do you know why? Because the "cure" is worse than what they are supposed to treat.
- rumblestrut 14y agoSorry to sound skeptical, but back in the day cancer was killed twice a week on Digg.
- EricDeb 14y agoThe thing is - we really only need one cure for a particular strand of cancer. Once we've actually done it we've done it. Bearing this in mind I think these stories deserve a fair amount of optimism.
- pyoung 14y agoWhen it comes to medical science, I would take skepticism over optimism any day. Many promising drugs have made it through the first rounds of trials, only to fall flat later on. Let's save the optimism for drugs that actually make it through to market.
- refurb 14y agoWhat do you mean by "strand of cancer"? In any given tumor, there are multiple cells lines each with their own set of mutations. That's what makes curing cancer so difficult. http://pipeline.corante.com/archives/2011/04/05/so_you_thought_breast_cancer_was_complicated.php http://pipeline.corante.com/archives/2011/04/05/so_you_thoug... This is a review of a very interesting paper recently published. 50 women with breast cancer had their tumors sequenced. The result? 1700 distinct mutations and the most common three mutations only showed up in 10% of patients. My personal belief is that cancer will never be "cured" in the literal sense of the word. Many cancers will become chronic conditions like AIDS where life expectancy is reduced, but people diagnosed will still get to enjoy a majority of the average life span.
- ippisl 14y agoIf there are so many strains of cancer for each patient, those patients do have multiple diseases and we should treat them with multiple drugs. There's a medical device that lets you test the response of the patient's biopsy to multiple drug combinations. I wonder if scaling this by:creating huge libraries of cancer drugs that only passed animal safety trials, using this test device to find the most effective combination of large amounts of drugs(maybe even combine drugs that fit the genetic profile of the biopsy strains) and using the combination but carefully managing dosage not to create toxicity , could be useful and practical to fight those mutation rich cancers ?
- mcs 14y agoand we'll never hear about this again
- ars 14y agoA while ago someone on HN suggested that whenever he reads about something like this he creates an alert in google news for keywords, and then forgets about it. If anything comes of it, you'll get a notice.
- bedris 14y agoThis study details the use of a peptide-drug conjugate; these are drugs with peptides (small proteins) chemically conjugated to cytotoxic drugs. The idea behind these conjugated drugs is that the peptide portion of the drug hones in on a specific biological target and the conjugated cytotoxic drug then kills the cells that have been recognized by the peptide (think warhead and payload). In this case, the peptide recognized prostate-specific membrane antigen, which is expressed on prostate cancer cells, and the cytotoxic drug was one derived from Thapsia garganica, the toxic weed (cytotoxic drugs being isolated from plants is nothing new, of course). A more common class of these conjugated therapies are called antibody-drug conjugates[1], where an antibody molecule (instead of a peptide) is linked to a cytotoxic drug. There is currently one of these drugs, Brentuximab vedotin, FDA-approved for the treatment of cancer[2]. There are many more under preclinical or clinical development. [1] http://en.wikipedia.org/wiki/Antibody-drug_conjugate http://en.wikipedia.org/wiki/Antibody-drug_conjugate [2] http://en.wikipedia.org/wiki/Brentuximab_vedotin http://en.wikipedia.org/wiki/Brentuximab_vedotin
- presidentender 14y agoSo if prostate cancer has metastasized, and we target the cancer, do we do so at the hazard of exposing the healthy prostate cells to the same fate? Do the cells of other cancer-prone organs produce similarly specific antigens? If so, how do we avoid the situation where we eliminate (for instance) melanoma tumors of the brain and lungs only to have the patient's skin kill itself off completely?
- bedris 14y agoI think that all of your questions come down to two core concepts: therapeutic index and antigen stability. For therapeutic index, you want to identify and target antigens that show the largest difference between cancerous tissues and normal tissues (i.e., antigens with a large therapeutic index). In other words, you'd want your drug to bind to an antigen that's present at a higher level on the prostate cancer cells than the normal prostate cells, such that the normal cells are spared. For antigen stability, you ideally want your drug to target an antigen whose expression is maintained in metastatic lesions. In other words, if a cancer metastasizes from a primary site to a distant organ, and the antigen your drug targets is maintained on the cancerous cells that have made their way to the distant site, then that is a more therapeutically amenable target then one whose expression is lost upon tumor metastasis. Do those explanations answer your questions well? Let me know if you'd like me to clarify more.
- EdwardTattsyrup 14y agoShrinking tumors is good. It's also important to stop cancer from metastasizing. I guess this drug might end up being used as a long term "maintenance" therapy. But I personally hope for a cancer therapy which goes beyond playing whack-a-mole against tumors. Maybe one day they'll gain a more fundamental understanding. Maybe one day they'll actually know why the body begins to form these tumors, why its built-in anti-cancer mechanisms fail or become overwhelmed, and, most important, how to restore or unblock the body's own ability to control and limit cancer cells.
- agumonkey 14y agoNot necessarily. There was some sad findings that tumor shrinking chemicals caused fragmentation and mobility. I've recently talked with a student researching on Warburg Effect http://en.wikipedia.org/wiki/Warburg_effect http://en.wikipedia.org/wiki/Warburg_effect , linking switch in metabolic regime (mitochondrial damage) to disabling the apoptosis mechanism. Their idea is to repair mitochondria so that cells will terminate themselves as usual using nanoparticules.
- robbiep 14y agoI don't think there is any great mystery there - mutation and copy errors create the initial conditions that lead to loss of function of tumor supressor genes or in of function in oncogenes, caused by known risk factors and some unknown risk factors we are still elucidating. There isn't a much more fundamental understanding that can be gained. We know all of this, we are beginning to elucidate the chromosomal translocations and karyotypes that seem to appear in certain families of cancers (and a specific cancer type will have the same 'assortment' of chromosomal typings) all that remains is to continue to design increasingly effective anti-cancer agents, one part of which this article is explaining. I don't believe there will be a single magic bullet, however treatments that have an immunological basis (See this NEJM paper that offers incredible hope for CLL - http://dx.doi.org/10.1056/NEJMoa1103849 http://dx.doi.org/10.1056/NEJMoa1103849 ) Or antibody based Rx coupled to cytotoxics or radiologicals as an adjuvant Rx, as well as the success of the designed molecules such as Imatinib etc all bode well for the future. Unfortunately the big C will evolve it's way out of many of these therapies (Imatinib etc inhibit fusion proteins created in aberrant cells that lead to proliferation, slowing but not necessarily stopping growth, so the cell evolves around it)
- traughber 14y agoI wish publications would wait for Phase 2 data before publishing sensationalist headlines like this. In this case, they have yet to even complete enrollment for the Phase 1 trial.
- refurb 14y agoI would wholeheartedly agree. Most Phase I work is exploratory and things like statistical rigor and blinding participants are ignored (and for good reason, those things don't come cheap). Phase I data is useful for toxicity data, but I wouldn't trust Phase I efficacy data in the least.
- pmiller2 14y agoYou're exactly right. In grad school, a friend of mine working on a PhD. in biological sciences once casually told me he'd discovered 4 new antibiotics in the course of his research. Of course, I was floored, until I thought to ask what his definition of "antibiotic" was. Turns out that at the stage he was working on, all it meant was the compound killed bacteria, not that it was at all useful for treating infections.
- TomAnthony 14y agoTo someone with a limited understanding of biology and chemistry, the logic behind this sounds good and the initial results seem promising. Yet, as people have commented, there are many similar stories that crop up. Can anyone in the know shed some light on how often these things fail and at what phase they normally do so? Basically - how excited should I actually be?
- robbiep 14y agobe cautiously optimistic. It's real research that has worked in animal models. It remains to be seen whether it will be as effective in humans. Additionally, shrinking a tumour is a long way from a cure. For example - The drug Ipilimumab (melanoma) was shown in clinical trials to increase median survival from 6.4 months to 10 months. Some people may have disease-free recurrence for significantly longer than they would have, some may actually be 'cured' (Disease-free survival for 5 years is a fairly standard medical definition of 'cure'), others die at the same time, or a week, or a month, later than they would have anyway. For all of these drugs, there is no magic bullet, the tumour will evolve around the mechanism.. My understanding of the subject (final year medical student) has lead me to believe that an immunological approach will be best (See my post which links to a nejm article further down the page) hope this helps your understanding
- cwjacklin 14y agohey robbie, i am working on a crowd sourced site to find evidence based treatment options for a disease. i would like to get feedback from you as you are a med student. would you reach out? my contact is my uesrname at gmail thanks.
- tokenadult 14y agoI took care to read the fine submitted article (based on a press release) and most of the preceding twenty-some comments before replying here. Comments to the effect that we often see stories like this based on press releases that don't translate into clinically useful treatments are correct. Anyone who has been on Hacker News as long as I have has seen dozens upon dozens of stories about breakthrough medical treatments that don't turn out to be breakthroughs. As usual, here in this thread I recommend Peter Norvig's article "Warning Signs in Experimental Design and Interpretation" about how to read research reports in general. http://norvig.com/experiment-design.html http://norvig.com/experiment-design.html Medical research is slow and painstaking. There has been genuine progress in medical research in my lifetime. (My mother was a nurse in our state's largest research hospital, and medical research was a subject of dinner table conversation in my home.) But false starts have been numerous. There are a great many medical treatments that have been proposed in my lifetime that have not been proven to be both safe and effective for treating what they purport to treat. Peter Norvig's article provides a good checklist of all the ways that optimistic initial reports can turn out to be wrong, of which "too few subjects" especially applies here. I reply over and over and over again on threads like this here on Hacker News because I did grow up with a strong interest in medical research--and some anecdotes about medical research that went awry--and because I know that legitimate medical researchers sometimes find their work hyped by the university press office or funding agencies far beyond their own more cautious statements. But here on Hacker News we may as well learn how to be discerning readers. Let's not just believe what we want to believe, which is the cognitive bias all human beings have, but let's test factual statements for strong evidence and make sure that the experimental procedures reported in some new study mentioned in a press release really support a grand conclusion. It's too early here to say "Drug made from toxic weed kills cancer" in a way that is safe and effective for a broad range of human patients for even the one kind of cancer that is mentioned in the article submitted here. I'm glad someone is working on this, but it's way too early to declare that we've found a cancer cure through this work.
- aaronblohowiak 14y agoOne litmus test that I use for this: If there experimental design would also vett bleach, it's still too early.
- krollew 14y agoNice to know, but I bet It won't be used widely soon, no matter if it works or not. Medicine wants keep cancer pacients alive, not cure them. Curing is not profitable. If they (and people themselves) wanted us not to be sick, almost nobody would be.
- ars 14y agoThis again? It's nonsense. Why do people believe garbage like this?
- krollew 14y agoBecause see how healthy man can be if only he want? Ever tried? Moreover technology evolved so much and healthcare seams to work worse than before. Think about it, science can tell what happens billions of killometers away and what happens in subatomic scale and it can't find out how human body works enough to cure most common diseases? It doesn't convince me. And why not to believe? There are many people doing bad things. There are wars, animals are treated like garbage. Why not to believe someone want to make bussiness on disieses? How about remissions, why nobody believe they occur for a reason? People are too stupid to find out that reason? I don't think so. Or maybe am I wrong and scientists try to find out why they happen? Why basis of caring about health in mainstream medicine now are meds and vaccination and not healthy diet and doing sports? I use no drugs and I don't get sick. I used to, before i started to care what I eat and what I do for my health. Noone ever told me to do what I've done. I rather seen commercials of drugs that are not healthy and not realy work. Does anyone care about that psychedelic drugs relieve cluster headaches (where no other good working med is known)? Anyone cares MDMA decreases symptoms of Parcinson disease? Is it so difficult to find out why? I mean, if anybody except single scientists care? I don't mention how great can they impact on state of mind. Hemp is great painkiller, medicine for insomnia, and others. Why I can't use it to relieve my pain or to help myself fall asleep? Why medicine use much more dangerous drugs if hemp could be used? As far as I know It's illegal because someone don't want to admit it's useful for medical reasons. Medicine is so broken. For me someone want it to be broken or people in medicine are stupid. I can hardly believe they are so stupid so I'd rather believe second option. The fact that some people always wanted to enslave somehow other people. We had explicit enslavement and religion. Why medicine wouldn't be next one?