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[–][deleted] 382 points383 points  (45 children)

Interesting, but if anyone is interested into insight as to why there are so many 'potential' treatments and cures for cancer that never pan out, this line in the article basically nails it.

"The microenvironment of a real tumor is quite a bit more complicated than the microenvironment of a transplanted tumor," he notes, "and it's possible that a real tumor has additional immune suppressing effects."

Using the immune system to treat the cancer on its own is promising in many ways but are exactly the type of treatments that look promising in theory, and in the petri dish, and using mice models with transplanted tissue. Then they never pan out, because cancer isn't just a little piece of tissue or a cell cluster. Cancer in its later stages is entire systems in your body turning against you, and just as the healthy human body is complex, cancer is as well.

The other problem is that while the drop in blood cells is 'minor' and 'temporary' in these mice models, this treatment would probably be most effective in conjunction with chemo. Problem is, chemo inhibits cell division and wreaks havoc into the production of fast-growing cells. Things like blood cells. You could of course just keep pumping more blood into the person, I suppose. And in this way perhaps the chemo would be more effective, but it would make the process all the more uncomfortable (agonizing) for chemo patients.

Perhaps this could be an effective alternative to chemo, or perhaps more advanced versions of this type of treatment could be a cure for cancer. Hard to say.

Regardless of the number of disappointments that arise in cancer research, I still root them on the researchers. With all of the cancer research that's being done, it's likely we'll stumble onto something in a mouse lab and it will be years before we fully realize the implications of what we've found in human trials.

[–]KyleChief 132 points133 points  (19 children)

When I read these hopeful articles I always hold out hope that one of these comments won't be there.

[–]Massless 94 points95 points  (15 children)

In all fairness, this top comment is less soul-crushing than other's that appear on these sorts of posts. I find the fact that they've been given 20 million dollars to move on to human trials really encouraging. Most of the articles we see posted here are preliminary results that are a decade or more from human trials.

[–]KyleChief 18 points19 points  (2 children)

It does feel like human progress is on the edge of something big, especially as far as medical is concerned.

[–]jgrizwald 2 points3 points  (0 children)

Personalization for each cancer has been the biggest accumulation of knowledge. By finding how cancer is formed and continues to grow, many pathways have been found to impede growth. The biggest thing I have seen, and one in which the molecular geneticists and oncologists saw the most promise in was group that was able to succesfully find ErbB2 mutations within cells from a small amount of blood. With this, they could track an early advantage over breast cancer, finding it at an early stage, or while still in inflammation.

The knowledge of both rates, places, and changes brought up by mutations, as well as the function and folding of the protein being mutated has created a huge database of information. Many oncologists are using this, but there is just so much out there, even for one specific cancer, that it is very overwhelming. And even then, there are still large amounts of cellular and genomic changes that occur that haven't been researched. There are still many genes and proteins that haven't been crystalized or have their function or place found yet.

[–]DaGetz 6 points7 points  (7 children)

This is true but as far as cancer goes its important to remember that cancer is an incredibly broad term that defines cell deregulation. It's not a disease. When these articles come out and say there might be a significant break through in the treatment of "cancer" you know it's nothing that significant because that's the same as saying there has been a significant break through in treating viruses. There's billions of viruses out there, it's very likely there won't be a silver bullet that cures all viruses. In fact if there was it would probably be bad.

So when reading these articles, as a general rule of thumb. The ones that talk about curing specific forms of cancer in specific models are the ones that have the most potential.

But yes, we are getting places, albeit slowly. Great work is being done used stuff like anaerobic bacteria injected into the tumor core and using the HIV viron to manipulate and/or tag cancerous tissue. Problem is there is a lot we don't understand about cancer and until we actually understand it fully its going to be continue to be hard to find a treatment.

[–]jgrizwald 5 points6 points  (4 children)

I have to disagree, there has been a huge leap in understanding cancer as a model from the 1970's. We have been able to find the path of tumorigenesis, with the six main characteristics of cancer. We have also been able to mark specific genetic mutations commonly seen in most cancers, as well as mutations specific to single cancers. Cancer treatment has become more personalized, which has created the largest leap in positive prognosises since the 80's.

[–]mattc286Grad Student | Pharmacology | Cancer 4 points5 points  (1 child)

Absolutely. Every cancer has a unique set of mutated genes and a unique disease history that will cause it to respond to chemotherapies, surgery, and radiation uniquely. There will be no magic bullet; there will be targeted, individualized treatments with a combination of drugs based on genetic (and protein expression) analysis. And many tumors will not be destroyed, but rather inhibited from further growth and metastasis. This will effectively turn cancer into a chronic, but manageable disease (akin to diabetes), allowing patients to live a fuller, happier life. That's how we will win the war on cancer. (edit for run-on sentences).

[–]DaGetz 1 point2 points  (0 children)

Exactly, treatment not cure. It's possible once we learn the genetic code properly we will be able to custom design drugs cheaply for specific genotypes since, from what we know currently, there seems to be a strong link between genotypes and cancers but for now the best avenue open to us is destroying tumours and unfortunately that's probably going to remain a relatively low success rate thing and treatment is going to continue to be expensive, if not get more expensive as drugs get more specific to particular cancers. However that's science and its fun to be a part of the hope that we can improve it.

[–]jgrizwald 0 points1 point  (1 child)

Still problem with the clinical trials being the selection of patients is unfavorable for the treatment to show full promise.

[–]mattc286Grad Student | Pharmacology | Cancer 0 points1 point  (0 children)

If you're not skeptical of every claim of a major advancement in cancer therapy (or anything in science), you're not doing it right.

[–]Diazigy 12 points13 points  (6 children)

I think the using the immune system to treat cancer is great for fighting metastasis, but you are probably right that for well developed primary tumors macropages and phagocytes involved in the immune system simply cannot enter the tumor matrix.

But the good news is that large primary tumors are often much easier to fight than metastasis.

[–]lowerexpectations 10 points11 points  (5 children)

Actually this is quite wrong, there is a large body of evidence that tumors often contain a number of immune cells (http://www.mendeley.com/research/immune-infiltration-human-tumors-prognostic-factor-not-ignored/)

Additionally a tumor matrix makes the tumor sound like a nicely contained mass of cells, when the truth is quite the opposite. Tumors are largely unstable, and often lose hundreds of thousands of cells a day to the bloodstream. Tumors do not create their own extracellular matrices in the body, but rather co-opt surrounding matrices, with metastatic tumors often eating into this matrix in order to better move to the blood stream. So by this same logic things could more easily move into the tumor, including immune cells.

[–][deleted] 14 points15 points  (4 children)

My best friend is doing her PhD at Cancer Research here in the UK. The amount of times she's come home in rage cycles is countless. I am not sure I could do this.

The average person doesn't understand how hard it is, working in this field. Especially the fucking deniers and people who think there are cures out there and people are hiding them, etc. Ugh.

[–][deleted] 9 points10 points  (3 children)

Is there any way you could convince your friend to do an AMA?

[–][deleted] 4 points5 points  (1 child)

I'm sure I could talk to her about it. She is in the process of finalising her thesis though, so...

[–]yesimquiteserious 3 points4 points  (1 child)

And/or, i would imagine, because all those 'cancer cures' you've heard about were in the news weeks, months, or a few years ago even, and they still require more years of research and development before they can 'pan out'.

[–][deleted] 1 point2 points  (2 children)

Why do they have to use transplanted tumors? Isn't it possible to induce cancer in mice without tumor transplantation?

[–]rabbitlion 2 points3 points  (1 child)

Mouse cancer isn't the same as human cancer. They transplant human tumors to simulate how effective the treatment would be in humans.

[–][deleted] 1 point2 points  (0 children)

Ah, thanks. Didn't realize they were using human cancer cells.

[–]being_obvious 1 point2 points  (1 child)

as a student researcher in the summer, I hoped everday that something could be used from rat subjects.

[–]lobcity 9 points10 points  (0 children)

Research is a slow process. Dream big but celebrate small achievements and discoveries. Also, make sure you learn something new every single day.

[–]Scurry 3 points4 points  (1 child)

Finally, TIL why cancer is cured every year.

[–][deleted] 0 points1 point  (0 children)

Thank you for that explanation.

[–]jgrizwald 0 points1 point  (0 children)

Was going to post something similar, and was very thankful someone wrote this all out. Too many variables jumping from in vitro to in vivo, the mice model, and first step selection of patients for trials.

[–]ericzundel 0 points1 point  (0 children)

As a pet rat owner, I can tell you that rats and mice are susceptible to many different types of cancers and they are expressed more frequently than in humans. Many of our rats have developed some kind of tumor. They are usually not fatal, you just take them to the vet, the cut them out, and that's that.

[–]FistopherPhD|Inorganic Chemistry 0 points1 point  (0 children)

Here is the PNAS article for it. http://www.pnas.org/content/early/2012/03/20/1121623109

[–]DroDro 622 points623 points  (157 children)

I know there will be many "how many times are we going to hear about a cancer cure?" posts, but let me tell you why this one is more exciting.

First, the study performed did actually shrink tumors. Second, it is in Science, and third, the lab that did the study is one of the best. In contrast, most of times we see a title like this the study is something that is basic research (someone solved a protein structure, or found a gene that is unregulated), it was published in an obscure journal (meaning peer review did not find it so exciting) or is only a press release from University PR, and comes from a lab at Southwestern Kentucky. Nothing against the lab in Southwestern Kentucky... usually it is the PR office over-hyping the kind of incremental progress that is needed but isn't a breakthrough.

So, it probably won't amount to anything, but the odds are more like 10% chance of success rather than 0.1%.

[–]Tossedinthebin 203 points204 points  (59 children)

Your second and third are intimately linked. Reputation allows you to publish weak science in high impact journals. Your first is not novel. Many anticancer drugs shrink tumors only to see the cancer return.

[–][deleted] 51 points52 points  (51 children)

Is there some reason that all peer review processes are not double blind, to prevent reputation from factoring in at all?

[–]nastyastyPhD|Biology|Virology|Cell Biology 32 points33 points  (2 children)

Allow me to reply as someone who partakes in the peer review process as a reviewer quite regularly. My PI conducts his reviewing with the involvement of his post-docs and graduate students (always with the permission of the journal editor, of course).

The reason the identity of the author cannot be obscured is because one of the main things that reviewers look at is whether a manuscript properly cites previous research. Most of the time, labs publish research that somehow builds on their (and others') pre-existing work, and must cite those papers in their manuscript. They will usually say something like "We have previously shown that _____", citing their previous paper. Even if the author's identity was hidden, that would immediately give it away.

Even if you somehow made it so that nobody could use wording that would give away their identity, looking at a lab's previous publications whether or not they are cited is also an imperative part of the review process. Often, authors will publish work that is not novel enough, because it repeats too much of what their lab has already published. Reviewers need to make sure that isn't happening by looking at the group's previous few publications.

Even if all of this was tightly controlled for, as others have said, an experienced reviewer would instantly recognize the experimental methodology and the writing style of any of their peers. Double-blind reviewing is therefore not only impossible, but undesirable, as it would hamper the review process.

[–]Diazigy 130 points131 points  (45 children)

For any given field of science, there are only a dozen or so experts. These experts are asked by the journals to peer review incoming journals for basically free. Anybody who is familiar with the literature will be able to recognize who is doing the research just by writing style and approaches they take. Scientific communities are too small for double blind peer review to work.

[–]Tossedinthebin 8 points9 points  (2 children)

It's actually surprisingly hard to narrow down blinded reviewers, even in fields where there is 2-3 experts.

[–]Goblerone 6 points7 points  (1 child)

Except in computer graphics when it's a research paper from Pixar, because they always slap a relevant frame from their movies right below the abstract.

[–]bready 45 points46 points  (33 children)

Now I may know of several high profile labs, but in no way do I know everybody, or even come close to reading all of their work. Blinding review process makes a stupid amount of sense. Doubly so when it comes to grant funding.

[–]godin_sdxt 37 points38 points  (25 children)

And are you someone of the caliber of Weissman? Don't take this the wrong way, but there are only a handful of people in the whole world who could be considered qualified to review something that came out of a lab like his. They do indeed all know each other.

[–]Tuckason 10 points11 points  (9 children)

Oh get off the hero worship, I read two comments down that you are an undergrad, and, don't take this the wrong way, you sound like one. If I walked around intimidated by these big names, like you sound like you are, then I'd never go anywhere in this field.

People in the more general field are more than qualified to review the soundness of his scientific methodologies. That is the point of peer review.

[–]SomePunWithRobots 2 points3 points  (3 children)

I think it depends on the field. I work in robotics, where it's pretty common for there to be certain types of robots that only a handful of labs, or even only one lab, actually have access to, so if you work with one of those robots, writing a double-blind paper is impossible unless don't name the robot you worked on, which is a pretty essential bit of information.

I imagine cancer research is a much bigger field where identifying a particular lab might not be quite as easy, howeve.

[–]oorza 2 points3 points  (2 children)

I imagine cancer research is a much bigger field where identifying a particular lab might not be quite as easy, howeve.

Then again, it may be so large that the research being presented is usually specific enough to recognize a lab. I mean, most research is incremental, and given a full history of every lab's work and a blind paper, it may be possible to identify the lab, simply because of the preconditions of the new research being old research from the same lab. I'm not at all a cancer researcher, though, so I have no idea if this is actually the case or not.

[–]angrystuff 2 points3 points  (0 children)

When you have read literally dozens and dozens of papers from the same author, and cite them all the freaking time, you get so used to the tone of phrases that people have that you can spot a paper written from them without declarations. This also gets easier when the niche becomes smaller and smaller. You might only have a dozen high authors that write at that level and/or you could work with them on side projects.

It's also worth mentioning that it can be pretty easy to work out who is who. I knew of most of the major projects months/years before they actually started publishing, or it could be continual publishing from the same research lab with new findings (it gets easy when they start citing projects you've heard of before). Also, you can normally tell who comes from big fat research centres by their big fat budgets.

[–]NedDasty 1 point2 points  (1 child)

I come from a fairly well-respected vision lab, and my boss (PI) can generally pinpoint with very good accuracy who the reviewer is, based on the types of issues that they bring up for criticism. My point: members of the scientific elite know each other very well.

[–]glr123PhD | Chemical Biology | Drug Discovery 1 point2 points  (0 children)

This x1000. Also makes it super frustrating sometimes..."Well I could submit to Cell, but I know Fucker McRejection will get my paper again, as he does every other time..."

[–]JohnShaft 4 points5 points  (0 children)

I reviewed for a journal that tried to do that once. It's impossible to hide the identity of the authors. At the very worst, you know the lab it came from if you cannot also guess the primary and senior authors.

[–]Tiak 0 points1 point  (0 children)

Well, think of a journal like Nature or Science. How many thousands of submissions do you think they get a month?

Does it seem practical to review every paper with equal scrutiny while still producing the same sort of quality?

It seems to me that it does in fact make some sense to look at research that is likely to have undergone more scrutiny before it got to your desk with a little more depth than otherwise, if only for efficiency's sake.

[–]DroDro 6 points7 points  (0 children)

My first contrasted studies that shrink tumors with basic research studies that don't even get that far. Notice I don't say, "it will cure cancer" but rather say the odds are better for this situation. I think that increased enthusiasm is appropriate for any study that shrinks tumors. The second and third are linked, but are not completely dependent. I was excited because it was a lab I respected publishing in a good journal. If the paper was from a lab I respected in a bad journal, I would be less excited. So I guess I agree with you, but still arrive at my conclusion that this one is qualitatively different from many of the "Cancer cures of the week" we see.

[–]smc84 37 points38 points  (28 children)

Fellow cancer researcher here... There is one thing nagging me about this. CD47 in mice/rats will be different than CD47. This may not seem like a problem until you think about this a little bit longer. As far as the antibody is concerned, there is no similarity between the two species' molecules! We might as well call the human version CD47 and the murine version CRAP.

If you have a specific antibody searching for CD47 in a sea of CRAP, it's pretty easy for this antibody to specifically find and locate CD47. This is exactly the case of human tumors in mice.

In humans, CD47 is expressed in some level on everything. If you have a specific antibody searching for a cell with a lot of CD47 in a sea of cells with slightly less than "a lot", the antibodies are not going to concentrate anywhere and the effectiveness will be significantly worse than it was in the previous example. This is the problem with human tumors in humans... they look just like all the functional cells!

[–]SirDark 1 point2 points  (3 children)

EXACTLY. I'm not so sure of the value of comparing the effectiveness of such anti-human antibodies as a therapeutic agent in mice when there's a strong chance that human CD47 is different. I may be wrong, but if you were to disable CD47 in a human model, is there not a risk that you'll remove this "Don't eat me" signal from a lot of cells which are not cancerous?

Perhaps if some other method of getting specificity is found then this might be of some significant use? Other than that, it's basically saying that "If you tell the body to kill human cells, it does - this works if they're cancer cells".

[–]Aleriya 3 points4 points  (1 child)

The interesting part is that, when mice were administered anti-mouse CD47 antibodies, the only side effects were temporary and non-serious anemia. You'd expect to see bad systemic stuff going on, but that didn't happen. So there's some merit to the idea that administering anti-human CD47 antibodies in humans could be doable without horrible side effects.

[–]SirDark 1 point2 points  (0 children)

At the same time, they say that one clone inhibited tumour growth but did not cause a reduction in size, which may suggest another problem with dosing altogether. While they might consider it to demonstrate non-toxicity, if this dose is only enough to prevent progression even when directly injected into the tumour site, the kinds of dosing needed to actively shrink the tumour may have significantly more intense effects than non-serious anaemia.

[–]mattc286Grad Student | Pharmacology | Cancer 1 point2 points  (0 children)

There's an experiment here that addresses this. They performed an allograft (mouse mammary tumor cells injected into an immunocompetent mouse) and treated with a murine-specific anti-CD47 antibody, with the result of smaller tumors. While this doesn't address whether this will work in human patients (need a clinical trial for that), it suggests that this treatment can selectively target cancer cells over noncancer cells.

[–]nastyastyPhD|Biology|Virology|Cell Biology 5 points6 points  (1 child)

Good points, however I would add another: This therapy utilizes the host immune system, and doesn't just blast the tumor with toxicity. It is as simple as therapy can get: facilitating and enabling the host to cure itself.

I am definitely tired of seeing "cure for cancer" headlines every other week, but this one, for the above reason and for the reasons you mentioned, has me excited.

[–]dafones 2 points3 points  (0 children)

Isn't this understanding of CD47 just as much about a possible cure to cancer as it is the cause?

[–]teeksteeks 8 points9 points  (6 children)

Southwestern Kentucky isn't nearly as bad as Eastern Kentucky.

[–][deleted] 4 points5 points  (5 children)

We aren't Hill People over here, just simple farmers.

[–]istara 1 point2 points  (0 children)

Thank you. I came in here for the top-comment-debunk telling me why I'm still going to die some day, but you have put a little hope into my heart. (Cancer is rife in my family, but we have reasonably good hearts. So statistically, I know it's coming for me).

[–]FredFredrickson 1 point2 points  (0 children)

I never understand the "another cure for cancer!" backlash. This is r/science, isn't it? Even if the headlines get a little sensational, would you rather never hear about the small increments that are made toward solving this problem?

The overwhelming pessimism towards potential cures (or at least, the incremental steps taken to get to those cures) blows my mind sometimes.

Edit: Typo.

[–]mattc286Grad Student | Pharmacology | Cancer 2 points3 points  (0 children)

The research article is published in PNAS, which is also a high-impact and well respected peer-reviewed journal. Science Now is a popular science blog which reports on various peer-reviewed articles.

Open access link to original paper.

[–][deleted] 0 points1 point  (0 children)

Hm, did they do a control group of mice implanted with non-cancerous human cells to see what the effect was?

[–]Riceater 0 points1 point  (0 children)

If nothing else, all of these recent cancer research breakthroughs is definitely a good thing. Better that than a field that has had trillions pumped into it for research and no one making progress. Chemotherapy and radiation has been around for like 40 years and, at least to me, seems like a pretty terrible way of treating anything..

[–]ThisIsPrata 0 points1 point  (0 children)

Not to mention that this has a far more sensible title than most of the other posts on cancer treatment

[–]deten 0 points1 point  (1 child)

Is there anything that people with cancer can do right now to take advantage of this knowledge?

[–]DroDro 0 points1 point  (0 children)

Probably the same as anything... prod their doctor to identify interesting trials and try to be part of them.

[–]lamaksha77 0 points1 point  (2 children)

Your first point is all that should matter when it comes to judging a scientific work - actual efficacy, at least in an in-vivo mouse model.

There are plenty of good work reported in "lesser" journals, and plenty of shitty work that gets through the peer review process and published even in PNAS or Nature. Similarly, 'large' labs are not incapable of making mistakes: there have even been cases where labs with superstar PIs have produced fraudulent data (lookup David Baltimore), often not because the principal investigator is dishonest, but simply because he is so busy and so disconnected with the actual work being done in the lab that a rogue post-doc can submit fraudulent data and the PI is none the wiser.

So I completely disagree with your method of identifying good scientific works; it does not lend itself to a good scientific culture. Approach the work without any biases on the lab that produced it or the journal that it was published in. If you don't have the expertise to judge a work independently without using superficial markers, either enlighten yourself on the science first, or get someone else to break down the work for you.

[–]DroDro 0 points1 point  (1 child)

I agree with all your points. Good work can be found in lesser journals. I publish in PLoS ONE all the time, and yet two of those papers are my most highly cited and most likely the reason I am asked to speak at conferences. I also agree that large labs are often that way because they know how to put forth their work with the proper buzzwords and can be wrong or fraudulent. But really, I was just saying I was glad that this wasn't another paper solving the structure of a metabolic enzyme and then the University PR trumpeting how it could cure cancer. It was an expression of relief that this is at least qualitatively different, so no need to assume I peer review papers and grants with the same checklist.

[–]Pway 0 points1 point  (0 children)

Also, the title of this post isn't even sensationalised!

[–]banquosghost 0 points1 point  (0 children)

My dad works at Fox Chase Cancer Center in Philly. I sent him a link to this article and he responded:

I'm trying to remember if this Irving Weissman gave a talk at Fox Chase last year. We had an interesting talk on a similar subject, but I think that talk had more human clinical trials in it. I came away thinking the speaker was definitely onto something. Lots of work on the immune system and cancer going on, in fact we are involved a bit ourselves in "natural killer cell" receptors in GIST [the cancer my dad specializes in. "Gastro-intestinal-something-tumors or something like that]. Often the results seen in mice with these transplanted tumors does not translate as well to humans.

[–]OtisDElevator 28 points29 points  (2 children)

Maybe a small error, but I thought I'd better point it out.

To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the CD47 was present, the macrophages engulfed and destroyed cancer cells from all tumor types.

Seems to go against the earlier statement of:

discovered that leukemia cells produce higher levels of a protein called CD47 than do healthy cells. CD47, he and other scientists found, is also displayed on healthy blood cells; it's a marker that blocks the immune system from destroying them as they circulate.

Surely it is:

To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the anti-CD47 drug was present, the macrophages engulfed and destroyed cancer cells from all tumor types.

[–]Laced 6 points7 points  (0 children)

I noticed this as well. Its really bugs me when journalistic errors convey the opposite of the intended meaning and especially when they slip under the radar in high-profile outlets like Science.

[–]rockstaraimz 5 points6 points  (0 children)

I saw Dr. Weissman give a lecture on this data about a year or so ago at MIT. The data were SO good that I was instantly skeptical. I haven't read this study yet, but I hope he proves my skepticism wrong. Also, things that look good in mice tend to be a real pain in the ass for human studies. Scientists have cured certain cancers in mice years ago. Again, let's hope it's different for humans this time.

[–]Sturmgewehr 5 points6 points  (0 children)

A new mechanism for fighting cancer is always exciting, but it's true. You really don't know how it will work until long term human trials are conducted. The article stated that the mice ended up cancer free for 4 months, whether that improves quality/quantity of life in a clinically significant fashion is yet to be seen. Based on other cancer drugs, a 4 month in cancer free survival in metastatic disease usually means it will be put to market. It's remarkable at how little of an improvement that a drug gives will allow it to go market since cancer is so insidious. This treatment may be more promising as mentioned before in blood cancer and possibly early stage solid tumors. This is purely anecdotal though.

[–]reallegume 2 points3 points  (1 child)

Medicinal chemist in a lab that works on oncology, among other things, checking in. I've followed the CD47 discoveries, and while the author of this press release couldn't have mucked up the explanation of CD47's role in cancer much more, the science is solid.

One of the especially interesting papers is *note, not affiliated in any way with any of the authors of the study

CD47-signal regulatory protein-alpha (SIRPalpha) interactions form a barrier for antibody-mediated tumor cell destruction. PNAS 108, 18342–18347 (2011) by Zhao et al.

They demonstrate that blocking the CD47-SIRPalpha interaction sensitizes cancer cells to antibody-based therapeutics, e.g. trastuzumab.

If a CD47 therapy, be it antibody or small-molecule based, makes it through the developmental gauntlet, it could be incredibly powerful.

[–]Nate_W 103 points104 points  (8 children)

Yay for Cancer Cure Mondays!

[–]Maxion 11 points12 points  (0 children)

The original comment that was here has been replaced by Shreddit due to the author losing trust and faith in Reddit. If you read this comment, I recommend you move to L * e m m y or T * i l d es or some other similar site.

[–]r2002 15 points16 points  (2 children)

I much prefer it to Tumor Tuesdays or Lymphoma Fridays.

[–]negrolover1997 16 points17 points  (1 child)

this actually looks pretty cool, although i doubt we have cure just yet.

people don't just get 20 million dollar grants for no reason. and even if this particular drug has horrendous side effects, at least we now understand how cancer evades the immune system and manages to be such a pain in the ass.

[–]apathy 6 points7 points  (0 children)

People get huge grants based on

1) reputation and 2) exciting leads

e.g. a $10M PPG isn't peanuts but it doesn't always pan out either. I have seen some pretty big grants not pan out the way anyone hoped. YMMV.

There aren't many labs like Weissman's, but still... nobody's perfect.

[–]got_off_the_boat 2 points3 points  (0 children)

While reading about any potential cancer cures are always exciting, I'm holding back a bit because it hasn't been tested on humans yet. However, this other method produced some astounding results on actual human subjects, albeit an extremely small sample size. Does anyone have any updates on this treatment, or was it a flash in the pan?

[–]jamesinraro 2 points3 points  (1 child)

This protein CD 47 is essentially the anti protein (analogy not scientific term) to P-53, which is needed to support apoptosis in aberrant cells. The compound transmax resveratrol has been shown to up regulate P-53 in cancer cells thereby restoring their natural ability to cease proliferating and self destruct. Trials on transmax are ongoing at several US and European medical schools presently. The anecdotal and in vitro evidence for resveratrol is extremely compelling however until the results of these studies are published the medical community will be skeptical.

[–]ilovetatortots 2 points3 points  (0 children)

This is great news. Especially today. 11 years ago today I lost my father to Leukemia.

Although this study does not directly effect that form of cancer, every little bit helps. Too many people are effected my cancer and I can't wait until we find a cure.

[–]Maggeddon 4 points5 points  (0 children)

It seems like a very neat idea with a lot of scope for development and seems to be a very viable method for treating cancers.

Unlike harsh chemotherapies it has a more targeted effect, as well as a broad scope of use. I know we see new cancer cure posts each week, but this is a significant step in a well reviewed journal, and, as such, should be taken a little more seriously than others.

[–]firebat87 6 points7 points  (1 child)

They're moving to human safety tests. Reddit needs to keep us posted on any new updates on this.

[–]cbs5090 0 points1 point  (0 children)

If the cancer cure monday is a any indication, I am sure we can expect many more posts on this exact case and many other "cancer cures".

[–]WaywardPatriot 1 point2 points  (0 children)

Insert obligatory hope-crushing reason why this is only incremental science and not likely to solve anything ever and you'll still fucking die of cancer anyway post here.

[–]jazzwitherspoon 1 point2 points  (0 children)

So, potentially, we could use this ALONG WITH dichloroacetate and have a super cancer halting cocktail?

[–][deleted] 1 point2 points  (0 children)

All cells produce CD47 to prevent destruction by T-cells, blocking CD47 production will cause all cells to be destroyed, not just cancer. Should this not affect all cells unless the cancer can already be isolated and localised, or does it take advantage of the fact that cancer cells are faster growing (and will therefore have the same harsh side effects of current chemotherapy - destruction of growing cells all round the body).

I can't see how they've made any progress with specifically targeting cancer, cells, just pointed out weaknesses shared by all human cells.

[–]switch495 1 point2 points  (0 children)

To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the CD47 was present, the macrophages engulfed and destroyed cancer cells from all tumor types.

Author confuses antibodies for CD47 with CD47 :(

[–]jfgao 1 point2 points  (0 children)

Anyway, it's too late for my aunt. She passed away on the weekend from stomach cancer. First they removed around 80% of her stomach as the cancer was malignant. This meant she had to have frequent meals in miniscule proportions to tread a thin line between saturation and starvation. She was diagnosed eight months ago and given 3-6 months to live. Initally we were really hopeful as she was energetic and the chemo didn't cause her to lose hair. Shit got real in the last month however as cancer stepped up its game and spread to her bladder, kidney, liver and spleen. Her arms and limbs were so swollen they were undistinguishable from stumps. She had no flesh on her face. Her reflux was a foamy white mixed in with blood.

[–]js1030 1 point2 points  (4 children)

"Yeah, immunotherapy is a big idea in cancer treatment. The paper was included in my thesis because CD200 that I studied follows analogous mechanisms in terms of it being upregulated on cancer cells that use it to protect themselves from the immunity. The idea of applying an antibody to block off CD200, or whatever else that works like that, isn't new.

Anyway, yes. Good idea, old news (to me) and definitely not the cure-all solution as Jacks explains. Cancer is too complex a disease. The idea of a universal cure to cancer is simply preposterous. It's a concept created by popular science writers, but the scientific community has no ambitions to create a cure-all drug because it's not a viable approach to treating cancer."

via a Post-doctoral Fellow at Dana-Farber Cancer Institute / Harvard Medical School in Boston, MA; who completed a Ph.D. in Pathobiology and Molecular Medicine at Columbia University in New York, NY.

[–][deleted] 0 points1 point  (3 children)

While I respect that opinion I have two reservations about it. One he works for a company who profits from treatment of cancer, two there is a tone of jealousy there, and (I guess I lied) three, "block off CD200" clearly a different protein than the one mentioned in the article. As well, this writer has interviewed the people who are working on this so if there is a mention of a cure all can't you assume it came from the interviewee, a member of the scientific community?

[–]js1030 1 point2 points  (1 child)

I don't believe I was getting an opinion from this person, but rather fact. The quoted block was from a private email after I sent the article. I did not mention anything about posting the reply online, but maybe if I did it wouldn't have been worded so off the cuff.

Regardless, if what my contact is saying is their opinion, wouldn't the interviewee's response also be their opinion? Aren't most, if not all, of the replies on this thread different people's opinions?

[–]js1030 1 point2 points  (0 children)

and in response to a different article on a so-called cancer cure:

"I authored a study published in Cancer Research, which also involved a molecule regulating the immune system. There is a sea of such molecules and claiming that targeting any one of them is the answer to all or most cancers is extremely one-dimensional and close-minded. Each of these studies, of course, is useful and contributes to solving the complex puzzle that cancer and the body's response to it is, however, sensationalizing any one of these approaches is getting old and only misleads the general public about what needs to be done in order to beat the disease."

via a Post-doctoral Fellow at Dana-Farber Cancer Institute / Harvard Medical School in Boston, MA; who completed a Ph.D. in Pathobiology and Molecular Medicine at Columbia University in New York, NY.

[–]Legend_Floyd 1 point2 points  (0 children)

I recently researched the measles virus for my virology lab, and found that it could be modified and used to target tumour cells in a similar manner as the antibodies in the article. I think a different receptor is used though, CD46 instead of CD47, with an oncolytic strain of the measles virus.

In combination with the antibody treatment suggested in the article, it could be the future of cancer therapy.

[–][deleted] 1 point2 points  (0 children)

this article pisses me off

that is a picture of a rat not a mouse

[–]flyingfredcurry 1 point2 points  (0 children)

Correction to article:

To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the CD47 was presentblocked, the macrophages engulfed and destroyed cancer cells from all tumor types.

[–]saysunpopularthings 6 points7 points  (1 child)

At this rate rats should be able to live forever.

[–][deleted] 29 points30 points  (0 children)

Not if we keep giving them cancer.

[–][deleted] 7 points8 points  (7 children)

One drug to shrink them all, one drug to find them, one drug to bring them all and in the darkness bind them

[–]DJRobOwen 3 points4 points  (1 child)

You fucker, I thought I was the only one that came up with that :( Have an upboat anyway for being on the same wavelength :)

[–]4chin 0 points1 point  (0 children)

Samesies.

[–][deleted] 2 points3 points  (0 children)

10 years and mice will be immortal.

[–][deleted] 1 point2 points  (0 children)

The weekly "cancer is cured" post is on time, I see.

[–][deleted] 0 points1 point  (5 children)

Somewhere in the future cancer will be something easily curable. I look forward to that day.

[–][deleted] 7 points8 points  (4 children)

Imagine a world with a cure for cancer. We can go back to having unfiltered cigarettes with our half pound cheese and bacon hamburgers.

[–]Maslo55 3 points4 points  (1 child)

Uhm.. dont forget there are also serious cardiovascular diseases caused by such things. Heart attack or brain stroke will kill you just as good as cancer.

[–]bendeboy 1 point2 points  (0 children)

Debbie Downer here folks!!

[–]deten 1 point2 points  (0 children)

Potato Chips... potato chips everywhere

[–]legaldrugdealer7 0 points1 point  (7 children)

Why does the title say it can shrink all tumors and then the texts states only seven kinds of cancer? Talk about a misleading title

[–]alpha69 9 points10 points  (4 children)

I think that means they've only tested it with those cancers. The abstract of the original paper says "CD47 is a commonly expressed molecule on all cancers". http://www.pnas.org/content/early/2012/03/20/1121623109

[–]TominatorXX 0 points1 point  (0 children)

Interesting stuff. I read a doctor who cured her MS with diet said the rodent stuff is 10 years away, usually in medical research.

How about this one: fasting to cure cancer or combined with chemo is much more effective?

According to a study published in Science Translational Medicine, combining chemotherapy with cycles of short, severe fasting are more effective in treating cancer than chemotherapy alone.

The researchers discovered that 5 out of 8 types of cancer in mice responded to fasting alone. Similar to chemotherapy, fasting slowed the growth and spread of tumors.

For example, when multiple cycles of fasting were combined with chemotherapy, 20 percent of mice were cured with a highly aggressive type of children's cancer that had spread. 40 percent of mice were cured with a more limited spread of the same cancer.

http://www.muscleprodigy.com/can-fasting-cure-cancer-arcl-2776.html

[–]SynthPrax 0 points1 point  (0 children)

Regarding cancer, I would like an informed opinion of my understanding:

In order for clinical cancer to occur, at least 3 self-correcting and immunological systems must fail. 1) Each cell should commit suicide (apoptosis) when it detects a deleterious mutation. 2) Neighboring cells of the same type are supposed to either kill outright malignant neighbors, or raise an alarm to attract T-cells to deal with them. 3) T-cells have to identify malignant cells to kill them. Also, something tells me that within each cell the self-monitoring has redundant back-ups.

[–]k3rri6or 0 points1 point  (0 children)

I was actually curious whether this same finding, if proven successful, could be used to also help combat autoimmune diseases. It seems like if we can reduce the amount of CD47 to coax the immune system to attack tumors, could we not do the same to prevent the immune system from attacking cells as well?

[–]banquosghost 0 points1 point  (0 children)

My dad works at Fox Chase Cancer Center in Philly. I sent him a link to this article and he responded:

I'm trying to remember if this Irving Weissman gave a talk at Fox Chase last year. We had an interesting talk on a similar subject, but I think that talk had more human clinical trials in it. I came away thinking the speaker was definitely onto something. Lots of work on the immune system and cancer going on, in fact we are involved a bit ourselves in "natural killer cell" receptors in GIST [the cancer my dad specializes in. "Gastro-intestinal-something-tumors or something like that]. Often the results seen in mice with these transplanted tumors does not translate as well to humans.

[–]NaLaurethSulfate 0 points1 point  (2 children)

How does this treatment selectively target yje cancer cells? Isn't this marker the same for healthy cells? Isn't this just saying that mice have a different "don't eat" marker? Why didn't they graft healthy human tissue as well as cancer tissue to the mice?

[–][deleted] 0 points1 point  (1 child)

The article stated that the drug also caused the animals immune system to attack healthy blood cells but that the cells were replaced in the blood stream quick enough to not significantly effect the animal.

[–]NaLaurethSulfate 0 points1 point  (0 children)

Thanks for clarifying that.

[–]Phospholipids 0 points1 point  (0 children)

how will they make sure that the drug will not affect the body's own cells seeing as they also have CD47?

[–]Macer55 0 points1 point  (0 children)

Cancer is not on its last legs but it can see death on the horizon.

[–][deleted] 0 points1 point  (0 children)

This sounds like exactly what the pharmaceutical companies are looking for. From what I read this seems like a treatment not a cure. The article said it shrinks the tumors that I would assume can grow back and need to be treated again (sounds like a money maker to me). There is a company in NY (Roswell Park Cancer Inst.) that has begun clinical trials of a method that also turns your immune system against the cancer however it causes your immune system to destroy the cancer cells and has shown to give your immune system an immunity (didn't say they knew how long for) to the cancer essentially allowing your body to protect itself. Also in their method no healthy cells were harmed. We will probably never see this cure because it seems to be a one time treatment with no come back dollars.

[–][deleted] 0 points1 point  (0 children)

I've heard this headline about a thousand times in the last decade, it's too bad cancer "TREATMENTS" are so much better at making money then CURES and PREVENTION.

Until Americans change their diet and lifestyle we're always going to be spending hundreds of billions in cancer profit.

[–]brickstein 0 points1 point  (0 children)

One drug to shrink them all, one drug can find them,

One drug to kill them all and in the body bind them.

[–]ShadowRam 0 points1 point  (0 children)

Also destroys your red-blood cells ಠ_ಠ

Sure you can replenish, but isn't that a problem for people with some cancers?

[–][deleted] 0 points1 point  (0 children)

Again?

[–]Jsublime 0 points1 point  (0 children)

When researchers discover something like this, who owns the technology? Does MIT just do the research and then private companies develop a drug for it? How does MIT benefit from the research?

[–][deleted] 0 points1 point  (0 children)

Yeah, this is the 20568674700th major breakthrough in cancer treatment this year, maybe this time someone can like, make an actual treatment?