This popped up in /r/worldnews yesterday with another source, where /u/sharplydressedman gave it some context [1].
> I hate to be a buzzkill, but the linked article is very sensationalist ... it entirely misses the point of the research published by the Anastasiadis lab (pubmed link [2]). Being able to stop or revert transformed cells in vitro is not new, we've been able to stop or revert tumor cells for decades....
> Tldr of this is that this is unexciting unless you're a researcher studying E-cadherin/B-catenin, and means very little to someone outside of the cell biology field.
/u/squaresarerectangles provided a link to the original Nature Cell Biology paper, reproduced in citation [3].
Not to mention that killing cancer cells, which can be done in umpteen way in vitro and in vivo today, seems superior to reverting cells to normal, except on unusual circumstances.
That is, I assume one would want to have a tumor die rather just stabilize as it's cell reverted to normal (if that's even possible). Also killing cells on the outside of tumor seems the most effective way to deliver drugs to the cells on the inside of a tumor.
(Just speaking from common sense, if there's something I'm missing, I'd be interested).
Isn't the big question WHY that cancer cell developed inside a human body in the first place? I mean, if it happened once, what would prevent it from happening again?
It is. There are a ridiculously large number of cancers and they are all different. Even something seemingly simple like "lung cancer" can be divided into several high level diseases, each of which have their own subcategories.
People who expect a one size fits all solution to cancer will be sorely mistaken
“We believe that loss of the apical PLEKHA7-microprocessor complex is an early and somewhat universal event in cancer,” he adds. “In the vast majority of human tumor samples we examined, this apical structure is absent"
I'm not saying you're wrong, but this seems to be suggesting that treatments based on this mechanism could potentially be used to treat the vast majority of cancers. You're saying this is wrong?
Sure, and they might be right. But history is rich with these sorts of things. The number of common cancer attributes are legion, e.g. MYC mutations, but to date it always turns out that the total story is complex enough that it doesn't matter.
Cancer is a type or classification of diseases. There are many cancerous diseases. It could very well be that they're related, but we shouldn't assume that unless proven. However, looking for similarities and patterns is a good thing nonetheless.
The classification of "being a cancer" does imply (rightly) that there are similarities. The question is if this helps us in treating the cause or not.
I feel that perhaps saying "cancerous diseases" is clearer than saying "cancers".
I'm an absolute layman, so I'm more curious here whether I am wrong: So far I've always understood that, however different a cancer may develop, all kinds of cancers have roughly the same cause: Some event corrupts a cell's DNA such that:
a) The corruption cannot be repaired;
b) The cell still survives;
c) The mechanisms that normally regulate cell division are impaired, causing the cell to continually divide.
d) The daughter cells also have DNA corruptions with the same properties.
Of course, depending on the nature of the DNA corruption and on what cells were corrupted, the resulting illnesses may be vastly different, as well as the strategies to combat them. But couldn't you at least look for ways to prevent cancer universally if you somehow address this common cause?
The thing is, your given (some event corrupts the cell's DNA) needs to be examined. Let's agree that some event corrupts the cell's DNA as you suggest, and then follow up with some questions.
1) Where in the enormous strand was it corrupted?
1a) Was it one place, or several?
2) What corrupted it?
2a) Again, was it one cause, or five different causes,
three of which we don't know about and can't currently track?
3) Does the mechanism of action (the thing that caused the mutation) change the way a specific pathology progresses, even if it's a similar mutation in the same area? (yes)
So that's sort of the problem with cancer research. They're not trying to solve a single problem with a bunch of different presentations, they're trying to solve a fuckton of problems with a similar number of presentations, some of which are similar even though they have different roots.
>I feel that perhaps saying "cancerous diseases" is clearer than saying "cancers".
I would argue that it's not. People use 'cancerous' as an adjective describing things that aren't cancer all the time. Of course, if you're only using 'cancerous' to refer to cancers (I.e., in the context of pathology,) then just call them cancers.
Yeah, it feels like they're not different diseases at all, merely different dialects of the same disease (my words, a tad hand-wavey). I understand the need to be precise about the wording and the willingness to not let people get their hopes up too much, but I feel that this "a bunch of different diseases" concept is introducing a whole slew of misconceptions in the mix as well.
Cancer is one disease like infectious disease is one disease. Some things we thought were different are now seen as similar (BRAF V600E, for example), but the genes and proteins involved are usually radically different, one to the next. If anything, it's striking that our morphological classifications have withstood genetic scrutiny at all.
Except that infectious diseases have innumerable, dissonant final effects on the body. Cancers all basically do the same thing to different parts of the body. Which is why the notion of cutting the symptom (uncontrolled, mutated, undying cells) can be considered.
In my world, cancer is simply a cell, or group of cells, which lives inside the human body, that the human body treats as part of itself. But these cells are more interested in their own survival than the survival of the body. It's when a group of cells "dissent", so to speak, and start prioritizing themselves over the rest of the cells in the body.
This is it. This is what we should be focusing on with all the cancer research funds available. Cancer is just a data corruption in the cell DNA and we have a few methods of fixing data in the digital world.
Cancer can mean different things. Would you consider a viral infection "just data corruption"? The virus "corrupts" a cell's DNA to manufacture more virus. Nothing is "just" when it comes to code that's been running for billions of years.
A hard tumor (say bone cancer/osteosarcoma) is vastly different than say leukemia.
Cancers types are Carcinoma (surfaces of the body i.e. skin), Sarcoma (tumors that originate in hard or soft tissue i.e. bone cancer), Lukemia (start in the blood, no tumors), Lymphoma (Hodgkin, Non-Hodgkin), Multiple Myeloma (starts in plasma cells), Melanoma (skin cancer), Brain and spinal cords, Germ cell (starts in sperm or egg cells but can be anywhere in the body), Neuroendocrine tumors (from cells that produce hormones), Carcinoid tumors (slow growing tumors in the rectum and small intestine and spreads to the liver).
The thing that a sizable amount of cancer research funds should focus on is preventation of telomere extension. Selectively or periodically turn off all mechanisms of telomere extension, which covers telomerase activities and ALT, the alternative lengthening of telomeres processes. All cancers abuse telomere extension in order to thrive, it is required for rapid cellular replication. Normal cells are not so much in need of it, so turn it all of for some period of time until the cancer is gone then restore telomere extension capabilities. This will work for all cancer types.
Telomerase interdiction can be achieved via RNAi or similar methods, while the hurdle to blocking ALT is that it isn't well understood at this time; the targets till need to be listed and understood. It will probably be the case that targeting telomere extension interdiction to cancer cells will be superior or even necessary, but fortunately selective targeting of cancer cells is a going concern in research, with considerable progress achieved already and more in the works.
It seems more & more the solutions to the big 3 diseases: cancer, heart disease, and dementia/alz, involve direct DNA / RNA / Mitohcondrial DNA reprogramming.
It would then seem prudent to ASAP get your own DNA sequenced. As time goes on, you collect more & more DNA damage & probably your original DNA becomes harder & harder to find.
DNA damage is not a major issue at all. Most of the damage can be "reversed" by looking at your close relatives since it's single nucleotide mutations.
Right now you can't even get the genome sequenced without gaps for a reasonable price. The current $1000 genome is 30x coverage which leaves some parts unsequenced. You can probably infer what some of those sequences should be, but that would be much harder than reversing potential DNA damage over your lifetime.
But even if we had the whole thing sequenced, modifying DNA in some or every cell is definitely not easy and in some cases impossible. Also, all current methods have all kinds of side effects.
Finally, even if you had some dangerous DNA mutation reversed, it may not help if a mutation induced cascade already began.
Eh, genome engineering is a possible solution to those problems, but that doesn't mean that it has to be the only solution. I'm working on genome engineering solutions for a couple of cancers right now-- we're close to solving problems in vitro, but that doesn't mean these treatments can be transferred to actual sick human subjects successfully.
Genome engineering is white hot right now, sailing off of CRISPR. Wait five years, see what pans out. I highly doubt that we'll have cures in hand on that timescale, but we can hope! I expect that genome engineering will improve human health vastly, but it's not going to be as easy as they make it out to be.
A last tidbit: like all medical interventions, genome engineering has side effects, too. They're largely side effects that have never been seen or treated before, and they can frequently be fatal or severe. I wouldn't expect that there is an incentive for these side effects to go away unless they're fatal more than 10% of the time.
What this group is doing has been pursued for quite a while, and many people have laid claim to finally cracking it, so I'm skeptical. It'll be a good while before this kind of intervention is finished being refined in vitro, nevermind in vivo.
(Sorry for being naive) What is the discovery of this finding - is it the Chemistry of reprogramming the cells or a spontaneous way to evolve these cells back to their original code?
What do you mean by a "spontaneous way to evolve these cells back to their original code"? The cells' genetic code (DNA) itself not changing, but not every gene in a genome is expressed in equal amounts or at the same time. In addition to encoding genes that "do stuff", the genome also codes for helper molecules which regulate the expression of these "action genes/proteins" in response to stimulus and environmental conditions. Modifying or replacing these helper molecules can therefore change the fate of the overall cell without even touching the main "action genes".
suspect it would go better with a bit of NLP or training of the brain to stop them from doing whatever they did in the first place that programmed those cells wrong. :)
not sure what the downvote is for, im assuming its because you suspect a mutagen like pesticide is directly responsible for the mutation that causes cancer cells to grow. bbbut my government lobbyists and their scientists recommended eating pesticide sprayed foods for 100 years, because spraying lemon juice on the foods was more expensive than pesticide. typical hacker news downvote because its actually a good idea thats not in your college text books.
> I hate to be a buzzkill, but the linked article is very sensationalist ... it entirely misses the point of the research published by the Anastasiadis lab (pubmed link [2]). Being able to stop or revert transformed cells in vitro is not new, we've been able to stop or revert tumor cells for decades....
> Tldr of this is that this is unexciting unless you're a researcher studying E-cadherin/B-catenin, and means very little to someone outside of the cell biology field.
/u/squaresarerectangles provided a link to the original Nature Cell Biology paper, reproduced in citation [3].
[1] https://www.reddit.com/r/worldnews/comments/3idyjg/us_scient...
[2]http://www.ncbi.nlm.nih.gov/pubmed/26302406
[3]http://www.nature.com/ncb/journal/vaop/ncurrent/full/ncb3227...