Potentially Reprogramming Cancer Cells Back to Normal Cells
neurosciencenews.com
neurosciencenews.com
> 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...
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).
http://www.nature.com/ncb/journal/vaop/ncurrent/full/ncb3227...
I fell like Cancer is an umbrella term for several different little monsters.
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?
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".
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 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.
Therefore a benign tumor is much closer related to a cancerous tumor that to leukemia.
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).
Cancer definition - The bad cells can spread to other areas of the body. Benign tumors do not spread into, or invade, nearby tissues. - http://www.cancer.gov/about-cancer/what-is-cancer
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 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.
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.
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.
From: http://fqxi.org/community/podcast/2014.10.02 (the extended version of this interview is also available)
[1]: http://cancer-insights.asu.edu/2012/02/is-cancer-an-ancient-...
We added the qualifier "potentially" from the article's first paragraph.