"Spontaneous" cancer development

[MarkE]

I have a question regarding cancer. It is broadly accepted that this is a genetical mutation inside a cell that often has an external/environmental cause, such as oncogenes in food sources, or UV light, but it is thought that it could also actually happen 'spontaneously'. This sounds mechanical, instead of a living organism with a ‘purpose’ or an ‘intention’ of any kind. But if you look at the process itself, it doesn’t seem solely and purely mechanical at all, but rather intentional. Let me describe the process of 'spontaneous' cancer development:

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The human body is well prepared to prevent the development of cancer. Cancer will only develop if protein coding genes are affected, so we have an overwhelming amount of noncoding DNA (junk DNA). If however a mutation occurs on the coding region of our genome, this can be repaired. A cell therefore has two tumour suppressor genes, one from each parent. Only when both of them are damaged a cell is able to grow uncontrollably. So if only one of the two tumour suppressor gene gets broken, it will be repaired by the other tumour suppressor gene as soon as possible. We have trillions of cells, so the chances are already be very small that this second tumour suppressor gene of the same allele of the same chromosome of the same cell will be damaged before the second one gets repaired, but it does happen. So when this can’t be repaired, the cell has another trick up its sleeve to prevent the development of cancer: the cell will initiate programmed cell death (apoptosis). But this suicidal attempt of a cell, to save the other cells from cancer, is prevented, so cell death can not take place. Not only that, but the exact opposite happens: growth factors are being promoted. Still, there’s no deadly cancer developed, because a cancer cell becomes lethal when metastasis occurs (the spreading of a cancer cell to other parts of the body). This now full-grown cancer will leave the group and enter a blood vessel, and continues its journey by itself.

Does this still sounds spontaneous and and mechanical, instead of planned or intentional in any way? Well, let’s continue the progress. The cancer cell can’t just breach through the wall of a blood vessel, so how to overcome this obstacle? The cancer cell will eat his way through (with the enzyme 'protease' and so called MMPs to break the tissue). After it has gained access to blood vessel, it now flows along the current the bloodstream and stops when it has 'arrived' (how does it know where to stop?) and repeats the same process by eating his way out of the blood vessel. The cancer cell is now finally able to proliferate and make copies of itself. It also makes certain proteins to signal blood vessels, who will react to this signal to start feeding it with blood (angiogenesis), and thereby enabling further growth of the tumour. Telomerase suddenly becomes active (a normal somatic cell doesn’t have telomerase because normal cell should die at some point, only stem cells and germ line cells have telomerase), which basically means that now this cancer cell will also become immortal.

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This process this doesn’t seem pregrogrammed and mechanical to me. There seems to be some kind of intentional step by step process. There are too much steps involved to be seen as some kind of random and spontaneous process. I’m not saying it’s intelligent or must have consciousness, but the way the scientific community thinks about cancer doesn’t quite do it for me. Lots of parasites also show to be able to think several steps ahead, and need several hosts to end up in the host they finally need to reproduce in. Tapeworms and other parasitic flatworms for instance have complex lifecycles in which specific developmental stages are completed in a sequence of several different hosts. Plasmodium (malaria) first goes to liver cells (it knows where the liver is located) where it reproduces asexually, burst open, next goes to blood cells where reproduces sexually, burst open, and partly develops into gametocytes (reproductive organs) to start the whole cycle over again, when another mosquito bites the host, and the parasite can move into the salivary glands of another mosquito. Again, lots of steps are involved, this time of an actual organism (protozoa) that is considered alive, but the process looks a lot like the development of cancer, which is thought to be not alive.

Why isn’t cancer considered more of an intentional process (or at least more than just 'spontaneous')?

Edited February 19, 2018 by MarkE

[Silvestru]

I cannot speak much about cancer but we find many "suspiciously clever" ways of survival in nature.

Your story made me think of https://en.wikipedia.org/wiki/Dicrocoelium_dendriticum - a parasite that goes through a very lengthy process to grow and live. (I bolded the parts which I find scary)

Quote

 

The first intermediate host, the terrestrial snail (Cochlicopa lubrica in the United States), consumes the feces, and becomes infected by the larval parasites. The larvae (or miracidium) drill through the wall of the gut and settle in its digestive tract, where they develop into a juvenile stage. The snail attempts to defend itself by walling the parasites off in cysts, which it then excretes and leaves behind in the grass or substrate.

The second intermediate host, an ant (Formica fusca in the United States^[13]), uses the trail of snail slime as a source of moisture. The ant then swallows a cyst loaded with hundreds of juvenile lancet flukes. The parasites enter the gut and then drift through its body. Most of the cercariae encyst in the haemocoel of the ant and mature into metacercariae, but one moves to the sub-esophageal ganglion (a cluster of nerve cells underneath the esophagus). There, the fluke takes control of the ant's actions by manipulating these nerves.^[14] As evening approaches and the air cools, the infected ant is drawn away from other members of the colony and upward to the top of a blade of grass. Once there, it clamps its mandibles onto the top of the blade and stays there until dawn. Afterward, it goes back to its normal activity at the ant colony. If the host ant were to be subjected to the heat of the direct sun, it would die along with the parasite. Night after night, the ant goes back to the top of a blade of grass until a grazing animal comes along and eats the blade, ingesting the ant along with it, thus putting lancet flukes back inside their host. They live out their adult lives inside the animal, reproducing so that the cycle begins again.Infected ants may contain 100 metacercariae, and a high percentage of ants may be infected. Typical infections in cattle may be in the tens of thousands of adult worms.^[18]

 

 

 

 

This parasite becomes snail excrement to get eaten by ants to mind control them to live and reproduce inside cows to eventually go out as cow dung..... 

Apologies for not providing input on the specific Cancer topic.

[CharonY]

There are too many misconceptions in OP to address them all. Just a short list: 

- error in replication/repair are common and spontaneous while not being targeted.

- there are more than on or two genes that are relevant to control cell replication

- mutations in non-coding areas can also contribute to tumorgenesis (mostly by altering regulation)

As a whole there is a need to understand that proliferating cells are common and essential in our body. However, the do not do us harm because of a host of things fantastically not going wrong. Cancer cells have reverted to some of these features, but with the checks and balances off, so to speak.

Overall the premise is inherently faulty and does not justify the amount of extrapolation.

[MarkE]

@CharonY Yes you’re right, cancer is a much more complex process, but I think you’re missing the point I’m trying to make.  

For instance, it’s true that our junk DNA is not completely inert. Ancient long noncoding RNAs for instance are actively regulated in organisms, and mostly involved in its early development (because all vertebrates look alike in the early fetal stage). These ncRNAs contribute to diseases, including cancer, and can cause alterations in the behaviour of cancer cells. When histone-modifying enzymes (called ‘major repressor’, found in certain cancers) are overexpressed they're able to make modifications that leads to gene expression. This overexpression of ncRNAs make cancer cells more likely to metastasis.

I haven't even mentioned oncoviruses, viral agents that are suspected of causing cancer, or carcinogenic bacteria that are known or suspected to cause cancer as well.

So yes, I was oversimplifying the cancer process, but that’s not the point. I don’t think we need to fully grasp the entire cancer process to be able to see how it’s behaving in this step by step way, and how it can’t be a totally spontaneous unintentional process (at least, that’s not how I’m interpreting it). 

@Silvestru I think it’s incredible to see examples such as these. How is this parasite able to know what would happen after he climbs to the top of a blade of grass, and what would happen next, and next? Is it ‘thinking’ towards a goal, or is it instinctively preprogrammed, like ‘if:snail, then: go to respiratory pore’, and next ‘if:ant, then: go to the top of a blade of grass”? Just like a squirrel, who has no prefrontal cortex, yet it plans ahead by storing nuts for the winter, instinctively.

If this is indeed the case, where's the evidence for this preprogrammed behaviour in its genome? Does the scientific community have evidence for these kinds of causal correlations, and know which genes are responsible for what behaviour?

Edited February 20, 2018 by MarkE

[Endy0816]

Its not really deliberate though, they're randomly accessing the code that can allow a cell to 'go mobile'. Think they are helped by some of the immune cells to do so.

Retroviral activity is pretty random as well. They are not very selective in their multiple insertions, leading them to break things. Part of why CRISPR is such a big deal, far more percise.

[CharonY]

4 hours ago, MarkE said:

So yes, I was oversimplifying the cancer process, but that’s not the point. I don’t think we need to fully grasp the entire cancer process to be able to see how it’s behaving in this step by step way, and how it can’t be a totally spontaneous unintentional process (at least, that’s not how I’m interpreting it).

Intention requires adding a layer of complexity to it. I.e. it requires additional mechanisms and thus higher evidence level than assuming a mostly randomized process. Of course, there are hotspots for certain types of mutation, but they are not confined to cell-cycle control systems and again, there are more elements than you initially proposed. If we start from faulty premises we won't come to realistic outcomes. Also note that while the processes of cancer, and tissue turnover in general, is complex, there is a lot of knowledge out there and dismissing it and building a parallel narrative based on assumptions is just not going to cut it.

Also note that non-coding RNA are still identifiable as they still need to be transcribed. I was more broadly referring to untranscribed sequences which play mainly regulatory roles.  

[Adelin]

I find this a very "sensible topic". I was reading about this last night. It's very important for scientists to study it more and more and also get financial support from our governments.

 

Edited April 26, 2018 by Phi for All
commercial links removed per rule 2.7