I'd like to address an issue which is not that well-resolved in my mind. That is, do cancer cells arise from any cell of the body or only from stem cells? I believe that differentiated cells are subject to the Hayflick limit and, as such, will self-destruct (apoptosis) if they are unable to establish contact with the pre-assigned cell neighbors. But stem cells have built-in immortality. (I wish I had a subscription or access to journals so that I can cite the literature for every point I make. Unfortunately, I have to rely on the media to bring me news of new developments) That immortality may be checked by what are called Natural Killer Cells but if a stem cell should lose contact and start to reprogram it's phenotypic expression before NKC's have had a chance to stop them, they will begin to express one CRF after another and thereby avoid detection just like a parasite would do.
Perhaps a little graphics is in order. You are a cell. You reach out with molecules similar to antibodies (I believe) in order to establish contact with your neighbor. You do not make contact and then there is a decision process that's activated. If, after waiting a preordained time, you do not make contact, begin to express some other antibody and check for contact. Now, the exact queue of CRF's that's used by a cell undergoing redevelopment is not known. I believe it may be advantage for the cell to exhibit CRF's that are near its immediate pedigree or near those cells that, earlier in development, had expressed CRF's that were still of the general tissue type in question. "Going back in time" repeats so that at some point, if you express, let's say, an extra early embryonic progenitor to the adult liver cell, you may find yourself no longer expressing liver cells but, rather, an earlier developmental branch that eventually would express mesadermal tissue from an early embryo or blastocyst, even. Trophoblastic cells that differentiated into the placenta seem to express CRF's and other characteristics found in many cancer cells. Indeed, the trophoblast has been called parasitic by some--metastatic by others.
When we figure out the exact program that's executed by the normal developing cell, we would be very close to a cancer cure because we could direct any cell into behaving like the cell that would be least injurious to the patient. For example, if we knew the pathway or programming sequence that the cancerous genome was undergoing , we would be able to provide that cell with the right CRF's that would cause it to develop into something relatively innocuous like connective tissue.
If the cancer is very far progressed, we might then have one cure for all as the necessary clues to take a cell from, let's say, a trophoblast to connective tissue would be the same. Well, here's where I think the promise might be delayed.
The reason is this: for the longest time, we have had to defend against parasites. You can't blame the parasite for it only recognizes the host as a suitable environment in which to live. Now, the parasite is a wily creature indeed. That means that we have to be one step ahead.
Let's imagine what would happen if we only expressed a single unique CRF for any given tissue and everyone else on the planet expressed the same one. In such a scenario, a parasite would have it easy because it need only express that one CRF that would disguise it as a liver cell, let's say. It could then live out the rest of it's lowly existence in someone's liver. To prevent this from happening, the host would, I think, establish a mechanism whereby it's liver CRF was different from that of most other people. If such a case proves to be correct, as I think it will, you can see how the total repertoire of CRF's might be a bit complex. I don't think that an maximum variability is in play but, if it were, I would not be surprised. I just think that to evade parasite you would only need a certain amount under the maximum.
I've addressed this elsewhere, but why is it that a cell needs to know where it is. Why does a stem cell need to know that it just gave rise to a liver daughter cell and that it--the stem cell--still is in the liver? I would submit that a homogeneous arrangement of differentiated cells is much better than a haphazard heterogeneous collection. But why? Well, form follows function for one. A bone cell in the lungs is not conducive to good lung function. Neurons in the blood stream would surely clog things up--you get the idea. In a slightly different vein, you would not want a gastric cell in the brain producing hydrochloric acid or a pancreatic cell in the heart producing digestive enzymes. You would not want skin cells populating the cornea with their light-absorbing melanin. The list goes on for every cell of the body. But what of development? Here again, extremely important, because you do not want your brain any further south than your palate. Every developing cell needs to know where it is in order to produce the final design. Chemotaxic agents play a role but only to establish broad patterns of migration.
Perhaps a little graphics is in order. You are a cell. You reach out with molecules similar to antibodies (I believe) in order to establish contact with your neighbor. You do not make contact and then there is a decision process that's activated. If, after waiting a preordained time, you do not make contact, begin to express some other antibody and check for contact. Now, the exact queue of CRF's that's used by a cell undergoing redevelopment is not known. I believe it may be advantage for the cell to exhibit CRF's that are near its immediate pedigree or near those cells that, earlier in development, had expressed CRF's that were still of the general tissue type in question. "Going back in time" repeats so that at some point, if you express, let's say, an extra early embryonic progenitor to the adult liver cell, you may find yourself no longer expressing liver cells but, rather, an earlier developmental branch that eventually would express mesadermal tissue from an early embryo or blastocyst, even. Trophoblastic cells that differentiated into the placenta seem to express CRF's and other characteristics found in many cancer cells. Indeed, the trophoblast has been called parasitic by some--metastatic by others.
When we figure out the exact program that's executed by the normal developing cell, we would be very close to a cancer cure because we could direct any cell into behaving like the cell that would be least injurious to the patient. For example, if we knew the pathway or programming sequence that the cancerous genome was undergoing , we would be able to provide that cell with the right CRF's that would cause it to develop into something relatively innocuous like connective tissue.
If the cancer is very far progressed, we might then have one cure for all as the necessary clues to take a cell from, let's say, a trophoblast to connective tissue would be the same. Well, here's where I think the promise might be delayed.
The reason is this: for the longest time, we have had to defend against parasites. You can't blame the parasite for it only recognizes the host as a suitable environment in which to live. Now, the parasite is a wily creature indeed. That means that we have to be one step ahead.
Let's imagine what would happen if we only expressed a single unique CRF for any given tissue and everyone else on the planet expressed the same one. In such a scenario, a parasite would have it easy because it need only express that one CRF that would disguise it as a liver cell, let's say. It could then live out the rest of it's lowly existence in someone's liver. To prevent this from happening, the host would, I think, establish a mechanism whereby it's liver CRF was different from that of most other people. If such a case proves to be correct, as I think it will, you can see how the total repertoire of CRF's might be a bit complex. I don't think that an maximum variability is in play but, if it were, I would not be surprised. I just think that to evade parasite you would only need a certain amount under the maximum.
I've addressed this elsewhere, but why is it that a cell needs to know where it is. Why does a stem cell need to know that it just gave rise to a liver daughter cell and that it--the stem cell--still is in the liver? I would submit that a homogeneous arrangement of differentiated cells is much better than a haphazard heterogeneous collection. But why? Well, form follows function for one. A bone cell in the lungs is not conducive to good lung function. Neurons in the blood stream would surely clog things up--you get the idea. In a slightly different vein, you would not want a gastric cell in the brain producing hydrochloric acid or a pancreatic cell in the heart producing digestive enzymes. You would not want skin cells populating the cornea with their light-absorbing melanin. The list goes on for every cell of the body. But what of development? Here again, extremely important, because you do not want your brain any further south than your palate. Every developing cell needs to know where it is in order to produce the final design. Chemotaxic agents play a role but only to establish broad patterns of migration.
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