How would you go about reprogramming cancer cells back to normalcy? You would first identify the most likely candidate(s) for Cell Recognition Factor(s) and determine how they change during the development of, let's say, a pancreatic cell. From the time of the first egg mass to mature adult cell, what CRF's were being expressed?
Take these and chemically attach them to a carrier that is able to diffuse through tissue. Inject the complex into the blood or lymphatic system. Repeat the cocktail until normalcy is achieved. Once we know the exact sequence that particular CRF's are expressed, we can just inject stage-specific CRF's in a particular sequence.
A difficulty that I'm hoping does not present itself is that of individual variations in CRF's. We may not want to have to design a sequence on an individual basis. It would be much better, at least initially, if one sequence for differentiation of pancreas cells was the same for all individuals.
Essential elements of this theory:
A. With the exception of lymphocytes, cells should not have the capability of existing anywhere in an organism.
B. Apoptosis or Killer cell is activated to eliminate "foreigners" that attempt to exist in an inappropriate location.
C. Cells that lose contact begin expressing earlier CRF's. This encourages Killer Cell targeting. If not killed, cells begin other reprogramming activity.
D. Once a CRF is expressed that is "early" enough, the cell begins acting like early embryo cells and exibit migratory (metastatic) behavior.
E. If the cell is supplied with early CRF's, it could be reprogrammed into a differentiated state.
Note: Cancer cells do communicate which each other but because they are embryonic, they continually seek CFR's that are not there. Even at the most primitive stages, the cancer cell is expecting other signals that are not being provided. Perhaps the womb had CRF's. If I were searching for CRF candidates to use in cancer, I would start with that very earliest of environments.
Recently, in one of the few papers that I could access free, I came across a statement saying that HDAC inhibitors could be used to bring on differentiation. HDAC modifies histones so that they bind more strongly with DNA. If you inhibit this action, you increase transcription, and cancer cells have been seen to differentiate to a normal state upon being treated with an HDAC inhibitor. These findings support the CRF theory of cancer because the cancer cell, now with a less restricted genome, begins to express the right CRF for its present niche.
Take these and chemically attach them to a carrier that is able to diffuse through tissue. Inject the complex into the blood or lymphatic system. Repeat the cocktail until normalcy is achieved. Once we know the exact sequence that particular CRF's are expressed, we can just inject stage-specific CRF's in a particular sequence.
A difficulty that I'm hoping does not present itself is that of individual variations in CRF's. We may not want to have to design a sequence on an individual basis. It would be much better, at least initially, if one sequence for differentiation of pancreas cells was the same for all individuals.
Essential elements of this theory:
A. With the exception of lymphocytes, cells should not have the capability of existing anywhere in an organism.
B. Apoptosis or Killer cell is activated to eliminate "foreigners" that attempt to exist in an inappropriate location.
C. Cells that lose contact begin expressing earlier CRF's. This encourages Killer Cell targeting. If not killed, cells begin other reprogramming activity.
D. Once a CRF is expressed that is "early" enough, the cell begins acting like early embryo cells and exibit migratory (metastatic) behavior.
E. If the cell is supplied with early CRF's, it could be reprogrammed into a differentiated state.
Note: Cancer cells do communicate which each other but because they are embryonic, they continually seek CFR's that are not there. Even at the most primitive stages, the cancer cell is expecting other signals that are not being provided. Perhaps the womb had CRF's. If I were searching for CRF candidates to use in cancer, I would start with that very earliest of environments.
Recently, in one of the few papers that I could access free, I came across a statement saying that HDAC inhibitors could be used to bring on differentiation. HDAC modifies histones so that they bind more strongly with DNA. If you inhibit this action, you increase transcription, and cancer cells have been seen to differentiate to a normal state upon being treated with an HDAC inhibitor. These findings support the CRF theory of cancer because the cancer cell, now with a less restricted genome, begins to express the right CRF for its present niche.
Comments