Researchers are still trying to use embryonic stem cells (ES) to cure disease and continue to encounter tumor formation. A recent study did something along the right lines when it co-transplanted bone marrow stem cells (BMSC)along with ES. There were no tumors formed during the 5 weeks of the study. To me, this indicates that the BMSC had started to revert back to ES and these provided the CRF's required by the original ES to prevent them from forming tumors.
What needs to be done is to search for CRF's in embryonic tissues. The main difficulty here is which of the hundreds of molecules on the cell surface are CRF's. I am working on trying to identify candidates for this role. One that caught my eye was the SSEA or stage-specific embryonic antigen because this theory requires that there be stage specificity. A candidate that I focused on back in the 70's when I first came up with the CRF theory were the glycoconjugates simply because they play a role in such phenomena as apoptosis and migration, and there are so many of them but I need to see them characterized as stage-specific.
To recap, these are the requirements for CRF's: stage-specificity, involvement in cell adhesion, involved in a mechanism to reprogram the genome, long-term stability or efficient turnover mechanisms. A problem I've recently grappled with is the possibility that there might exist a one to many arrangement between the CRF and the particular stage of differentiation. It is conceivable that differentiation via CRF's could take place using a minimal number of embryonic and adult CRF's. I think of the four-color map theorem wherein it was proven that no matter how many countries (tissues) to have, only four colors (CRF's) are needed. Of course, because tissues are three dimensional, you would definitely need more than four colors (6?)
With regard to the reprogramming, molecular proof of a genetic mechanism that could support CRF's was recently reported at esciencenews.com on 5/12/08. They wrote that global genetic silencing occurs at the moment of differentiation. Also, the genome remains flexible right up until the end stages. They used microarrays to show genomic expression. I was not able to ascertain exactly how active genes were differentiated from inactive but I assume that some chemical modification of the chromosomes is at play. Once we identify the chemical species of the CRF molecules, we would probably use microarrays to chart the CRF's at each stage of differentiation. Then with the program on hand, we can play gene operator and supply the cancer with the needed CRF's. Initially, we would probably opt to create a ubiquitous adult cell type like connective tissue or capillary cell. The same technology could also be used to ensure that ES or adult stem cells end up as intended in the patient.
What needs to be done is to search for CRF's in embryonic tissues. The main difficulty here is which of the hundreds of molecules on the cell surface are CRF's. I am working on trying to identify candidates for this role. One that caught my eye was the SSEA or stage-specific embryonic antigen because this theory requires that there be stage specificity. A candidate that I focused on back in the 70's when I first came up with the CRF theory were the glycoconjugates simply because they play a role in such phenomena as apoptosis and migration, and there are so many of them but I need to see them characterized as stage-specific.
To recap, these are the requirements for CRF's: stage-specificity, involvement in cell adhesion, involved in a mechanism to reprogram the genome, long-term stability or efficient turnover mechanisms. A problem I've recently grappled with is the possibility that there might exist a one to many arrangement between the CRF and the particular stage of differentiation. It is conceivable that differentiation via CRF's could take place using a minimal number of embryonic and adult CRF's. I think of the four-color map theorem wherein it was proven that no matter how many countries (tissues) to have, only four colors (CRF's) are needed. Of course, because tissues are three dimensional, you would definitely need more than four colors (6?)
With regard to the reprogramming, molecular proof of a genetic mechanism that could support CRF's was recently reported at esciencenews.com on 5/12/08. They wrote that global genetic silencing occurs at the moment of differentiation. Also, the genome remains flexible right up until the end stages. They used microarrays to show genomic expression. I was not able to ascertain exactly how active genes were differentiated from inactive but I assume that some chemical modification of the chromosomes is at play. Once we identify the chemical species of the CRF molecules, we would probably use microarrays to chart the CRF's at each stage of differentiation. Then with the program on hand, we can play gene operator and supply the cancer with the needed CRF's. Initially, we would probably opt to create a ubiquitous adult cell type like connective tissue or capillary cell. The same technology could also be used to ensure that ES or adult stem cells end up as intended in the patient.
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