Recently, I was glad to hear that STAP (stimulus-triggered acquisition of pluripotency) had been produced by subjecting white blood cells to various stressful environments. The one originally mentioned in the lay press was an acid bath. That result was what I predicted would happen when any cell population is prevented from sensing its environment. I had surmised that the acid environment was denaturing the CRF (cell recognition factors) that enabled the cell to determine location.
More recently, however, there has been talk of retracting. I think the results will be shown to be valid. With such an important discovery, in the rush to publish, mistakes are almost sure to be made in presentation. This latest report says that there was some irregularity with some of the images and it hinted at non-reproducibility. I see little chance that there was an attempt to deceive as in that one famous case at Sloan-Kettering where a scientist had clearly fudged his results--I believe by putting certain mice into the wrong treatment group.
A mobile cell like a mature white cell needs to know if it should attack. If acid is disrupting communications, the white cell would have no option but to revert to an earlier part of the differentiation sequence or program. They also tried low-oxygen and physical disruption of cell membrane. These were not found to be as effective as the acid bath. Low oxygen would not usually be a problem because white cells often have to operate in areas of low oxygen as you might find in infections and early tumors. Disrupting their outer membrane might be hit or miss as reprogramming would only occur (as per my CRF theory) if the CRFs were physically excised; and this would be problematic if the white cells used were in a chemotaxic mode and sensors "bunched up" along the line of travel.
My theory predicts that if certain similar disruptions could be made to the membrane CRFs of mature non-immune cells, you would also see transitions to STAP cells. The caveat being, of course, that such cells are more prone to go into programmed cell death when a loss of CRFs occur. We might need to use cells with mutations in their apoptosis and/or EMT and/or Death Receptor genes, for instance. A much more difficult process. I would like to know if there was a rationale was for using white blood cells other than that it makes sense that a readily available and accessible cell be harvested form the patient (I just hope they were circulating white blood cells with a minimally invasive procedure for harvesting).
More recently, however, there has been talk of retracting. I think the results will be shown to be valid. With such an important discovery, in the rush to publish, mistakes are almost sure to be made in presentation. This latest report says that there was some irregularity with some of the images and it hinted at non-reproducibility. I see little chance that there was an attempt to deceive as in that one famous case at Sloan-Kettering where a scientist had clearly fudged his results--I believe by putting certain mice into the wrong treatment group.
A mobile cell like a mature white cell needs to know if it should attack. If acid is disrupting communications, the white cell would have no option but to revert to an earlier part of the differentiation sequence or program. They also tried low-oxygen and physical disruption of cell membrane. These were not found to be as effective as the acid bath. Low oxygen would not usually be a problem because white cells often have to operate in areas of low oxygen as you might find in infections and early tumors. Disrupting their outer membrane might be hit or miss as reprogramming would only occur (as per my CRF theory) if the CRFs were physically excised; and this would be problematic if the white cells used were in a chemotaxic mode and sensors "bunched up" along the line of travel.
My theory predicts that if certain similar disruptions could be made to the membrane CRFs of mature non-immune cells, you would also see transitions to STAP cells. The caveat being, of course, that such cells are more prone to go into programmed cell death when a loss of CRFs occur. We might need to use cells with mutations in their apoptosis and/or EMT and/or Death Receptor genes, for instance. A much more difficult process. I would like to know if there was a rationale was for using white blood cells other than that it makes sense that a readily available and accessible cell be harvested form the patient (I just hope they were circulating white blood cells with a minimally invasive procedure for harvesting).
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