Why do zebras have stripes, asked Alan Turing just before he died from self inflicted causes. The answer was, just at the time of Watson and Crick, because cells communicate with each other and turn genes on and off in an almost wave like fashion.
Two years ago we write a paper regarding flower patterns and used the term Turing Tessellation. This means that cells produce proteins in an epigenetic manner and the proteins directly or as a result of the control they have on other molecules, communicate cell to cell, and this is what causes flower patterns.
In a recent paper in Cell and reported in Medical News Today the authors show that in Melanoma the stem cell theory, namely that it is just one single cell that goes wild is proven wrong in melanoma. What happens simply is that the cells "communicate" a la Turing, and then when proteins which control malignant cells start flowing they set off a chain reaction a la Turing and as we had shown in a paper a few years ago. The cells pop up elsewhere. The metastasis is not from the single stem cell escaping but from the proteins going wild.
The reporter in Medical News Today writes:
Scientists at The Wistar Institute offer a new explanation for the persistent ability of melanoma cells to self-renew, one of the reasons why melanoma remains the deadliest form of skin cancer. The concept of the "dynamic stemness" of melanoma can explain why melanoma cells behave like both conventional tumor cells and cancer stem cells.
The researchers write in the May 14 issue of the journal Cell that - contrary to other published reports - melanoma does not appear to follow the hierarchic cancer stem cell model, where a single malignant "mother cell" both reproduces to produce new mother cells and differentiates to produce the bulk tumor population. Instead, all melanoma cells equally harbor cancer stem cell potential and are capable of inducing new tumors. Their findings reveal the unique biology of melanoma, and suggest that melanoma requires a new therapeutic approach.
They continue:
The present study arose when Roesch discovered a link between the potential of JARID1B to decrease proliferation of melanoma cells and control stemness. He decided to see whether JARID1B could be a marker of slow growing melanoma stem cells. Initially, the results were promising, he says. JARID1B-expressing cells were slow-growing (as stem cells often are), and rare, accounting for about 5 percent of the tumor population. "At this point we were really happy because we thought we had found a cancer stem cell marker," Roesch said.
But then, two unexpected results occurred. First, Roesch found that all melanoma cells were equally capable of initiating tumors in a mouse model, regardless of whether they expressed JARID1B or not. Second, he found that JARID1B expression did not conform to the traditional model of stem cell development - cells that expressed the gene could turn it off, and cells that didn't, could turn it on. In other words, the gene's expression was plastic, rather than stable. "Basically, our data suggest that every melanoma cell can serve as source for indefinite replenishment of the tumor," said Roesch.
Thus it is the cell to cell flow, the building and decaying of protein concentrations which set off the malignant melanocytes.
The Cell article summarizes the following key points:
Two years ago we write a paper regarding flower patterns and used the term Turing Tessellation. This means that cells produce proteins in an epigenetic manner and the proteins directly or as a result of the control they have on other molecules, communicate cell to cell, and this is what causes flower patterns.
In a recent paper in Cell and reported in Medical News Today the authors show that in Melanoma the stem cell theory, namely that it is just one single cell that goes wild is proven wrong in melanoma. What happens simply is that the cells "communicate" a la Turing, and then when proteins which control malignant cells start flowing they set off a chain reaction a la Turing and as we had shown in a paper a few years ago. The cells pop up elsewhere. The metastasis is not from the single stem cell escaping but from the proteins going wild.
The reporter in Medical News Today writes:
Scientists at The Wistar Institute offer a new explanation for the persistent ability of melanoma cells to self-renew, one of the reasons why melanoma remains the deadliest form of skin cancer. The concept of the "dynamic stemness" of melanoma can explain why melanoma cells behave like both conventional tumor cells and cancer stem cells.
The researchers write in the May 14 issue of the journal Cell that - contrary to other published reports - melanoma does not appear to follow the hierarchic cancer stem cell model, where a single malignant "mother cell" both reproduces to produce new mother cells and differentiates to produce the bulk tumor population. Instead, all melanoma cells equally harbor cancer stem cell potential and are capable of inducing new tumors. Their findings reveal the unique biology of melanoma, and suggest that melanoma requires a new therapeutic approach.
They continue:
The present study arose when Roesch discovered a link between the potential of JARID1B to decrease proliferation of melanoma cells and control stemness. He decided to see whether JARID1B could be a marker of slow growing melanoma stem cells. Initially, the results were promising, he says. JARID1B-expressing cells were slow-growing (as stem cells often are), and rare, accounting for about 5 percent of the tumor population. "At this point we were really happy because we thought we had found a cancer stem cell marker," Roesch said.
But then, two unexpected results occurred. First, Roesch found that all melanoma cells were equally capable of initiating tumors in a mouse model, regardless of whether they expressed JARID1B or not. Second, he found that JARID1B expression did not conform to the traditional model of stem cell development - cells that expressed the gene could turn it off, and cells that didn't, could turn it on. In other words, the gene's expression was plastic, rather than stable. "Basically, our data suggest that every melanoma cell can serve as source for indefinite replenishment of the tumor," said Roesch.
Thus it is the cell to cell flow, the building and decaying of protein concentrations which set off the malignant melanocytes.
The Cell article summarizes the following key points:
- The H3K4 demethylase JARID1B marks a subpopulation of slow-cycling melanoma cells
- The JARID1B+ subpopulation is required for continuous tumor maintenance
- Cells can lose or gain JARID1B expression and do not follow a stem cell hierarchy
- Tumor initiation is not necessarily linked with tumor maintenance
This observation will undoubtedly change the "paradigm" in a Kuhn sense in viewing cancer. We have argued this for a few years now but it will take time for researchers to understand its implications in the full. For this we must thank Alan Turing.
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