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During the 1960s and 1970s, a great deal of research was done on a class of viruses that affects rodents and birds and causes tumors in those species. The motivation for a lot of this research was the idea that similar viruses might cause tumors in humans, but in fact it's turned out that there are very few viruses that cause tumors in humans. Nevertheless, the study of these rodent viruses has been enormously fruitful in helping us to understand human cancer, and that's the basis of this story.
One of the viruses that was studied in those years had two peculiarities. One was that it had lost most of the genes that it needed to reproduce itself. It could only reproduce if a helper virus was present in the same cell to supply the missing functions. The second peculiarity was that in place of the genes that were required for reproduction of the virus was another gene that had actually been picked up at some point in the history of this virus when it went through rats, and it picked up a rat gene and incorporated it into its own genome.
At the same time that a lot of work was going on on these viruses, other scientists were studying other aspects of tumor formation, in particular, the action of carcinogenic agents, chemicals and X-rays and ultraviolet light. As you all know, human cells can turn into tumor cells under the influence of such agents. The tumor-like properties of those cells are inherited by all the daughter cells through many generations and, moreover, almost all chemicals that turn out to be carcinogens are also able to cause mutations.
Another observation was that in tumor cells, many of the chromosomes seemed to have altered structures. So, all of these observations and others certainly suggested that changes in DNA might be involved in the development of tumor cells. By about 1980, it became possible to test that hypothesis directly.
If you have human tumor cells produced in laboratory dishes or isolated from the tumor itself, then perhaps they have a gene or genes in them which is responsible for the fact that they're tumor cells. If you isolate the DNA from the cells and cut it up into more or less gene-sized pieces and then put it on top of mouse cells growing in a dish, the mouse cells can take up pieces of this DNA, and any mouse cell that picks up a piece of DNA that carries on it a gene that can cause a tumor will begin to grow like tumor cells, and its progeny will grow rapidly and form a tight little cluster on the cell.
Now it's possible to pick such cells off and isolate the DNA from them and also separate the human DNA sequence that might have caused the tumor-like property from the bulk of the mouse sequences and to clone that DNA. And when you do that and put that DNA, which is now pure sequence, back in mouse cells, many of the cells become tumor-like rather than just a rare few. And such a gene, such a DNA sequence, bears the name of an oncogene.
please change the tittle
swaraj0007 3 years ago 16
@ShaolinViolin mutations of the RAS protein leads to it constantly being activated and therefore constantly promoting transcription and cell proliferation. This growth is uncontrolled because RAS can no longer be turned off and that is how cancers form.
POPsPuravida 1 year ago 4