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Sometimes cancer arises when you have crossing over between non-homologous chromosomes. In the process, a chimeric protein arises. A chimeric protein is a protein that consists of parts of two separate proteins spliced together. In this way, cancer cells end up producing a substance (in this case a protein) that is absent in a healthy person. A good example ...


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There is indeed a positive correlation between gastric reflux disease and esophageal cancer, and also between stomach ulcerations and stomach cancer. There are more than one possible mechanisms for these correlations to arise, but what you are proposing is definitely a prime suspect. ...


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Telomeres are at the end of the chromosomes and get shorter with every cell division, since the lagging strand is missing a start point for the DNA polymerase. This limits the number of cell divisions to 40 to 60 before the cells go into senescence and stop dividing (they are not dying at this point). This phenomenon is called the "Hayflick limit". Cell ...


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In some types of cancer cells, an enzyme called telomerase can actually rebuild the telomeres, making a cell appear "younger" than it actually is and preventing it from senescing (reaches a point where it stops dividing). Telomerase, a eukaryotic ribonucleoprotein (RNP) complex, helps to stabilize telomere length in human stem cells, reproductive cells ...


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There are, indeed, several such mAb based treatments. From the Mayo Clinic: The monoclonal antibody drug rituximab (Rituxan) attaches to a specific protein (CD20) found only on B cells, one type of white blood cell. Certain types of lymphomas arise from these same B cells. When rituximab attaches to this protein on the B cells, it makes the cells more ...


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It would not be possible to differentiate CSC from normal population non-invasively and select them out. You may do a single cell expression analysis to say if a CSC is present in a population or not but there is no magic bullet method for eliminating them. Also there are several oncogenes and some of them are also required for usual stem cell function. HAT ...


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The cells never died in the sense that they kept replicating, individual cells still died. They were safely cultured in petri dishes before Henrietta Lacks died. The cells came from a tumor that developed from her cervix. The cervical cancer cells had developed high telomerase activity. Telomerase builds telomeres on the ends of DNA, protecting the ...


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The processes of apoptosis is not so simple, there is a lot of genes and proteins that participate in it. In cancer cells some of them mutate and not working properly. Lack of apoptosis is the main problem in cancer. If cell not working properly, it dies. But not in cancer. So theoretically, yes. If we will fix the apoptosis, the cell probably will die. ...


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In the most technical sense, yes. In a practical sense, no. Average background radiation dose from food and water sources is ~.3 mSv according to the UN. Given that it takes 1 full Sv to increase cancer risk by ~5-6%, it seems unlikely that, under normal conditions, variability in consumption of water will change risk in a significant fashion. Now, when ...



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