The phenomenon of oncogene addiction describes cancer cell dependence on individual oncogenes to sustain the malignant phenotype. There has been clinical evidence to support the idea of oncogene addiction. One area oncogene addiction has been seen is in Chronic myeloid leukemia also known as CML. In CML there is an abnormality in chromosome 22. A translocation event happens where RAG cuts some of the Abl gene and more of the Bcr gene. When they come together and combine, it forms an alternative chromosome 22 referred to as Philadelphia chromosome. CML is essentially driven by the BCR-ABL mutant oncogene as its addiction. This was demonstrated in patients through the clinical responses attained with the kinase inhibitor imatinb, which targets BCR-ABL. It is further supported by genetic mechanisms of resistance that vastly led to reactivation of BCR-ABL kinase activity. Another example is antiandrogens. These are used as a treatment for prostate cancer. They are also known to be ‘lineage addicted’ to AR and have recurrent AR amplifications or mutations upon resistance to first line therapeutic techniques. Overall, medicine continues to advance and we are seeing other ways to support the phenomenon of oncogene addiction.
Comments
Comment II
I think this paragraph is very straight forward. I would suggest to make the closing sentence less broad and more specific to the paragraph itself. Also very good use of scientific language. Another suggestion would be to switch the lower case of myeloid leukemia to uppercase.
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This paragraph was very infromative and well writen. One comment I would have is that it might be beneficial to give a quick overview as to what BCR-ABL and AR are. That way there, if a non-scientifically gifted person reads it, they will understand what you are saying.