12.2 Research Assignment: Chronic Myeloid Leukemia

Chronic Myeloid Leukemia
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Chronic Myeloid Leukemia
Protein kinases are enzymes that chemically add phosphate groups to other proteins with the aim of modifying them (Howard Hughes Medical Institute, 2017). This means that even the protein which are changed will result in functional changes, associated with the way they interact with other proteins, their cellular location and enzymes.
The facilitation of the phosphorylation processes is made possible through the donation of the phosphate molecule which comes from the adenosine triphosphate (ATP), which is a universal donor for Phosphoryl (Howard Hughes Medical Institute, 2017).
The BCR-ABL kinase is caused by genetic mutations that result in the development of chronic myeloid leukemia.
Between the BCR-ABL and the ABL, the two have different binding sites. This is relative to the fact that they have been modified differently; this is with reference to the BCR-ABL due to mutations.
Every other cell in a human body has 23 pairs of chromosomes. During translocation of the chromosomal material some parts of the chromosome 22 goes to 9 and the vice versa. This then results in a shorter chromosome 22. This leads to the formation of a new gene that is generally referred to as the BCR-ABL an oncogene. It is this gene that then causes the cancer cells, CML (Howard Hughes Medical Institute, 2017).
The drug developed by scientists to treat CML was referred to as Gleevec.
This is a drug that works by blocking the binding cites for the BCL-ABL and the prevents the unregulated activity.
Some of the patients developed resistance after long use, this is relative to the fac...