الفهرس 
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Abstract
Myeloid leukaemia in remission (CML) is a clonal stem cell illness defined by the proliferation of granulocytic components at all stages of development and the acquisition of an oncogenic BCR/ABL fusion protein, which is typically caused by a reciprocal translocation (9;22)(q34;q11). The chromosome from Philadelphia (Ph) is another name for the t(9;22), named for the city where Nowell and Hungerford first discovered it in 1960..
With a peak incidence at age 53, the prevalence of CML rises with age. Children can be afflicted, however it is uncommon, and men are affected more frequently than women (3:2). Most of the time, the reason of CML is unknown, yet radiation exposure might cause CML to manifest.
Regarding cellular development and function, hematopoiesis in CML is clonal and results from a self-renewing, hematopoietic pluripotent stem cell. However, the number of white blood cells has been steadily increasing (WBC). The BCR-ABL fusion gene product is the genetic signature of CML. Its acquisition is a type of molecular and cellular flaws that leads to CML, most likely during the division of a pluripotent stem cell.
Widely acknowledged proof that the neoplastic clone begins in a very primitive pluripotent stem cell is the unmistakable discovery of Ph chromosomes in all blood cell types, including B and T cells. The Abelson (ABL) nine chromosome oncogene and the area of the breakpoint cluster (BCR) on chromosome 22 frequently reciprocally translocate to produce this fusion protein. A third (or more) chromosome may occasionally be involved in a complex translocation (such as a three-way), but the BCR/ABL fusion product is always present.