It is important to note that cancer start immediately the cell within the body tries to develop out of control. Therefore, the cells can spread to other sections of the body, making the whole body to become cancerous. Chronic myeloid leukemia (CML), may be considered as a paradigm in the current ontology. CML is commonly referred to as chronic myelogenous leukemia. CML is a type of cancer that begins when some blood-forming cell of the bone marrow. For the case of CML, the genetic adjustments take place an initial (immature) stage of the myeloid cells: these cells are the ones responsible for making red blood cell, platelet and other types of white blood cell. The myeloid cells do not make up the lymphocytes. Usually, these adjustments of the change forms result in an abnormal gene known as BCR-ABL, which changes the cell to a CML cell. The genetic fusion in the BCR-ABL leads to the formation of protein with unusual tyrosine kinase element which is regarded as a pathogenic factor contributing to the existence of this disease (Miao et al. pg 53). As for the leukemia cell grow gradually within the bone marrow and spreading into the blood.
Meanwhile, the cell also spreads to other sections of the body, including the liver and spleen: research has shown that CML is a common leukemia and can often change to fast-growing acute leukemia which is challenging to treat. But what is leukemia?: this is a type of cancer which also starts within the blood-forming cell existing in the bone marrow. Whenever one of the cells remodels and become a leukemia cell, it does not grow the way it should. In most occasions, it does divide into the new cell as a quicker rate- these leukemia cells do not die as expected, but instead continue to build up in the bone marrow. For the case of acute, chronic leukemia, the cell mature partially, such cell may appear to be normal, but in the real sense, they are not.
These cells do not fight bacteria and microorganisms within the body as white blood cells. Studies have shown that leukemia cells tend to live longer compared to other functional cells. They cause abnormal crowding of the bone marrow resulting in severe problems. The result is the crowding out of the cells. At a given stage, the leukemia cells get out of the bone marrow and spread into the body bloodstream, causing the white blood cells (WBCs) to increase in their number. However, the leukemia cells can spill to other vital body organs and adversely affect the general functioning of the body.
Most importantly, unlike the other types of cancer that begins in the respective organs of the body, leukemia starts from the bone marrow and spills over the entire parts of the body system. Not all chronic leukemia is similar. Determining the specific type of leukemia assists professional healthcare providers to protect each patient’s prognosis and recommends the best treatment plans (Miao et al. pg 17).
The epidemiology and etiology
The CML is the disorder of myeloproliferation that is affecting the stem of hematopoietic cells. It is occurring within all various groups of ages though, predominantly it is the disease of the adults, which accounts for 20% leukemia within the adults. The data about the lack is very reliable, especially with the countries that are poor with their resources, the extrapolation of the data available suggest about the CML affecting the patients above 100,000 in total worldwide every year and represent the significant burden of health within the global. Therefore, the CML incidences have been approximated at 1 to 2 on every 100,000 of the population yearly.
Consequently, there have always been 10 to 12 cases about the CML (Eichhorst et al. pg 78). The age which is median for the leukemia presentation remains at between 45 and 55 years that account to 20% of adults being affected by the disease. According to the effect of leukemia, the people who are usually affected most are the males as compared to the females with the ratio of 2:1.
Pathology of Chronic Myelocytic Leukemia (CML)
The breakthrough in the pathogenesis e of CML was the Nowell's landmark invention of the Ph chromosome and its links to the illness. The Ph chromosome is a result of the reciprocal transferring occurring between the elongated chromosomes of nine and twenty-two. The t(9;22)(q34;q11) frequently adds up three component of the ABL gene from the chromosome forming section of the BCR gene on the chromosome; the result is a hybrid BCR-ABL gene that is reproduced into a chimeric BCR-ABL messenger of the RNA. This ABL gene comprises of 11 exons, and the first exon constitutes two variants, namely 1a and 1b. This gene inscribes an endless expressed, a non-receptor tyrosine kinase with an approximate molar mass of 145KD. The isoforms of the ABL genes are usually derived for the explicit spilling of the initial exon. The breakpoint stage of the ABL gene can happen in a section which is largest the 300kilobase, but often before exon 2. The ABL exons that are 2 to 1 are put in the part of the BCR sections. The main breakpoint cluster section (M-bar) of the BCR gene existing in the chromosome (22) is situated between the exon 12 and 16 and often extends to about 3.5kb. The fusion of the two components, namely: b2a2 and b3a2, are formed and each translated into a chimeric protein commonly known as 210kD. In 95% BCR-ABL present in the CML, chance are the leukemic cells can comprise of b2a2 or b3a2 transcripts, and the remaining percentage (5%) can result in alternative spilling events which result in the expression of both the fusion elements (Eichhorst et al. pg 78). The prognosis and treatment for CML patients and similar to patients with b2a2 and b3a2 transcripts, with higher amounts of platelets for patients with b3a2 transcripts.
The BCR-ABL protein
The leukemogenic potential of the BCR-ABL takes place due to the fact that the tyrosine kinase activities of the ABL protein are usually controlled within the activated combination of the oncoprotein. It is important to note that the ABL proteins are non-receptor tyrosine kinase which plays a vital role when it comes on signal transfer and control of cell growth (). There exist two isoforms within the ABL, namely: isoform 1a and isoform 1b, these isoforms are often sown at the higher level of hematopoietic progenitor cell activities. Moreover, the isoforms are situated at the glycine residue of the N-sections. Failure of the myristoylation process to occur in the ABL encourages the events o
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