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group_5_presentation_3_-_chronic_myeloid_leukemia [2017/11/28 10:11] yousis |
group_5_presentation_3_-_chronic_myeloid_leukemia [2018/01/25 15:18] (current) |
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| **Figure 1**: normal blood versus blood of a CML patient. | **Figure 1**: normal blood versus blood of a CML patient. | ||
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| + | Link to PPT presentation: https://docs.google.com/a/mcmaster.ca/presentation/d/1yjxDywKLHAQyuMUwxRe52624DxmA9ek-3qR8e3BM-jw/edit?usp=sharing | ||
| ====== Introduction ====== | ====== Introduction ====== | ||
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| * **Myelogenous Leukemias**: develop from abnormal myeloid stem cells | * **Myelogenous Leukemias**: develop from abnormal myeloid stem cells | ||
| - | Moreover, the types of leukemia are further grouped based on how quickly the leukemia develops and grows. Acute leukemias start suddenly, developing within days or weeks, and chronic leukemias develop slowly over months or years. The four main types of leukemia are outlined in figure X below. | + | Moreover, the types of leukemia are further grouped based on how quickly the leukemia develops and grows. Acute leukemias start suddenly, developing within days or weeks, and chronic leukemias develop slowly over months or years. The four main types of leukemia are outlined in figure 3 below. |
| {{::screen_shot_2017-11-07_at_4.24.53_pm.png?600|}} | {{::screen_shot_2017-11-07_at_4.24.53_pm.png?600|}} | ||
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| === Complete Blood Count (CBC) === | === Complete Blood Count (CBC) === | ||
| - | This is often a routine test showing the number of red blood cells, white blood cells, and platelets in the blood. In a patient with CML, leukocytosis is seen with a remarkable left shift (Quintás-Cardama and Cortes, 2006). This means that there are a high number of immature white blood cells present in the blood, as a result of their early release from the bone marrow. Leukocytosis is most prevalent in basophils and eosinophils. Red blood cells are usually present in less than normal levels, as they are outnumbered by the white blood cells (Sessions, 2007). This usually results in mild anemia. The platelet count may also be slightly elevated, but this case of thrombocytosis does not result in any symptoms directly related to it (Sessions, 2007). | + | This is often a routine test showing the number of red blood cells, white blood cells, and platelets in the blood. In a patient with CML, leukocytosis is seen with a remarkable left shift (Quintás-Cardama and Cortes, 2006). This means that there are a high number of immature white blood cells present in the blood, as a result of their early release from the bone marrow. Leukocytosis is most prevalent in basophils and eosinophils. Red blood cells are usually present in less than normal levels, as they are outnumbered by the white blood cells (Sessions, 2007). This usually results in mild anemia. The platelet count may be less than normal, as the WBC production outcompetes it (Sessions, 2007). |
| {{:cml_blood_smere_.jpg?300|}} | {{:cml_blood_smere_.jpg?300|}} | ||
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| <box 35% round right | > {{ ::screen_shot_2017-11-10_at_8.57.39_am.png?410 |}} </box| Figure 7: Reciprocal translocation of the BCR protein and ABL gene generating an oncogene that constitutively activates unregulated myeloid cell growth leading to CML. > In 1960, Peter Nowell and David Hungerford, working in Philadelphia, described a consistent chromosomal abnormality in patients with CML (Druker, 2008). They consistently reported an acrocentric chromosome that was thought to be a chromosomal deletion (Druker, 2008). Through this discovery, CML became known as the first human malignant disease to be linked to an acquired genetic abnormality (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). | <box 35% round right | > {{ ::screen_shot_2017-11-10_at_8.57.39_am.png?410 |}} </box| Figure 7: Reciprocal translocation of the BCR protein and ABL gene generating an oncogene that constitutively activates unregulated myeloid cell growth leading to CML. > In 1960, Peter Nowell and David Hungerford, working in Philadelphia, described a consistent chromosomal abnormality in patients with CML (Druker, 2008). They consistently reported an acrocentric chromosome that was thought to be a chromosomal deletion (Druker, 2008). Through this discovery, CML became known as the first human malignant disease to be linked to an acquired genetic abnormality (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). | ||
| - | The characteristic genetic abnormality of CML, the Philadelphia chromosome, is present in the bone marrow cells of more than 90% of all patients with CML (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). The reciprocal chromosomal translocation between the long arms of chromosomes 9 and 22, as illustrated below in figure x, is the hallmark of CML (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). This process fuses the Abelson murine Leukemia viral oncogene homolog (ABL) on chromosome 9 with the breakpoint cluster region (BCR) protein on chromosome 22, generating an oncogene that encodes the BCR-ABL protein, a constitutively active cytoplasmic form of the ABL kinase (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). It is this translocation of the two chromosomes and consequent expression of the BCR-ABL kinase that is considered to be the initiating factor in the pathogenesis of CML (Smith, Burthem, & Whetton, 2003). Furthermore, this reciprocal translocation occurs only in somatic cell lines and ultimately, the BCR-ABL fusion kinase leads to increased and unregulated growth of myeloid cells in the bone marrow. | + | The characteristic genetic abnormality of CML, the Philadelphia chromosome, is present in the bone marrow cells of more than 90% of all patients with CML (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). The reciprocal chromosomal translocation between the long arms of chromosomes 9 and 22, as illustrated below in figure 7, is the hallmark of CML (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). This process fuses the Abelson murine Leukemia viral oncogene homolog (ABL) on chromosome 9 with the breakpoint cluster region (BCR) protein on chromosome 22, generating an oncogene that encodes the BCR-ABL protein, a constitutively active cytoplasmic form of the ABL kinase (Kantarjian, Talpaz, Giles, O’Brien, & Cortes, 2006). It is this translocation of the two chromosomes and consequent expression of the BCR-ABL kinase that is considered to be the initiating factor in the pathogenesis of CML (Smith, Burthem, & Whetton, 2003). Furthermore, this reciprocal translocation occurs only in somatic cell lines and ultimately, the BCR-ABL fusion kinase leads to increased and unregulated growth of myeloid cells in the bone marrow. |
| ==== The "Philadelphia Chromosome" ==== | ==== The "Philadelphia Chromosome" ==== | ||
