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group_5_presentation_3_-_chronic_myeloid_leukemia [2017/11/28 16:03] mohamesb [Chronic Myeloid Leukemia] |
group_5_presentation_3_-_chronic_myeloid_leukemia [2018/01/25 15:18] (current) |
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| ====== Chronic Myeloid Leukemia ====== | ====== Chronic Myeloid Leukemia ====== | ||
| - | {{::screen_shot_2017-10-01_at_6.19.43_pm.png?525|}} | + | {{ ::screen_shot_2017-10-01_at_6.19.43_pm.png?525 |}} |
| - | **Figure 1**: Normal blood versus blood of a CML patient. | + | **Figure 1**: normal blood versus blood of a CML patient. |
| - | LS4M03 CML ppt slides: https://docs.google.com/presentation/d/1yjxDywKLHAQyuMUwxRe52624DxmA9ek-3qR8e3BM-jw/edit?usp=sharing | + | 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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| <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" ==== | ||
