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group_5_presentation_3_-_chronic_myeloid_leukemia [2017/11/28 16:02]
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"​ ==== 
  
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