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{{Chronic myelogenous leukemia}}
 
{{Chronic myelogenous leukemia}}
{{CMG}} {{AE}} {{MJK}} {{SN}}
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{{CMG}} {{AE}}{{Badria}} {{MJK}} {{SN}}
 
==Overview==
 
==Overview==
In the 1840s, the first cases of [[chronic myelogenous leukemia]] ([[splenomegaly]] with high [[leukocyte]] count) was reported in France, Germany, and Scotland. In 1960, the association of [[Philadelphia chromosome]] with the [[pathogenesis]] of  [[chronic myelogenous leukemia]] was first discovered. In 1973, (9;22) [[Chromosomal translocation|translocation]] was first discovered.Definition of the [[BCR (gene)|breakpoint cluster region (BCR)]] on [[chromosome]] 22 was first reported in 1984 and the demonstration of the BCR-ABL transcript in CML was first discovered in 1985. From 1980 onwards [[allogeneic stem cell transplantation]] (SCT) became the treatment of choice for eligible patients. In 1998, the era of [[tyrosine kinase inhibitors]] (TKI) began.
+
In the 1840s, the first cases of [[chronic myelogenous leukemia]] ([[splenomegaly]] with high [[leukocyte]] count) was reported in France, Germany, and Scotland. In 1960, the association of [[Philadelphia chromosome]] with the [[pathogenesis]] of  [[chronic myelogenous leukemia]] was first discovered. In 1973, (9;22) [[Chromosomal translocation|translocation]] was first discovered.Definition of the [[BCR (gene)|breakpoint cluster region (BCR)]] on [[chromosome]] 22 was first reported in 1984 and the demonstration of the BCR-ABL transcript in CML was first discovered in 1985. From 1980 on wards [[allogeneic stem cell transplantation]] (SCT) became the treatment of choice for eligible patients. In 1998, the era of [[tyrosine kinase inhibitors]] (TKI) began.
 
==Historical Perspective==
 
==Historical Perspective==
Important dates in chronic myelogenous leukemia:
+
Important dates in [[chronic myelogenous leukemia]]:
 +
* The early history of [[leukemia]] reaches back 200 years.<ref name="pmid22033191">{{cite journal |vauthors=Kampen KR |title=The discovery and early understanding of leukemia |journal=Leuk. Res. |volume=36 |issue=1 |pages=6–13 |date=January 2012 |pmid=22033191 |doi=10.1016/j.leukres.2011.09.028 |url=}}</ref>
 +
* In 1811, Peter Cullen defined a case of splenitis acutus with un explainable milky [[blood]].
 +
* Alfred Velpeau, mentioned the [[leukemia]] associated symptoms, and observed [[pus]] in the [[Blood vessel|blood vessels]] (1825).
 +
* Alfred Donné, demonstrated a [[maturation]] arrest of the [[white blood cells]] (1844).
 +
* John Bennett named the disease leucocythemia, based on the microscopic collection of [[purulent]] leucocytes (1845)
  
* In 1845, Edinburgh pathologist John Hughes Bennett presented a “Case of Hypertrophy of the Spleen and Liver in which Death Took Place from Suppuration of the Blood” in the Edinburgh Medical Journal. <ref name="pmid17671636">{{cite journal |vauthors=Nowell PC |title=Discovery of the Philadelphia chromosome: a personal perspective |journal=J. Clin. Invest. |volume=117 |issue=8 |pages=2033–5 |date=August 2007 |pmid=17671636 |pmc=1934591 |doi=10.1172/JCI31771 |url=}}</ref>
+
* In 1845, Edinburgh pathologist, John Hughes Bennett, presented a “Case of [[Hypertrophy]] of the [[Spleen]] and [[Liver]] in which Death Took Place from Suppuration of the Blood” in the Edinburgh Medical Journal. <ref name="pmid17671636">{{cite journal |vauthors=Nowell PC |title=Discovery of the Philadelphia chromosome: a personal perspective |journal=J. Clin. Invest. |volume=117 |issue=8 |pages=2033–5 |date=August 2007 |pmid=17671636 |pmc=1934591 |doi=10.1172/JCI31771 |url=}}</ref>
* Only a few weeks later, Rudolf Virchow in Berlin published a very similar case.  
+
* Few weeks later, Rudolf Virchow, in Berlin published a similar case.  
* In 1872, Ernst Neumann stated that leukemia cells originated in the bone marrow.
+
* In 1872, Ernst Neumann stated that [[leukemia]] cells originated in the [[bone marrow]].
* The next decades described the differentiation into myeloid versus lymphoid and acute versus chronic leukemias.
+
* The next decades described the pathophysiologic differentiation into [[myeloid]] versus [[lymphoid]] and acute versus chronic [[Leukemia|leukemias]].
  
* In 1973, (9;22) translocation was discovery by Philadelphia cytogeneticists Peter Nowel and David Hungerford of an abnormally small G-group chromosome that we know as the Philadelphia chromosome (Ph).<ref name="pmid14480645">{{cite journal |vauthors=NOWELL PC, HUNGERFORD DA |title=Chromosome studies in human leukemia. II. Chronic granulocytic leukemia |journal=J. Natl. Cancer Inst. |volume=27 |issue= |pages=1013–35 |date=November 1961 |pmid=14480645 |doi= |url=}}</ref>
+
* In 1973, (9;22) translocation was discovery by Philadelphia cytogeneticists Peter Nowel and David Hungerford of an abnormally small G-group [[chromosome]] that we know as the Philadelphia chromosome (Ph).<ref name="pmid14480645">{{cite journal |vauthors=NOWELL PC, HUNGERFORD DA |title=Chromosome studies in human leukemia. II. Chronic granulocytic leukemia |journal=J. Natl. Cancer Inst. |volume=27 |issue= |pages=1013–35 |date=November 1961 |pmid=14480645 |doi= |url=}}</ref>
* In 1986 Janet Rowley recognized that Ph was the product of a reciprocal translocation between chromosomes 9 and 22.
+
* In 1986 Janet Rowley established that Ph was the product of a [[reciprocal translocation]] between chromosomes 9 and 22 which were termed as BCR and ABL
* In the 1980s, the translocation partners were identified as BCR and ABL
+
* This then lead to discovery of unregulated [[tyrosine kinase]] activity is critical to BCR-ABL’s ability to transform [[cells]].  
* This then lead to discovery of unregulated tyrosine kinase activity is critical to BCR-ABL’s ability to transform cells.
 
* A faithful murine disease model was established in 1990.
 
  
Historical perspective of treatment of [[chronic myelogenous leukemia]]:<ref name="Deininger2008">{{cite journal|last1=Deininger|first1=M. W.|title=Chronic Myeloid Leukemia: An Historical Perspective|journal=Hematology|volume=2008|issue=1|year=2008|pages=418–418|issn=1520-4391|doi=10.1182/asheducation-2008.1.418}}</ref>
+
=== '''Historical perspective of treatment of [[chronic myelogenous leukemia]]:''' ===
 
+
Treatment of [[Chronic myelogenous leukemia|chronic myeloid leukemia]] evolved over an era as described below. <ref name="Deininger2008">{{cite journal|last1=Deininger|first1=M. W.|title=Chronic Myeloid Leukemia: An Historical Perspective|journal=Hematology|volume=2008|issue=1|year=2008|pages=418–418|issn=1520-4391|doi=10.1182/asheducation-2008.1.418}}</ref>
Therapy developed slowly.
+
* In 1865, Heinrich Lissauer, described the use of [[arsenic]] in two patients with [[leukemia]].
* In 1865, Heinrich Lissauer described the use of arsenic in two patients with leukemia.
 
 
* In the 1920s, [[splenic]] [[irradiation]] was performed which resulted in symptomatic relief.
 
* In the 1920s, [[splenic]] [[irradiation]] was performed which resulted in symptomatic relief.
* In 1959 effective control of [[blood]] counts became possible with [[busulfan]].
+
* In 1959, effective control of [[blood]] counts became possible with [[busulfan]].
* Ten years later, first intervention with a better prognosis and better-tolerated hydroxyurea was discovered.
+
* Ten years later, [[hydroxyurea]] was discovered.
* In mid 1970's a breakthrough was achieved when the Seattle group described the disappearance of the Ph chromosome in CML patients who underwent allotransplant.
+
* In mid 1970's, a breakthrough was achieved when the Seattle group described the disappearance of the Ph chromosome in CML patients who underwent [[Allotransplantation|allotransplant]].
* Soon later, interferon-α was found to induce durable complete cytogenetic responses and long-term survival, although in only a small fraction of patients.  
+
* [[Interferon]] was discovered to stimulate cytogenetic responses and resultant long-term survival, however, only in a few patients.  
* In 1992, Alexander Levitzki proposed the use of ABL inhibitors to treat leukemias driven by ABL oncogenes.
+
* In 1992, Alexander Levitzki, proposed the use of ABL inhibitor.
* At about the same time, scientists at Ciba-Geigy had synthesized a potent inhibitor of ABL that was termed GCP57148B and is now known as imatinib.
+
* At about the same time, scientists at Ciba-Geigy synthesized, a strong inhibitor of ABL that was named GCP57148B and is now known as imatinib.
 
+
* For that 20% to 30% who fail [[imatinib]], second-line inhibitors are an effective salvage therapy.
* In 2008, the majority of patients diagnosed with chronic phase CML can expect to have durable responses with good quality of life.
+
* However, once the disease has progressed beyond the chronic phase, [[Allotransplantation|allotransplant]] is still the recommended.  
* For that 20% to 30% who fail imatinib, second-line inhibitors are an effective salvage strategy.
+
* Unfortunately, leukemia often persists in the best responders and the therapies directed at the BCR-ABL [[tyrosine kinase]] are unable to cure since they can not destroy CML stem cells.
* However, once the disease has progressed beyond the chronic phase, allotransplant is still the recommended treatment for all eligible patients.  
 
* Unfortunately, evidence is presented that leukemia may persist even in the best responders and that therapies directed at the BCR-ABL tyrosine kinase are not curative since they fail to eradicate the CML stem cells. Thus, the CML saga continues, and needs further improvement.
 
  
 
==References==
 
==References==

Latest revision as of 16:30, 6 November 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Badria Munir M.B.B.S.[2] Mohamad Alkateb, MBBCh [3] Sima NoorAli, M.D.

Overview

In the 1840s, the first cases of chronic myelogenous leukemia (splenomegaly with high leukocyte count) was reported in France, Germany, and Scotland. In 1960, the association of Philadelphia chromosome with the pathogenesis of chronic myelogenous leukemia was first discovered. In 1973, (9;22) translocation was first discovered.Definition of the breakpoint cluster region (BCR) on chromosome 22 was first reported in 1984 and the demonstration of the BCR-ABL transcript in CML was first discovered in 1985. From 1980 on wards allogeneic stem cell transplantation (SCT) became the treatment of choice for eligible patients. In 1998, the era of tyrosine kinase inhibitors (TKI) began.

Historical Perspective

Important dates in chronic myelogenous leukemia:

  • The early history of leukemia reaches back 200 years.[1]
  • In 1811, Peter Cullen defined a case of splenitis acutus with un explainable milky blood.
  • Alfred Velpeau, mentioned the leukemia associated symptoms, and observed pus in the blood vessels (1825).
  • Alfred Donné, demonstrated a maturation arrest of the white blood cells (1844).
  • John Bennett named the disease leucocythemia, based on the microscopic collection of purulent leucocytes (1845)
  • In 1845, Edinburgh pathologist, John Hughes Bennett, presented a “Case of Hypertrophy of the Spleen and Liver in which Death Took Place from Suppuration of the Blood” in the Edinburgh Medical Journal. [2]
  • Few weeks later, Rudolf Virchow, in Berlin published a similar case.
  • In 1872, Ernst Neumann stated that leukemia cells originated in the bone marrow.
  • The next decades described the pathophysiologic differentiation into myeloid versus lymphoid and acute versus chronic leukemias.
  • In 1973, (9;22) translocation was discovery by Philadelphia cytogeneticists Peter Nowel and David Hungerford of an abnormally small G-group chromosome that we know as the Philadelphia chromosome (Ph).[3]
  • In 1986 Janet Rowley established that Ph was the product of a reciprocal translocation between chromosomes 9 and 22 which were termed as BCR and ABL
  • This then lead to discovery of unregulated tyrosine kinase activity is critical to BCR-ABL’s ability to transform cells.

Historical perspective of treatment of chronic myelogenous leukemia:

Treatment of chronic myeloid leukemia evolved over an era as described below. [4]

  • In 1865, Heinrich Lissauer, described the use of arsenic in two patients with leukemia.
  • In the 1920s, splenic irradiation was performed which resulted in symptomatic relief.
  • In 1959, effective control of blood counts became possible with busulfan.
  • Ten years later, hydroxyurea was discovered.
  • In mid 1970's, a breakthrough was achieved when the Seattle group described the disappearance of the Ph chromosome in CML patients who underwent allotransplant.
  • Interferon-α was discovered to stimulate cytogenetic responses and resultant long-term survival, however, only in a few patients.
  • In 1992, Alexander Levitzki, proposed the use of ABL inhibitor.
  • At about the same time, scientists at Ciba-Geigy synthesized, a strong inhibitor of ABL that was named GCP57148B and is now known as imatinib.
  • For that 20% to 30% who fail imatinib, second-line inhibitors are an effective salvage therapy.
  • However, once the disease has progressed beyond the chronic phase, allotransplant is still the recommended.
  • Unfortunately, leukemia often persists in the best responders and the therapies directed at the BCR-ABL tyrosine kinase are unable to cure since they can not destroy CML stem cells.

References

  1. Kampen KR (January 2012). "The discovery and early understanding of leukemia". Leuk. Res. 36 (1): 6–13. PMID 22033191. doi:10.1016/j.leukres.2011.09.028. 
  2. Nowell PC (August 2007). "Discovery of the Philadelphia chromosome: a personal perspective". J. Clin. Invest. 117 (8): 2033–5. PMC 1934591Freely accessible. PMID 17671636. doi:10.1172/JCI31771. 
  3. NOWELL PC, HUNGERFORD DA (November 1961). "Chromosome studies in human leukemia. II. Chronic granulocytic leukemia". J. Natl. Cancer Inst. 27: 1013–35. PMID 14480645. 
  4. Deininger, M. W. (2008). "Chronic Myeloid Leukemia: An Historical Perspective". Hematology. 2008 (1): 418–418. ISSN 1520-4391. doi:10.1182/asheducation-2008.1.418. 

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