Difference between revisions of "Chronic myelogenous leukemia historical perspective"

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==Historical Perspective==
 
==Historical Perspective==
 
Important dates in chronic myelogenous leukemia:
 
Important dates in chronic myelogenous leukemia:
* In the 1840s, the first cases of chronic myelogenous leukemia was first reported.<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 1960, [[Philadelphia chromosome]] was first discovered by Peter Nowell and David Hungerford.
+
* 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 1973, (9;22) translocation was first discovered. 
+
* Only a few weeks later, Rudolf Virchow in Berlin published a very similar case.
* From 1980, [[allogeneic stem cell transplantation]] (SCT) became the treatment of choice for eligible patients.<ref name="pmid20875546">{{cite journal |vauthors=Goldman JM |title=Chronic myeloid leukemia: a historical perspective |journal=Semin. Hematol. |volume=47 |issue=4 |pages=302–11 |date=October 2010 |pmid=20875546 |doi=10.1053/j.seminhematol.2010.07.001 |url=}}</ref>  
+
* In 1872, Ernst Neumann stated that leukemia cells originated in the bone marrow.
* In 1984, definition of the breakpoint cluster region on chromosome 22 was first reported.
+
* The next decades described the differentiation into myeloid versus lymphoid and acute versus chronic leukemias.
* In 1985, the [[BCR|BCR-ABL]] transcript was first discovered.
+
 
* In 1998, the era of tyrosine kinase inhibitors (TKI) began.
+
* 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 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.  
 +
* 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>
 +
 
 +
Therapy developed slowly.
 +
* 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, first intervention with a better prognosis and better-tolerated 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.
 +
* Soon later, interferon-α was found to induce durable complete cytogenetic responses and long-term survival, although in only a small fraction of patients.  
 +
* In 1992, Alexander Levitzki proposed the use of ABL inhibitors to treat leukemias driven by ABL oncogenes.
 +
* 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.
 +
 
 +
* In 2008, the majority of patients diagnosed with chronic phase CML can expect to have durable responses with good quality of life.
 +
* For that 20% to 30% who fail imatinib, second-line inhibitors are an effective salvage strategy.
 +
* 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==

Revision as of 18:08, 18 October 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2] 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 onwards 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:

  • 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. [1]
  • Only a few weeks later, Rudolf Virchow in Berlin published a very similar case.
  • 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.
  • 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).[2]
  • In 1986 Janet Rowley recognized that Ph was the product of a reciprocal translocation between chromosomes 9 and 22.
  • 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.
  • A faithful murine disease model was established in 1990.

Historical perspective of treatment of chronic myelogenous leukemia:[3]

Therapy developed slowly.

  • 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, first intervention with a better prognosis and better-tolerated 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.
  • Soon later, interferon-α was found to induce durable complete cytogenetic responses and long-term survival, although in only a small fraction of patients.
  • In 1992, Alexander Levitzki proposed the use of ABL inhibitors to treat leukemias driven by ABL oncogenes.
  • 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.
  • In 2008, the majority of patients diagnosed with chronic phase CML can expect to have durable responses with good quality of life.
  • For that 20% to 30% who fail imatinib, second-line inhibitors are an effective salvage strategy.
  • 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

  1. 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. 
  2. NOWELL PC, HUNGERFORD DA (November 1961). "Chromosome studies in human leukemia. II. Chronic granulocytic leukemia". J. Natl. Cancer Inst. 27: 1013–35. PMID 14480645. 
  3. 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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