Myeloproliferative neoplasm historical perspective: Difference between revisions

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==Historical Perspective==
==Historical Perspective==
*In '''1892''', Sir Louis Vasquez described the first form of myeloproliferative disease in a patient. He described a patient with excess [[red blood cell]] production (eventually found to be [[polycythemia vera]], liver enlargement (hepatomegaly), and spleen enlargement (splenomegaly).<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref> It was thought that excess [[hematopoietic cell]] production resulted in organ enlargement. This was later termed extramedullary hematopoiesis.
*In '''1892''', Sir Louis Vasquez described the first form of myeloproliferative disease in a patient. He described a patient with excess [[red blood cell]] production (eventually found to be [[polycythemia vera]], [[liver]] enlargement ([[hepatomegaly]]), and [[spleen]] enlargement ([[splenomegaly]]). It was thought that excess [[hematopoietic cell]] production resulted in organ enlargement. This was later termed [[extramedullary hematopoiesis]].<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>


*In '''1903''', Sir William Osler later described a group of patients with elevated [[red blood cell]] counts.<ref name="pmid27884974">{{cite journal| author=Vannucchi AM| title=From leeches to personalized medicine: evolving concepts in the management of polycythemia vera. | journal=Haematologica | year= 2017 | volume= 102 | issue= 1 | pages= 18-29 | pmid=27884974 | doi=10.3324/haematol.2015.129155 | pmc=5210229 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27884974  }} </ref>
*In '''1903''', Sir William Osler later described a group of patients with elevated [[red blood cell]] counts.<ref name="pmid27884974">{{cite journal| author=Vannucchi AM| title=From leeches to personalized medicine: evolving concepts in the management of polycythemia vera. | journal=Haematologica | year= 2017 | volume= 102 | issue= 1 | pages= 18-29 | pmid=27884974 | doi=10.3324/haematol.2015.129155 | pmc=5210229 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27884974  }} </ref>


*In '''1934''', Alfred Goedel and Emil Epstein found that patients with thrombocytosis without erythrocytosis was a separate disease entity (later coined as [[essential thrombocythemia]]).<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>
*In '''1934''', Alfred Goedel and Emil Epstein found that patients with [[thrombocytosis]] without [[Polycythemia|erythrocytosis]] was a separate disease entity (later coined as [[essential thrombocythemia]]).<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>


*In '''1940''', Sir William Dameshek and Henthell described the clinical features of the myeloproliferative neoplasm now known as [[polycythemia vera]]. Patients were noted to have facial plethora, splenomegaly, elevated hemoglobin, and elevated platelet count.  
*In '''1940''', Sir William Dameshek and Henthell described the clinical features of the myeloproliferative neoplasm now known as [[polycythemia vera]]. Patients were noted to have facial [[Hypervolemia|plethora]], [[splenomegaly]], elevated [[hemoglobin]], and elevated [[platelet]] count.  


*In '''1951''', Sir William Dameshek, an American hematologist, discovered myeloproliferative neoplasms.<ref>{{cite journal |author = Dameshek W | title = Some speculations on the myeloproliferative syndromes. | journal = Blood | volume = 6 | issue = 4 | pages = 372-5 | year = 1951 | id = PMID 14820991}}</ref> Dr. Dameshek was a pioneer in the field and paved the way for future investigations into the details of this condition. He grouped a variety of conditions together and classified these individual conditions are myeloproliferative neoplasms.
*In '''1951''', Sir William Dameshek, an American hematologist, discovered myeloproliferative neoplasms. Dr. Dameshek was a pioneer in the field and paved the way for future investigations into the details of this condition. He grouped a variety of conditions together and classified these individual conditions are myeloproliferative neoplasms.<ref>{{cite journal |author = Dameshek W | title = Some speculations on the myeloproliferative syndromes. | journal = Blood | volume = 6 | issue = 4 | pages = 372-5 | year = 1951 | id = PMID 14820991}}</ref>


*In '''1967''', Fialkow and colleagues showed evidence for clonally-derived [[myelopoiesis]], based on studies showing the presence of the same ''G6PD'' polymorphism in erythrocytes and granulocytes. These studies suggested that one clone gave rise to multiple cell types.<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>
*In '''1967''', Fialkow and colleagues showed evidence for clonally-derived myelopoiesis, based on studies showing the presence of the same ''[[Glucose-6-phosphate dehydrogenase|G6PD]]'' polymorphism in [[Red blood cell|erythrocytes]] and [[Granulocyte|granulocytes]]. These studies suggested that one clone gave rise to multiple cell types.<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>


*In '''1976''', Adamson and colleagues showed evidence for panmyeloid clonal expansion, meaning that a single clone could give rise to multiple lineages including erythrocytes, granulocytes, and megakaryocytes.<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>
*In '''1976''', Adamson and colleagues showed evidence for panmyeloid clonal expansion, meaning that a single clone could give rise to multiple lineages including [[Red blood cell|erythrocytes]], [[Granulocyte|granulocytes]], and [[Megakaryocyte|megakaryocytes]].<ref name="pmid18779404">{{cite journal| author=Levine RL, Gilliland DG| title=Myeloproliferative disorders. | journal=Blood | year= 2008 | volume= 112 | issue= 6 | pages= 2190-8 | pmid=18779404 | doi=10.1182/blood-2008-03-077966 | pmc=2962533 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18779404  }} </ref>


*In '''2005''', Ross Levine and colleagues found that the ''JAK2'' ''V617F'' mutation was the molecular basis for [[polycythemia vera]], [[essential throbocythemia]], and [[myeloid metaplasia]] with [[myelofibrosis]].<ref name="pmid15837627">{{cite journal| author=Levine RL, Wadleigh M, Cools J, Ebert BL, Wernig G, Huntly BJ et al.| title=Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. | journal=Cancer Cell | year= 2005 | volume= 7 | issue= 4 | pages= 387-97 | pmid=15837627 | doi=10.1016/j.ccr.2005.03.023 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15837627  }} </ref> High-throughout sequencing of DNA was performed in patients who were diagnosed with these myeloproliferative neoplasms. Healthy persons were found to not harbor this mutation, suggesting high specificity of the mutation for myeloproliferative neoplasm. It was noted that the ''JAK2'' mutation resulted in a constitutively active tyrosine kinase.<ref>{{cite journal | author = Baxter EJ, Scott LM, Campbell PJ, et al. | title = Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. | journal = Lancet | volume = 365 | pages = 1054-1061 | year = 2005 | id = PMID 15781101}}</ref><ref>{{cite journal | author = James C, Ugo V, Le Couedic JP, et al. | title = A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. | journal = Nature | volume = 434 | issue = 7037 | pages = 1144–1148 | year = 2005 | id =PMID 15793561}}</ref><ref>{{cite journal | author = Levine RL, Wadleigh M, Cools J, et al. | title = Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis | journal = Cancer Cell | volume = 7 |issue = 4 | pages = 387–397  | year = 2005 | id = PMID 15837627}}</ref><ref>{{cite journal | author = Kralovics R, Passamonti F, Buser AS, et al. | title = A gain-of-function mutation of JAK2 in myeloproliferative disorders | journal = N Engl J Med | volume = 352 | issue = 17 | pages = 1779–1790 | year = 2005 | id = PMID 15858187}}</ref><ref>{{cite journal | author = Campbell PJ, Scott LM, Buck G, et al. | title = Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study | journal = Lancet | volume = 366 | issue = 9501 | pages = 1945–1953 | year = 2005 | id = PMID 16325696}}</ref> It was eventually noted that more than 95% of patients with [[polycythemia vera]] harbored the ''JAK2'' ''V617F'' mutation, and 55-60% of patients with myelofibrosis had the mutation. The mutation was also found to be in 50% of patients with primary myelofibrosis.
*In '''2005''', Ross Levine and colleagues found that the ''[[Janus kinase|JAK2]]'' ''V617F'' mutation was the molecular basis for [[polycythemia vera]], [[Essential thrombocytosis|essential thrombocythemia]], and [[myeloid metaplasia]] with [[myelofibrosis]].<ref name="pmid15837627">{{cite journal| author=Levine RL, Wadleigh M, Cools J, Ebert BL, Wernig G, Huntly BJ et al.| title=Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis. | journal=Cancer Cell | year= 2005 | volume= 7 | issue= 4 | pages= 387-97 | pmid=15837627 | doi=10.1016/j.ccr.2005.03.023 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15837627  }} </ref> High-throughput sequencing of [[DNA]] was performed in patients who were diagnosed with these myeloproliferative neoplasms. Healthy persons were found to not harbor this [[mutation]], suggesting high specificity of the [[mutation]] for myeloproliferative neoplasm. It was noted that the ''[[Janus kinase|JAK2]]'' mutation resulted in a constitutively active [[tyrosine kinase]].<ref>{{cite journal | author = Baxter EJ, Scott LM, Campbell PJ, et al. | title = Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders. | journal = Lancet | volume = 365 | pages = 1054-1061 | year = 2005 | id = PMID 15781101}}</ref><ref>{{cite journal | author = James C, Ugo V, Le Couedic JP, et al. | title = A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera. | journal = Nature | volume = 434 | issue = 7037 | pages = 1144–1148 | year = 2005 | id =PMID 15793561}}</ref><ref>{{cite journal | author = Levine RL, Wadleigh M, Cools J, et al. | title = Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis | journal = Cancer Cell | volume = 7 |issue = 4 | pages = 387–397  | year = 2005 | id = PMID 15837627}}</ref><ref>{{cite journal | author = Kralovics R, Passamonti F, Buser AS, et al. | title = A gain-of-function mutation of JAK2 in myeloproliferative disorders | journal = N Engl J Med | volume = 352 | issue = 17 | pages = 1779–1790 | year = 2005 | id = PMID 15858187}}</ref><ref>{{cite journal | author = Campbell PJ, Scott LM, Buck G, et al. | title = Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study | journal = Lancet | volume = 366 | issue = 9501 | pages = 1945–1953 | year = 2005 | id = PMID 16325696}}</ref> It was eventually noted that more than 95% of patients with [[polycythemia vera]] harbored the ''[[Janus kinase|JAK2]]'' ''V617F'' mutation, and 55-60% of patients with [[myelofibrosis]] had the [[mutation]]. The [[mutation]] was also found to be in 50% of patients with [[Myelofibrosis|primary myelofibrosis]].


*In '''2006''', Pikman and colleagues found that the ''MPL'' ''W515L'' mutation was associated with myeloproliferative neoplasms.<ref name="pmid16834459">{{cite journal| author=Pikman Y, Lee BH, Mercher T, McDowell E, Ebert BL, Gozo M et al.| title=MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. | journal=PLoS Med | year= 2006 | volume= 3 | issue= 7 | pages= e270 | pmid=16834459 | doi=10.1371/journal.pmed.0030270 | pmc=1502153 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16834459  }} </ref> It was noted that, in patients without the ''JAK2'' ''V617F'' mutation, the ''MPL'' mutation served as the pathogenic stimulus for myeloproliferation via activation of ''JAK-STAT'' signaling.<ref name="pmid16834459">{{cite journal| author=Pikman Y, Lee BH, Mercher T, McDowell E, Ebert BL, Gozo M et al.| title=MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. | journal=PLoS Med | year= 2006 | volume= 3 | issue= 7 | pages= e270 | pmid=16834459 | doi=10.1371/journal.pmed.0030270 | pmc=1502153 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16834459  }} </ref>
*In '''2006''', Pikman and colleagues found that the ''MPL'' ''W515L'' [[mutation]] was associated with myeloproliferative neoplasms.<ref name="pmid16834459">{{cite journal| author=Pikman Y, Lee BH, Mercher T, McDowell E, Ebert BL, Gozo M et al.| title=MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. | journal=PLoS Med | year= 2006 | volume= 3 | issue= 7 | pages= e270 | pmid=16834459 | doi=10.1371/journal.pmed.0030270 | pmc=1502153 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16834459  }} </ref> It was noted that, in patients without the ''[[Janus kinase|JAK2]]'' ''V617F'' [[mutation]], the ''MPL'' mutation served as the pathogenic stimulus for myeloproliferation via activation of [[JAK-STAT signaling pathway|''JAK-STAT'' signaling]].<ref name="pmid16834459">{{cite journal| author=Pikman Y, Lee BH, Mercher T, McDowell E, Ebert BL, Gozo M et al.| title=MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia. | journal=PLoS Med | year= 2006 | volume= 3 | issue= 7 | pages= e270 | pmid=16834459 | doi=10.1371/journal.pmed.0030270 | pmc=1502153 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16834459  }} </ref>


*In '''2007''', Scott and colleagues discovered that ''JAK2'' exon 12 mutations (which are distinct from the ''V617F'' mutation in exon 14) could result in [[polycythemia vera]].<ref name="pmid17267906">{{cite journal| author=Scott LM, Tong W, Levine RL, Scott MA, Beer PA, Stratton MR et al.| title=JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. | journal=N Engl J Med | year= 2007 | volume= 356 | issue= 5 | pages= 459-68 | pmid=17267906 | doi=10.1056/NEJMoa065202 | pmc=2873834 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17267906  }} </ref>
*In '''2007''', Scott and colleagues discovered that ''[[Janus kinase|JAK2]]'' exon 12 [[Mutation|mutations]] (which are distinct from the ''V617F'' [[mutation]] in exon 14) could result in [[polycythemia vera]].<ref name="pmid17267906">{{cite journal| author=Scott LM, Tong W, Levine RL, Scott MA, Beer PA, Stratton MR et al.| title=JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis. | journal=N Engl J Med | year= 2007 | volume= 356 | issue= 5 | pages= 459-68 | pmid=17267906 | doi=10.1056/NEJMoa065202 | pmc=2873834 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17267906  }} </ref>


*In '''2008''', the World Health Organization developed original criteria for the diagnosis of myeloproliferative neoplasm.<ref name="pmid27884974">{{cite journal| author=Vannucchi AM| title=From leeches to personalized medicine: evolving concepts in the management of polycythemia vera. | journal=Haematologica | year= 2017 | volume= 102 | issue= 1 | pages= 18-29 | pmid=27884974 | doi=10.3324/haematol.2015.129155 | pmc=5210229 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27884974  }} </ref>
*In '''2008''', the World Health Organization developed original criteria for the diagnosis of myeloproliferative neoplasm.<ref name="pmid27884974">{{cite journal| author=Vannucchi AM| title=From leeches to personalized medicine: evolving concepts in the management of polycythemia vera. | journal=Haematologica | year= 2017 | volume= 102 | issue= 1 | pages= 18-29 | pmid=27884974 | doi=10.3324/haematol.2015.129155 | pmc=5210229 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27884974  }} </ref>


*In '''2009''', Langemeijer and colleagues noted that ''TET2'' and ''ASXL1'' mutations and somatic copy-number loss were found to be associated with myeloproliferative neoplasms. These mutations were first found to be associated with [[myelodysplastic syndrome]]. These studies were conducted via [[single nucleotide polymorphism]] arrays and comparative genomic hybridization.
*In '''2009''', Langemeijer and colleagues noted that ''TET2'' and ''[[ASXL1]]'' [[Mutation|mutations]] and somatic copy-number loss were found to be associated with myeloproliferative neoplasms. These mutations were first found to be associated with [[myelodysplastic syndrome]]. These studies were conducted via [[single nucleotide polymorphism]] arrays and comparative [[Genomics|genomic]] hybridization.


*In '''2016''', the World Health Organization developed a revision for the diagnostic criteria for myeloproliferative neoplasm.
*In '''2016''', the World Health Organization developed a revision for the diagnostic criteria for myeloproliferative neoplasm.

Revision as of 14:09, 18 March 2019

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Mohamad Alkateb, MBBCh [2] Shyam Patel [3]

Overview

The first description of myeloproliferative neoplasm dates back to the late 19th century, when Sir Louis Vasquez studied a patient with excess red blood cells. Myeloproliferative neoplasm was first brought to attention as an important clinical entity by Dr. William Dameshek, an American hematologist, in 1951. In 2005, the link between the JAK2 mutation and polycythemia vera was discovered. The World Health Organization created diagnostic criteria for myeloproliferative neoplasms in 2008, and this was revised in 2016.

Historical Perspective

  • In 1903, Sir William Osler later described a group of patients with elevated red blood cell counts.[2]
  • In 1951, Sir William Dameshek, an American hematologist, discovered myeloproliferative neoplasms. Dr. Dameshek was a pioneer in the field and paved the way for future investigations into the details of this condition. He grouped a variety of conditions together and classified these individual conditions are myeloproliferative neoplasms.[3]
  • In 1967, Fialkow and colleagues showed evidence for clonally-derived myelopoiesis, based on studies showing the presence of the same G6PD polymorphism in erythrocytes and granulocytes. These studies suggested that one clone gave rise to multiple cell types.[1]
  • In 1976, Adamson and colleagues showed evidence for panmyeloid clonal expansion, meaning that a single clone could give rise to multiple lineages including erythrocytes, granulocytes, and megakaryocytes.[1]
  • In 2006, Pikman and colleagues found that the MPL W515L mutation was associated with myeloproliferative neoplasms.[10] It was noted that, in patients without the JAK2 V617F mutation, the MPL mutation served as the pathogenic stimulus for myeloproliferation via activation of JAK-STAT signaling.[10]
  • In 2008, the World Health Organization developed original criteria for the diagnosis of myeloproliferative neoplasm.[2]
  • In 2016, the World Health Organization developed a revision for the diagnostic criteria for myeloproliferative neoplasm.

References

  1. 1.0 1.1 1.2 1.3 Levine RL, Gilliland DG (2008). "Myeloproliferative disorders". Blood. 112 (6): 2190–8. doi:10.1182/blood-2008-03-077966. PMC 2962533. PMID 18779404.
  2. 2.0 2.1 Vannucchi AM (2017). "From leeches to personalized medicine: evolving concepts in the management of polycythemia vera". Haematologica. 102 (1): 18–29. doi:10.3324/haematol.2015.129155. PMC 5210229. PMID 27884974.
  3. Dameshek W (1951). "Some speculations on the myeloproliferative syndromes". Blood. 6 (4): 372–5. PMID 14820991.
  4. Levine RL, Wadleigh M, Cools J, Ebert BL, Wernig G, Huntly BJ; et al. (2005). "Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis". Cancer Cell. 7 (4): 387–97. doi:10.1016/j.ccr.2005.03.023. PMID 15837627.
  5. Baxter EJ, Scott LM, Campbell PJ; et al. (2005). "Acquired mutation of the tyrosine kinase JAK2 in human myeloproliferative disorders". Lancet. 365: 1054–1061. PMID 15781101.
  6. James C, Ugo V, Le Couedic JP; et al. (2005). "A unique clonal JAK2 mutation leading to constitutive signalling causes polycythaemia vera". Nature. 434 (7037): 1144–1148. PMID 15793561.
  7. Levine RL, Wadleigh M, Cools J; et al. (2005). "Activating mutation in the tyrosine kinase JAK2 in polycythemia vera, essential thrombocythemia, and myeloid metaplasia with myelofibrosis". Cancer Cell. 7 (4): 387–397. PMID 15837627.
  8. Kralovics R, Passamonti F, Buser AS; et al. (2005). "A gain-of-function mutation of JAK2 in myeloproliferative disorders". N Engl J Med. 352 (17): 1779–1790. PMID 15858187.
  9. Campbell PJ, Scott LM, Buck G; et al. (2005). "Definition of subtypes of essential thrombocythaemia and relation to polycythaemia vera based on JAK2 V617F mutation status: a prospective study". Lancet. 366 (9501): 1945–1953. PMID 16325696.
  10. 10.0 10.1 Pikman Y, Lee BH, Mercher T, McDowell E, Ebert BL, Gozo M; et al. (2006). "MPLW515L is a novel somatic activating mutation in myelofibrosis with myeloid metaplasia". PLoS Med. 3 (7): e270. doi:10.1371/journal.pmed.0030270. PMC 1502153. PMID 16834459.
  11. Scott LM, Tong W, Levine RL, Scott MA, Beer PA, Stratton MR; et al. (2007). "JAK2 exon 12 mutations in polycythemia vera and idiopathic erythrocytosis". N Engl J Med. 356 (5): 459–68. doi:10.1056/NEJMoa065202. PMC 2873834. PMID 17267906.