Oncogenes in myeloproliferative disorders

Ayalew Tefferi, D. Gary Gilliland

Research output: Contribution to journalArticle

133 Citations (Scopus)

Abstract

Myeloproliferative disorders (MPDs) constitute a group of hematopoietic malignancies that feature enhanced proliferation and survival of one or more myeloid lineage cells. William Dameshek is credited for introducing the term "MPDs" in 1951 when he used it to group chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) under one clinicopathologic category. Since then, other myeloid neoplasms have been added to the MPD member list: chronic neutrophilic (CNL), eosinophilic (CEL) and myelomonocytic (CMML) leukemias; juvenile myelomonocytic leukemia (JMML); hypereosinophilic syndrome (HES); systemic mastocytosis (SM); and others. Collectively, MPDs are stem cell-derived clonal proliferative diseases whose shared and diverse phenotypic characteristics can be attributed to dysregulated signal transduction - a consequence of acquired somatic mutations. The most recognized among the latter is BCR-ABL, the disease-causing mutation in CML. Other mutations of putative pathogenetic relevance in MPDs include: JAK2V617F in PV, ET, and PMF; JAK2 exon 12 mutations in PV; MPLW515L/K in PMF and ET; KITD816V in SM; FIP1L1-PDGFRA in CEL-SM; rearrangements of PDGFRB in CEL-CMML and FGFR1 in stem cell leukemia-lymphoma syndrome; and RAS/PTPN11/NF1 mutations in JMML. This increasing repertoire of mutant molecules has streamlined translational research and molecularly targeted drug development in MPDs.

Original languageEnglish (US)
Pages (from-to)550-566
Number of pages17
JournalCell Cycle
Volume6
Issue number5
StatePublished - Mar 1 2007

Fingerprint

Myeloproliferative Disorders
Stem cells
Oncogenes
Essential Thrombocythemia
Systemic Mastocytosis
Platelet-Derived Growth Factor beta Receptor
Signal transduction
Polycythemia Vera
Primary Myelofibrosis
Juvenile Myelomonocytic Leukemia
Mutation
Exons
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Molecules
Leukemia
Stem Cells
Pharmaceutical Preparations
Hypereosinophilic Syndrome
Translational Medical Research
Hematologic Neoplasms

Keywords

  • JAK2
  • JAK2V617F
  • Myelofibrosis
  • Polycythemia
  • Thrombocythemia

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Cite this

Tefferi, A., & Gilliland, D. G. (2007). Oncogenes in myeloproliferative disorders. Cell Cycle, 6(5), 550-566.

Oncogenes in myeloproliferative disorders. / Tefferi, Ayalew; Gilliland, D. Gary.

In: Cell Cycle, Vol. 6, No. 5, 01.03.2007, p. 550-566.

Research output: Contribution to journalArticle

Tefferi, A & Gilliland, DG 2007, 'Oncogenes in myeloproliferative disorders', Cell Cycle, vol. 6, no. 5, pp. 550-566.
Tefferi A, Gilliland DG. Oncogenes in myeloproliferative disorders. Cell Cycle. 2007 Mar 1;6(5):550-566.
Tefferi, Ayalew ; Gilliland, D. Gary. / Oncogenes in myeloproliferative disorders. In: Cell Cycle. 2007 ; Vol. 6, No. 5. pp. 550-566.
@article{4c9945b282464c7ca57be6dc73d99e77,
title = "Oncogenes in myeloproliferative disorders",
abstract = "Myeloproliferative disorders (MPDs) constitute a group of hematopoietic malignancies that feature enhanced proliferation and survival of one or more myeloid lineage cells. William Dameshek is credited for introducing the term {"}MPDs{"} in 1951 when he used it to group chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) under one clinicopathologic category. Since then, other myeloid neoplasms have been added to the MPD member list: chronic neutrophilic (CNL), eosinophilic (CEL) and myelomonocytic (CMML) leukemias; juvenile myelomonocytic leukemia (JMML); hypereosinophilic syndrome (HES); systemic mastocytosis (SM); and others. Collectively, MPDs are stem cell-derived clonal proliferative diseases whose shared and diverse phenotypic characteristics can be attributed to dysregulated signal transduction - a consequence of acquired somatic mutations. The most recognized among the latter is BCR-ABL, the disease-causing mutation in CML. Other mutations of putative pathogenetic relevance in MPDs include: JAK2V617F in PV, ET, and PMF; JAK2 exon 12 mutations in PV; MPLW515L/K in PMF and ET; KITD816V in SM; FIP1L1-PDGFRA in CEL-SM; rearrangements of PDGFRB in CEL-CMML and FGFR1 in stem cell leukemia-lymphoma syndrome; and RAS/PTPN11/NF1 mutations in JMML. This increasing repertoire of mutant molecules has streamlined translational research and molecularly targeted drug development in MPDs.",
keywords = "JAK2, JAK2V617F, Myelofibrosis, Polycythemia, Thrombocythemia",
author = "Ayalew Tefferi and Gilliland, {D. Gary}",
year = "2007",
month = "3",
day = "1",
language = "English (US)",
volume = "6",
pages = "550--566",
journal = "Cell Cycle",
issn = "1538-4101",
publisher = "Landes Bioscience",
number = "5",

}

TY - JOUR

T1 - Oncogenes in myeloproliferative disorders

AU - Tefferi, Ayalew

AU - Gilliland, D. Gary

PY - 2007/3/1

Y1 - 2007/3/1

N2 - Myeloproliferative disorders (MPDs) constitute a group of hematopoietic malignancies that feature enhanced proliferation and survival of one or more myeloid lineage cells. William Dameshek is credited for introducing the term "MPDs" in 1951 when he used it to group chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) under one clinicopathologic category. Since then, other myeloid neoplasms have been added to the MPD member list: chronic neutrophilic (CNL), eosinophilic (CEL) and myelomonocytic (CMML) leukemias; juvenile myelomonocytic leukemia (JMML); hypereosinophilic syndrome (HES); systemic mastocytosis (SM); and others. Collectively, MPDs are stem cell-derived clonal proliferative diseases whose shared and diverse phenotypic characteristics can be attributed to dysregulated signal transduction - a consequence of acquired somatic mutations. The most recognized among the latter is BCR-ABL, the disease-causing mutation in CML. Other mutations of putative pathogenetic relevance in MPDs include: JAK2V617F in PV, ET, and PMF; JAK2 exon 12 mutations in PV; MPLW515L/K in PMF and ET; KITD816V in SM; FIP1L1-PDGFRA in CEL-SM; rearrangements of PDGFRB in CEL-CMML and FGFR1 in stem cell leukemia-lymphoma syndrome; and RAS/PTPN11/NF1 mutations in JMML. This increasing repertoire of mutant molecules has streamlined translational research and molecularly targeted drug development in MPDs.

AB - Myeloproliferative disorders (MPDs) constitute a group of hematopoietic malignancies that feature enhanced proliferation and survival of one or more myeloid lineage cells. William Dameshek is credited for introducing the term "MPDs" in 1951 when he used it to group chronic myeloid leukemia (CML), polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF) under one clinicopathologic category. Since then, other myeloid neoplasms have been added to the MPD member list: chronic neutrophilic (CNL), eosinophilic (CEL) and myelomonocytic (CMML) leukemias; juvenile myelomonocytic leukemia (JMML); hypereosinophilic syndrome (HES); systemic mastocytosis (SM); and others. Collectively, MPDs are stem cell-derived clonal proliferative diseases whose shared and diverse phenotypic characteristics can be attributed to dysregulated signal transduction - a consequence of acquired somatic mutations. The most recognized among the latter is BCR-ABL, the disease-causing mutation in CML. Other mutations of putative pathogenetic relevance in MPDs include: JAK2V617F in PV, ET, and PMF; JAK2 exon 12 mutations in PV; MPLW515L/K in PMF and ET; KITD816V in SM; FIP1L1-PDGFRA in CEL-SM; rearrangements of PDGFRB in CEL-CMML and FGFR1 in stem cell leukemia-lymphoma syndrome; and RAS/PTPN11/NF1 mutations in JMML. This increasing repertoire of mutant molecules has streamlined translational research and molecularly targeted drug development in MPDs.

KW - JAK2

KW - JAK2V617F

KW - Myelofibrosis

KW - Polycythemia

KW - Thrombocythemia

UR - http://www.scopus.com/inward/record.url?scp=33947328520&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33947328520&partnerID=8YFLogxK

M3 - Article

C2 - 17351342

AN - SCOPUS:33947328520

VL - 6

SP - 550

EP - 566

JO - Cell Cycle

JF - Cell Cycle

SN - 1538-4101

IS - 5

ER -