Advances in the therapy of chronic idiopathic myelofibrosis

Cecilia Arana-Yi, Alfonso Quintás-Cardama, Francis Giles, Deborah Thomas, Antonio Carrasco-Yalan, Jorge Cortes, Hagop Kantarjian, Srdan Verstovsek

Research output: Contribution to journalReview article

Abstract

The molecular basis of chronic idiopathic myelofibrosis (CIMF) has remained elusive, thus hampering the development of effective targeted therapies. However, significant progress regarding the molecular mechanisms involved in the pathogenesis of this disease has been made in recent years that will likely provide ample opportunity for the investigation of novel therapeutic approaches. At the forefront of these advances is the discovery that 35%-55% of patients with CIMF harbor mutations in the Janus kinase 2 tyrosine kinase gene. Until very recently, the management of patients with CIMF involved the use of supportive measures, including growth factors, transfusions, or interferon, and the administration of cytoreductive agents, such as hydroxyurea and anagrelide. However, several trials have demonstrated the efficacy of antiangiogenic agents alone or in combination with corticosteroids. In addition, the use of reduced-intensity conditioning allogeneic stem cell transplantation has resulted in prolonged survival and lower transplant-related mortality.

Original languageEnglish (US)
Pages (from-to)929-943
Number of pages15
JournalOncologist
Volume11
Issue number8
DOIs
StatePublished - Sep 18 2006
Externally publishedYes

Fingerprint

Primary Myelofibrosis
Janus Kinase 2
Angiogenesis Inhibitors
Hydroxyurea
Stem Cell Transplantation
Protein-Tyrosine Kinases
Interferons
Intercellular Signaling Peptides and Proteins
Adrenal Cortex Hormones
Therapeutics
Transplants
Mutation
Survival
Mortality
Genes

Keywords

  • Myelofibrosis
  • Myeloproliferative disorders
  • Therapy

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Arana-Yi, C., Quintás-Cardama, A., Giles, F., Thomas, D., Carrasco-Yalan, A., Cortes, J., ... Verstovsek, S. (2006). Advances in the therapy of chronic idiopathic myelofibrosis. Oncologist, 11(8), 929-943. https://doi.org/10.1634/theoncologist.11-8-929

Advances in the therapy of chronic idiopathic myelofibrosis. / Arana-Yi, Cecilia; Quintás-Cardama, Alfonso; Giles, Francis; Thomas, Deborah; Carrasco-Yalan, Antonio; Cortes, Jorge; Kantarjian, Hagop; Verstovsek, Srdan.

In: Oncologist, Vol. 11, No. 8, 18.09.2006, p. 929-943.

Research output: Contribution to journalReview article

Arana-Yi, C, Quintás-Cardama, A, Giles, F, Thomas, D, Carrasco-Yalan, A, Cortes, J, Kantarjian, H & Verstovsek, S 2006, 'Advances in the therapy of chronic idiopathic myelofibrosis', Oncologist, vol. 11, no. 8, pp. 929-943. https://doi.org/10.1634/theoncologist.11-8-929
Arana-Yi C, Quintás-Cardama A, Giles F, Thomas D, Carrasco-Yalan A, Cortes J et al. Advances in the therapy of chronic idiopathic myelofibrosis. Oncologist. 2006 Sep 18;11(8):929-943. https://doi.org/10.1634/theoncologist.11-8-929
Arana-Yi, Cecilia ; Quintás-Cardama, Alfonso ; Giles, Francis ; Thomas, Deborah ; Carrasco-Yalan, Antonio ; Cortes, Jorge ; Kantarjian, Hagop ; Verstovsek, Srdan. / Advances in the therapy of chronic idiopathic myelofibrosis. In: Oncologist. 2006 ; Vol. 11, No. 8. pp. 929-943.
@article{69c3f2691ad5403cb488bf6f577558e4,
title = "Advances in the therapy of chronic idiopathic myelofibrosis",
abstract = "The molecular basis of chronic idiopathic myelofibrosis (CIMF) has remained elusive, thus hampering the development of effective targeted therapies. However, significant progress regarding the molecular mechanisms involved in the pathogenesis of this disease has been made in recent years that will likely provide ample opportunity for the investigation of novel therapeutic approaches. At the forefront of these advances is the discovery that 35{\%}-55{\%} of patients with CIMF harbor mutations in the Janus kinase 2 tyrosine kinase gene. Until very recently, the management of patients with CIMF involved the use of supportive measures, including growth factors, transfusions, or interferon, and the administration of cytoreductive agents, such as hydroxyurea and anagrelide. However, several trials have demonstrated the efficacy of antiangiogenic agents alone or in combination with corticosteroids. In addition, the use of reduced-intensity conditioning allogeneic stem cell transplantation has resulted in prolonged survival and lower transplant-related mortality.",
keywords = "Myelofibrosis, Myeloproliferative disorders, Therapy",
author = "Cecilia Arana-Yi and Alfonso Quint{\'a}s-Cardama and Francis Giles and Deborah Thomas and Antonio Carrasco-Yalan and Jorge Cortes and Hagop Kantarjian and Srdan Verstovsek",
year = "2006",
month = "9",
day = "18",
doi = "10.1634/theoncologist.11-8-929",
language = "English (US)",
volume = "11",
pages = "929--943",
journal = "Oncologist",
issn = "1083-7159",
publisher = "AlphaMed Press",
number = "8",

}

TY - JOUR

T1 - Advances in the therapy of chronic idiopathic myelofibrosis

AU - Arana-Yi, Cecilia

AU - Quintás-Cardama, Alfonso

AU - Giles, Francis

AU - Thomas, Deborah

AU - Carrasco-Yalan, Antonio

AU - Cortes, Jorge

AU - Kantarjian, Hagop

AU - Verstovsek, Srdan

PY - 2006/9/18

Y1 - 2006/9/18

N2 - The molecular basis of chronic idiopathic myelofibrosis (CIMF) has remained elusive, thus hampering the development of effective targeted therapies. However, significant progress regarding the molecular mechanisms involved in the pathogenesis of this disease has been made in recent years that will likely provide ample opportunity for the investigation of novel therapeutic approaches. At the forefront of these advances is the discovery that 35%-55% of patients with CIMF harbor mutations in the Janus kinase 2 tyrosine kinase gene. Until very recently, the management of patients with CIMF involved the use of supportive measures, including growth factors, transfusions, or interferon, and the administration of cytoreductive agents, such as hydroxyurea and anagrelide. However, several trials have demonstrated the efficacy of antiangiogenic agents alone or in combination with corticosteroids. In addition, the use of reduced-intensity conditioning allogeneic stem cell transplantation has resulted in prolonged survival and lower transplant-related mortality.

AB - The molecular basis of chronic idiopathic myelofibrosis (CIMF) has remained elusive, thus hampering the development of effective targeted therapies. However, significant progress regarding the molecular mechanisms involved in the pathogenesis of this disease has been made in recent years that will likely provide ample opportunity for the investigation of novel therapeutic approaches. At the forefront of these advances is the discovery that 35%-55% of patients with CIMF harbor mutations in the Janus kinase 2 tyrosine kinase gene. Until very recently, the management of patients with CIMF involved the use of supportive measures, including growth factors, transfusions, or interferon, and the administration of cytoreductive agents, such as hydroxyurea and anagrelide. However, several trials have demonstrated the efficacy of antiangiogenic agents alone or in combination with corticosteroids. In addition, the use of reduced-intensity conditioning allogeneic stem cell transplantation has resulted in prolonged survival and lower transplant-related mortality.

KW - Myelofibrosis

KW - Myeloproliferative disorders

KW - Therapy

UR - http://www.scopus.com/inward/record.url?scp=33748568166&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33748568166&partnerID=8YFLogxK

U2 - 10.1634/theoncologist.11-8-929

DO - 10.1634/theoncologist.11-8-929

M3 - Review article

C2 - 16951397

AN - SCOPUS:33748568166

VL - 11

SP - 929

EP - 943

JO - Oncologist

JF - Oncologist

SN - 1083-7159

IS - 8

ER -