Chronic myeloid leukemia: Pathophysiology and therapeutics

Seth J. Corey, Jorge Cortes

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disorder -characterized by a translocation between the long arms of chromosomes 9 and 22. Often referred to as the Philadelphia (Ph) chromosome, this genetic rearrangement results in an oncogenic tyrosine kinase, Bcr-Abl. The disease may smolder for years before terminating in a blast crisis. Once curable, mostly with bone marrow transplantation and only seldom with interferon alpha-based therapy, its management has been radically changed with the introduction of imatinib mesylate, an orally available Abl kinase inhibitor, in 1998. More common in adults, only an estimated 50 pediatric cases occur annually in North America. The treatment of CML will remain in flux as second-generation Bcr-Abl kinase inhibitors are studied clinically. Because of its rarity in pediatrics, clinical insights must come from -experience with adult CML. CML serves as the paradigm of how molecular understanding of a cancer's pathophysiology can produce a revolutionary form of -targeted therapy, providing hope for those pediatric cancers with a well-defined genetic lesion.

Original languageEnglish (US)
Title of host publicationMolecularly Targeted Therapy for Childhood Cancer
PublisherSpringer New York
Pages139-153
Number of pages15
ISBN (Print)9780387690605
DOIs
StatePublished - Dec 1 2010
Externally publishedYes

Fingerprint

Pediatrics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Chromosomes
Phosphotransferases
bcr-abl Fusion Proteins
Blast Crisis
Interferon-alpha
Chromosomes, Human, Pair 22
Philadelphia Chromosome
Myeloproliferative Disorders
Chromosomes, Human, Pair 9
Bone
Therapeutics
North America
Bone Marrow Transplantation
Fluxes
Neoplasms

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Corey, S. J., & Cortes, J. (2010). Chronic myeloid leukemia: Pathophysiology and therapeutics. In Molecularly Targeted Therapy for Childhood Cancer (pp. 139-153). Springer New York. https://doi.org/10.1007/978-0-387-69062-9_8

Chronic myeloid leukemia : Pathophysiology and therapeutics. / Corey, Seth J.; Cortes, Jorge.

Molecularly Targeted Therapy for Childhood Cancer. Springer New York, 2010. p. 139-153.

Research output: Chapter in Book/Report/Conference proceedingChapter

Corey, SJ & Cortes, J 2010, Chronic myeloid leukemia: Pathophysiology and therapeutics. in Molecularly Targeted Therapy for Childhood Cancer. Springer New York, pp. 139-153. https://doi.org/10.1007/978-0-387-69062-9_8
Corey SJ, Cortes J. Chronic myeloid leukemia: Pathophysiology and therapeutics. In Molecularly Targeted Therapy for Childhood Cancer. Springer New York. 2010. p. 139-153 https://doi.org/10.1007/978-0-387-69062-9_8
Corey, Seth J. ; Cortes, Jorge. / Chronic myeloid leukemia : Pathophysiology and therapeutics. Molecularly Targeted Therapy for Childhood Cancer. Springer New York, 2010. pp. 139-153
@inbook{1a19c208629a495f97dd0e79fd01ef2b,
title = "Chronic myeloid leukemia: Pathophysiology and therapeutics",
abstract = "Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disorder -characterized by a translocation between the long arms of chromosomes 9 and 22. Often referred to as the Philadelphia (Ph) chromosome, this genetic rearrangement results in an oncogenic tyrosine kinase, Bcr-Abl. The disease may smolder for years before terminating in a blast crisis. Once curable, mostly with bone marrow transplantation and only seldom with interferon alpha-based therapy, its management has been radically changed with the introduction of imatinib mesylate, an orally available Abl kinase inhibitor, in 1998. More common in adults, only an estimated 50 pediatric cases occur annually in North America. The treatment of CML will remain in flux as second-generation Bcr-Abl kinase inhibitors are studied clinically. Because of its rarity in pediatrics, clinical insights must come from -experience with adult CML. CML serves as the paradigm of how molecular understanding of a cancer's pathophysiology can produce a revolutionary form of -targeted therapy, providing hope for those pediatric cancers with a well-defined genetic lesion.",
author = "Corey, {Seth J.} and Jorge Cortes",
year = "2010",
month = "12",
day = "1",
doi = "10.1007/978-0-387-69062-9_8",
language = "English (US)",
isbn = "9780387690605",
pages = "139--153",
booktitle = "Molecularly Targeted Therapy for Childhood Cancer",
publisher = "Springer New York",

}

TY - CHAP

T1 - Chronic myeloid leukemia

T2 - Pathophysiology and therapeutics

AU - Corey, Seth J.

AU - Cortes, Jorge

PY - 2010/12/1

Y1 - 2010/12/1

N2 - Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disorder -characterized by a translocation between the long arms of chromosomes 9 and 22. Often referred to as the Philadelphia (Ph) chromosome, this genetic rearrangement results in an oncogenic tyrosine kinase, Bcr-Abl. The disease may smolder for years before terminating in a blast crisis. Once curable, mostly with bone marrow transplantation and only seldom with interferon alpha-based therapy, its management has been radically changed with the introduction of imatinib mesylate, an orally available Abl kinase inhibitor, in 1998. More common in adults, only an estimated 50 pediatric cases occur annually in North America. The treatment of CML will remain in flux as second-generation Bcr-Abl kinase inhibitors are studied clinically. Because of its rarity in pediatrics, clinical insights must come from -experience with adult CML. CML serves as the paradigm of how molecular understanding of a cancer's pathophysiology can produce a revolutionary form of -targeted therapy, providing hope for those pediatric cancers with a well-defined genetic lesion.

AB - Chronic Myeloid Leukemia (CML) is a clonal myeloproliferative disorder -characterized by a translocation between the long arms of chromosomes 9 and 22. Often referred to as the Philadelphia (Ph) chromosome, this genetic rearrangement results in an oncogenic tyrosine kinase, Bcr-Abl. The disease may smolder for years before terminating in a blast crisis. Once curable, mostly with bone marrow transplantation and only seldom with interferon alpha-based therapy, its management has been radically changed with the introduction of imatinib mesylate, an orally available Abl kinase inhibitor, in 1998. More common in adults, only an estimated 50 pediatric cases occur annually in North America. The treatment of CML will remain in flux as second-generation Bcr-Abl kinase inhibitors are studied clinically. Because of its rarity in pediatrics, clinical insights must come from -experience with adult CML. CML serves as the paradigm of how molecular understanding of a cancer's pathophysiology can produce a revolutionary form of -targeted therapy, providing hope for those pediatric cancers with a well-defined genetic lesion.

UR - http://www.scopus.com/inward/record.url?scp=84900224400&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84900224400&partnerID=8YFLogxK

U2 - 10.1007/978-0-387-69062-9_8

DO - 10.1007/978-0-387-69062-9_8

M3 - Chapter

AN - SCOPUS:84900224400

SN - 9780387690605

SP - 139

EP - 153

BT - Molecularly Targeted Therapy for Childhood Cancer

PB - Springer New York

ER -