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Chronic myeloid leukemia

Fioretos, Thoas LU (2015) In Cancer Cytogenetics p.153-174
Abstract

Chronic myeloid leukemia (CML) is a clonal bone marrow (BM) disease characterized by neoplastic overproduction of, mainly, granulocytes. The treatment of CML has changed dramatically with the introduction of tyrosine kinase inhibitors (TKIs) targeting the product of the underlying cytogenetic and molecular lesion in CML. The Philadelphia chromosome was the first consistent neoplasia-associated chromosomal abnormality reported; its discovery was a milestone in cancer cytogenetics. Treatment of CML has changed dramatically over the last decades. The chfromosome t(9;22) (q34;q11) or its variant translocations (seen in 5-10%) are detected in the great majority of BM cells from patients with CML.The introduction of imatinib and other TKIs... (More)

Chronic myeloid leukemia (CML) is a clonal bone marrow (BM) disease characterized by neoplastic overproduction of, mainly, granulocytes. The treatment of CML has changed dramatically with the introduction of tyrosine kinase inhibitors (TKIs) targeting the product of the underlying cytogenetic and molecular lesion in CML. The Philadelphia chromosome was the first consistent neoplasia-associated chromosomal abnormality reported; its discovery was a milestone in cancer cytogenetics. Treatment of CML has changed dramatically over the last decades. The chfromosome t(9;22) (q34;q11) or its variant translocations (seen in 5-10%) are detected in the great majority of BM cells from patients with CML.The introduction of imatinib and other TKIs has dramatically improved the clinical outcome for CML patients, and today, the vast majority of patients receiving TKI treatment in chronic phase (CP) remain in complete hematologic and cytogenetic remission with low to undetectable BCR-ABL1 fusion transcripts.

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Please use this url to cite or link to this publication:
author
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
Cancer cytogenetics, Chronic myeloid leukemia, Philadelphia chromosome, Tyrosine kinase inhibitors
in
Cancer Cytogenetics
editor
Heim, Sverre; Mitelman, Felix; and
pages
22 pages
publisher
Wiley-Blackwell
external identifiers
  • scopus:85015895170
ISBN
9781118795569
9781118795538
DOI
10.1002/9781118795569.ch8
language
English
LU publication?
yes
id
26761a2d-dc1f-4cd9-bcd1-fb486b010642
date added to LUP
2017-04-20 10:29:53
date last changed
2017-04-20 10:33:35
@inbook{26761a2d-dc1f-4cd9-bcd1-fb486b010642,
  abstract     = {<p>Chronic myeloid leukemia (CML) is a clonal bone marrow (BM) disease characterized by neoplastic overproduction of, mainly, granulocytes. The treatment of CML has changed dramatically with the introduction of tyrosine kinase inhibitors (TKIs) targeting the product of the underlying cytogenetic and molecular lesion in CML. The Philadelphia chromosome was the first consistent neoplasia-associated chromosomal abnormality reported; its discovery was a milestone in cancer cytogenetics. Treatment of CML has changed dramatically over the last decades. The chfromosome t(9;22) (q34;q11) or its variant translocations (seen in 5-10%) are detected in the great majority of BM cells from patients with CML.The introduction of imatinib and other TKIs has dramatically improved the clinical outcome for CML patients, and today, the vast majority of patients receiving TKI treatment in chronic phase (CP) remain in complete hematologic and cytogenetic remission with low to undetectable BCR-ABL1 fusion transcripts.</p>},
  author       = {Fioretos, Thoas},
  editor       = {Heim, Sverre and Mitelman, Felix},
  isbn         = {9781118795569},
  keyword      = {Cancer cytogenetics,Chronic myeloid leukemia,Philadelphia chromosome,Tyrosine kinase inhibitors},
  language     = {eng},
  pages        = {153--174},
  publisher    = {Wiley-Blackwell},
  series       = {Cancer Cytogenetics},
  title        = {Chronic myeloid leukemia},
  url          = {http://dx.doi.org/10.1002/9781118795569.ch8},
  year         = {2015},
}