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Kronisk myeloisk leukemi : Förebild för målstyrd terapi

Richter, Johan LU and Stenke, Leif (2017) In Läkartidningen 114(39). p.1574-1574
Abstract

Chronic myeloid leukemia (CML) pioneered as the first human malignancy linked to a specific cytogenetic aberration (the Philadelphia chromosome), which led the way to specific targeted therapies with imatinib (Glivec) and later tyrosine kinase inhibitors (TKI). Continuous TKI administration, blocking the oncogenic fusion protein Bcr-Abl, has revolutionized the outcome of CML, transforming an almost uniformly deadly disease into a chronic disorder with a near to normal life expectancy for many patients. There are now indications that, in a portion of patients achieving deep molecular responses, TKI treatment can be stopped without signs of relapse, indicating that these drugs may indeed induce cure. This is of particular importance since... (More)

Chronic myeloid leukemia (CML) pioneered as the first human malignancy linked to a specific cytogenetic aberration (the Philadelphia chromosome), which led the way to specific targeted therapies with imatinib (Glivec) and later tyrosine kinase inhibitors (TKI). Continuous TKI administration, blocking the oncogenic fusion protein Bcr-Abl, has revolutionized the outcome of CML, transforming an almost uniformly deadly disease into a chronic disorder with a near to normal life expectancy for many patients. There are now indications that, in a portion of patients achieving deep molecular responses, TKI treatment can be stopped without signs of relapse, indicating that these drugs may indeed induce cure. This is of particular importance since adverse events related to long-term TKI therapy, compromising quality of life, are now being increasingly recognized. With the recent introduction of generics the price of imatinib has dropped by more than 95% in Sweden, making an already cost effective treatment even more attractive.

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Abstract (Swedish)
Vid kronisk myeloisk leukemi har målstyrd, kontinuerlig behandling med tyro­sinkinashämmare lett till dramatiskt förbättrad överlevnad.
Please use this url to cite or link to this publication:
author
and
organization
alternative title
Chronic myeloid leukemia - A model disease for targeted therapy
publishing date
type
Contribution to journal
publication status
published
subject
in
Läkartidningen
volume
114
issue
39
pages
1 pages
publisher
Swedish Medical Association
external identifiers
  • scopus:85030256803
ISSN
0023-7205
language
Swedish
LU publication?
yes
id
31a29811-d33d-44e0-9df0-9f0644a8a3d7
date added to LUP
2017-11-03 09:55:07
date last changed
2022-03-09 07:07:54
@misc{31a29811-d33d-44e0-9df0-9f0644a8a3d7,
  abstract     = {{<p>Chronic myeloid leukemia (CML) pioneered as the first human malignancy linked to a specific cytogenetic aberration (the Philadelphia chromosome), which led the way to specific targeted therapies with imatinib (Glivec) and later tyrosine kinase inhibitors (TKI). Continuous TKI administration, blocking the oncogenic fusion protein Bcr-Abl, has revolutionized the outcome of CML, transforming an almost uniformly deadly disease into a chronic disorder with a near to normal life expectancy for many patients. There are now indications that, in a portion of patients achieving deep molecular responses, TKI treatment can be stopped without signs of relapse, indicating that these drugs may indeed induce cure. This is of particular importance since adverse events related to long-term TKI therapy, compromising quality of life, are now being increasingly recognized. With the recent introduction of generics the price of imatinib has dropped by more than 95% in Sweden, making an already cost effective treatment even more attractive.</p>}},
  author       = {{Richter, Johan and Stenke, Leif}},
  issn         = {{0023-7205}},
  language     = {{swe}},
  number       = {{39}},
  pages        = {{1574--1574}},
  publisher    = {{Swedish Medical Association}},
  series       = {{Läkartidningen}},
  title        = {{Kronisk myeloisk leukemi : Förebild för målstyrd terapi}},
  volume       = {{114}},
  year         = {{2017}},
}