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Author Topic: Ursache für Resistenz gegen Krebstherapien entdeckt  (Read 1192 times)

ama

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Ursache für Resistenz gegen Krebstherapien entdeckt
« on: April 27, 2007, 01:53:27 PM »

Der "Standard" hat eine gute Wissenschafts-Rubrik.

http://derStandard.at/Text/Corporate/?id=2860276

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derStandard.at | Wissenschaft | Mensch
27.04.2007 12:33

Ursache für Resistenz gegen Krebstherapien entdeckt

Rund ein Fünftel der Patienten gegen die Behandlung resistent, weil bei
ihnen ein so genanntes Onkogen aktiv wird Washington - Ein internationales
Forscherteam in den USA hat herausgefunden, weshalb eine gezielte Therapie
gegen Lungenkrebs bei manchen Patienten nicht wirkt. Rund ein Fünftel der
Patienten sei gegen die Behandlung resistent, weil bei ihnen ein so
genanntes Onkogen aktiv werde, ...
[...]

Die Studie wurde in der US-Fachzeitschrift "Science" veröffentlicht. Das
Verfahren ist vermutlich nicht nur bei Lungenkrebs wirksam.
(APA)

Abstract
MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling

http://www.sciencemag.org/cgi/content/abstract/1141478v1?

©derStandard.at 2007
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Der Abstract:

http://www.sciencemag.org/cgi/content/abstract/1141478v1?

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Home > Science Magazine > Science Express > Engelman et al.

Published Online April 26, 2007
Science DOI:
10.1126/science.1141478
Science Express
Index
Reports
Submitted on February 20, 2007
Accepted on April 11, 2007

MET Amplification Leads to Gefitinib Resistance in Lung Cancer by
Activating ERBB3 Signaling

Jeffrey A. Engelman 1, Kreshnik Zejnullahu 2, Tetsuya Mitsudomi 3,
Youngchul Song 4, Courtney Hyland 5, Joon Oh Park 2, Neal Lindeman 5,
Christopher-Michael Gale 6, Xiaojun Zhao 7, James Christensen 8, Takayuki
Kosaka 3, Alison J. Holmes 2, Andrew M. Rogers 7, Federico Cappuzzo 9,
Tony Mok 10, Charles Lee 5, Bruce E. Johnson 2, Lewis C. Cantley 4, Pasi
A. Jänne 2*

1 Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA;
Department of Systems Biology, Harvard Medical School, Boston, MA 02115,
USA; Department of Signal Transduction, Beth Israel Deaconess Medical
Center, Boston, MA 02115, USA.
2 Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, Boston,
MA 02115, USA;
Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA
02115, USA.
3 Department of Thoracic Surgery, Aichi Cancer Center Hospital, Nagoya
464-8681, Japan.
4 Department of Systems Biology, Harvard Medical School, Boston, MA 02115,
USA;
Department of Signal Transduction, Beth Israel Deaconess Medical Center,
Boston, MA 02115, USA.
5 Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115,
USA.
6 Department of Signal Transduction, Beth Israel Deaconess Medical Center,
Boston, MA 02115, USA.
7 Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA
02115, USA.
8 Pfizer Global Research and Development, Department of Research
Pharmacology, La Jolla Labs,
La Jolla, CA 92121, USA.
9 Istituto Clinico Humanitas, Department on Hematology-Oncology, Rozzano
20089, Italy.
10 Department of Clinical Oncology, Chinese University of Hong Kong,
Shatin, New Territories, Hong Kong, China.
* To whom correspondence should be addressed.
Pasi A. Jänne , E-mail: pjanne{at}partners.org

The epidermal growth factor receptor (EGFR) kinase inhibitors gefitinib
and erlotinib are used clinically for the treatment of lung cancers with
EGFR activating mutations, but the tumors invariably develop drug
resistance. To investigate resistance mechanisms, we isolated
gefitinib-resistant clones from an EGFR mutant lung cancer cell line. The
resistant cells displayed amplification of the MET oncogene and maintained
activation of ERBB3/PI3K/Akt signaling in the presence of gefitinib.
Inhibition of MET signaling in these cells restored their sensitivity to
gefitinib.
MET amplification was detected in 4 out of 18 (22%) lung cancer specimens
that had become resistant to gefitinib or erlotinib. Because amplified MET
activates the ERBB3/PI3K pathway in other tumor cell lines, our results
raise the possibility that MET amplification promotes drug resistance in
other ERBB-driven cancers.

© 2007 American Association for the Advancement of Science.All Rights Reserved.
AAAS is a partner of HINARI, AGORA, PatientInform, CrossRef, and COUNTER.
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