001     128518
005     20240228135104.0
024 7 _ |a 10.1182/blood-2013-12-538975
|2 doi
024 7 _ |a pmid:24916506
|2 pmid
024 7 _ |a 0006-4971
|2 ISSN
024 7 _ |a 1528-0020
|2 ISSN
037 _ _ |a DKFZ-2017-04534
041 _ _ |a eng
082 _ _ |a 610
100 1 _ |a Weisser, Martin
|b 0
245 _ _ |a PTK2 expression and immunochemotherapy outcome in chronic lymphocytic leukemia.
260 _ _ |a Stanford, Calif.
|c 2014
|b HighWire Press
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1523618544_30814
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Addition of rituximab (R) to fludarabine and cyclophosphamide (FC) has significantly improved patient outcomes in chronic lymphocytic leukemia (CLL). Whether baseline gene expression can identify patients who will benefit from immunochemotherapy over chemotherapy alone has not been determined. We assessed genome-wide expression of 300 pretreatment specimens from a subset of 552 patients in REACH, a study of FC or R-FC in relapsed CLL. An independent test set was derived from 282 pretreatment specimens from CLL8, a study of FC or R-FC in treatment-naïve patients. Genes specific for benefit from R-FC were determined by assessing treatment-gene interactions in Cox proportional hazards models. REACH patients with higher pretreatment protein tyrosine kinase 2 (PTK2) messenger RNA levels derived greater benefit from R-FC, with significant improvements in progression-free survival, independent of known prognostic factors in a multivariate model. Examination of PTK2 gene expression in CLL8 patients yielded similar results. Furthermore, PTK2 inhibition blunted R-dependent cell death in vitro. This retrospective analysis from 2 independent trials revealed that increased PTK2 expression is associated with improved outcomes for CLL patients treated with R-FC vs FC. PTK2 expression may be a useful biomarker for patient selection in future trials. These trials were registered at www.clinicaltrials.gov as #NCT00090051 (REACH) and #NCT00281918 (CLL8).
536 _ _ |a 313 - Cancer risk factors and prevention (POF3-313)
|0 G:(DE-HGF)POF3-313
|c POF3-313
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Antibodies, Monoclonal, Murine-Derived
|2 NLM Chemicals
650 _ 7 |a RNA, Messenger
|2 NLM Chemicals
650 _ 7 |a RNA, Neoplasm
|2 NLM Chemicals
650 _ 7 |a Rituximab
|0 4F4X42SYQ6
|2 NLM Chemicals
650 _ 7 |a Cyclophosphamide
|0 8N3DW7272P
|2 NLM Chemicals
650 _ 7 |a Focal Adhesion Kinase 1
|0 EC 2.7.10.2
|2 NLM Chemicals
650 _ 7 |a PTK2 protein, human
|0 EC 2.7.10.2
|2 NLM Chemicals
650 _ 7 |a Vidarabine
|0 FA2DM6879K
|2 NLM Chemicals
650 _ 7 |a fludarabine
|0 P2K93U8740
|2 NLM Chemicals
700 1 _ |a Yeh, Ru-Fang
|b 1
700 1 _ |a Duchateau-Nguyen, Guillemette
|b 2
700 1 _ |a Palermo, Giuseppe
|b 3
700 1 _ |a Nguyen, Tri Quang
|0 0000-0002-6769-8664
|b 4
700 1 _ |a Shi, Xiaoyan
|b 5
700 1 _ |a Stinson, Susanna Y
|b 6
700 1 _ |a Yu, Nancy
|b 7
700 1 _ |a Dufour, Annika
|b 8
700 1 _ |a Robak, Tadeusz
|b 9
700 1 _ |a Salogub, Galina N
|b 10
700 1 _ |a Dmoszynska, Anna
|b 11
700 1 _ |a Solal-Celigny, Philippe
|b 12
700 1 _ |a Warzocha, Krzysztof
|b 13
700 1 _ |a Loscertales, Javier
|b 14
700 1 _ |a Catalano, John
|b 15
700 1 _ |a Larratt, Loree
|b 16
700 1 _ |a Rossiev, Viktor A
|b 17
700 1 _ |a Bence-Bruckler, Isabelle
|b 18
700 1 _ |a Geisler, Christian H
|b 19
700 1 _ |a Montillo, Marco
|b 20
700 1 _ |a Fischer, Kirsten
|b 21
700 1 _ |a Fink, Anna-Maria
|b 22
700 1 _ |a Hallek, Michael
|b 23
700 1 _ |a Bloehdorn, Johannes
|b 24
700 1 _ |a Busch, Raymonde
|b 25
700 1 _ |a Benner, Axel
|0 P:(DE-He78)e15dfa1260625c69d6690a197392a994
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|u dkfz
700 1 _ |a Döhner, Hartmut
|b 27
700 1 _ |a Valente, Nancy
|b 28
700 1 _ |a Wenger, Michael K
|b 29
700 1 _ |a Stilgenbauer, Stephan
|b 30
700 1 _ |a Dornan, David
|b 31
773 _ _ |a 10.1182/blood-2013-12-538975
|g Vol. 124, no. 3, p. 420 - 425
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909 C O |o oai:inrepo02.dkfz.de:128518
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Marc 21