Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study.

Standard

Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study. / Schneider, Claus-Peter; Heigener, David; Schott-von-Römer, Kathrin; Gütz, Sylvia; Laack, Heinz-Eckart; Digel, Werner; Guschall, Wolf-Rüdiger; Franke, Andreas; Bodenstein, Heinrich; Schmidtgen, Claudia; Reck, Martin.

In: J THORAC ONCOL, Vol. 3, No. 12, 12, 2008, p. 1446-1453.

Research output: SCORING: Contribution to journalSCORING: Journal articleResearchpeer-review

Harvard

Schneider, C-P, Heigener, D, Schott-von-Römer, K, Gütz, S, Laack, H-E, Digel, W, Guschall, W-R, Franke, A, Bodenstein, H, Schmidtgen, C & Reck, M 2008, 'Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study.', J THORAC ONCOL, vol. 3, no. 12, 12, pp. 1446-1453. <http://www.ncbi.nlm.nih.gov/pubmed/19057271?dopt=Citation>

APA

Schneider, C-P., Heigener, D., Schott-von-Römer, K., Gütz, S., Laack, H-E., Digel, W., Guschall, W-R., Franke, A., Bodenstein, H., Schmidtgen, C., & Reck, M. (2008). Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study. J THORAC ONCOL, 3(12), 1446-1453. [12]. http://www.ncbi.nlm.nih.gov/pubmed/19057271?dopt=Citation

Vancouver

Bibtex

@article{db1f796842dc4abfbdc3cc76c8a3da1e,
title = "Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study.",
abstract = "INTRODUCTION: Relationships between clinical outcomes and epidermal growth factor receptor (EGFR)-related tumor markers were investigated in patients with advanced non-small cell lung cancer. METHODS: Patients with stage IIIB/IV non-small cell lung cancer (0-2 prior regimens) received erlotinib (150 mg PO per day). Response and survival were evaluated, and tumor samples were assessed by immunohistochemistry (EGFR, phosphorylated mitogen-activated protein kinase, and phosphorylated AKT protein expression), fluorescence in situ hybridization (FISH; EGFR gene copy number), and DNA sequencing (EGFR, KRAS gene mutations). RESULTS: Among 311 patients, 8% had a complete/partial response; the disease control rate was 66%. Median Overall survival (OS) was 6.1 months; 1-year survival rate was 27.2%. Two of 4 patients with EGFR mutations had tumor responses, versus 2/68 with wild-type EGFR (p = 0.014). Progression-free survival (PFS) (HR = 0.31) and OS (HR = 0.33) were significantly prolonged in patients with EGFR mutations. Response rate was significantly higher in patients with EGFR FISH-positive (17%) than FISH-negative tumors (6%), and both PFS (HR = 0.58) and OS (HR = 0.63) significantly favored patients with EGFR FISH-positive tumors; median OS was 8.6 months in the EGFR FISH-positive group. None of 17 patients with a KRAS mutation had a tumor response, but the impact of KRAS mutation status on survival outcomes was of borderline statistical significance. Neither phosphorylated mitogen-activated protein kinase nor phosphorylated AKT immunohistochemistry status had a significant effect on PFS and OS with erlotinib. CONCLUSIONS: The presence of EGFR mutations and EGFR FISH-positive tumors may predispose patients to achieving better outcomes on erlotinib, but may have a beneficial impact on prognosis (irrespective of treatment). Prospective, placebo-controlled studies are needed to determine the predictive value of the putative biomarkers.",
author = "Claus-Peter Schneider and David Heigener and Kathrin Schott-von-R{\"o}mer and Sylvia G{\"u}tz and Heinz-Eckart Laack and Werner Digel and Wolf-R{\"u}diger Guschall and Andreas Franke and Heinrich Bodenstein and Claudia Schmidtgen and Martin Reck",
year = "2008",
language = "Deutsch",
volume = "3",
pages = "1446--1453",
journal = "J THORAC ONCOL",
issn = "1556-0864",
publisher = "International Association for the Study of Lung Cancer",
number = "12",

}

RIS

TY - JOUR

T1 - Epidermal growth factor receptor-related tumor markers and clinical outcomes with erlotinib in non-small cell lung cancer: an analysis of patients from german centers in the TRUST study.

AU - Schneider, Claus-Peter

AU - Heigener, David

AU - Schott-von-Römer, Kathrin

AU - Gütz, Sylvia

AU - Laack, Heinz-Eckart

AU - Digel, Werner

AU - Guschall, Wolf-Rüdiger

AU - Franke, Andreas

AU - Bodenstein, Heinrich

AU - Schmidtgen, Claudia

AU - Reck, Martin

PY - 2008

Y1 - 2008

N2 - INTRODUCTION: Relationships between clinical outcomes and epidermal growth factor receptor (EGFR)-related tumor markers were investigated in patients with advanced non-small cell lung cancer. METHODS: Patients with stage IIIB/IV non-small cell lung cancer (0-2 prior regimens) received erlotinib (150 mg PO per day). Response and survival were evaluated, and tumor samples were assessed by immunohistochemistry (EGFR, phosphorylated mitogen-activated protein kinase, and phosphorylated AKT protein expression), fluorescence in situ hybridization (FISH; EGFR gene copy number), and DNA sequencing (EGFR, KRAS gene mutations). RESULTS: Among 311 patients, 8% had a complete/partial response; the disease control rate was 66%. Median Overall survival (OS) was 6.1 months; 1-year survival rate was 27.2%. Two of 4 patients with EGFR mutations had tumor responses, versus 2/68 with wild-type EGFR (p = 0.014). Progression-free survival (PFS) (HR = 0.31) and OS (HR = 0.33) were significantly prolonged in patients with EGFR mutations. Response rate was significantly higher in patients with EGFR FISH-positive (17%) than FISH-negative tumors (6%), and both PFS (HR = 0.58) and OS (HR = 0.63) significantly favored patients with EGFR FISH-positive tumors; median OS was 8.6 months in the EGFR FISH-positive group. None of 17 patients with a KRAS mutation had a tumor response, but the impact of KRAS mutation status on survival outcomes was of borderline statistical significance. Neither phosphorylated mitogen-activated protein kinase nor phosphorylated AKT immunohistochemistry status had a significant effect on PFS and OS with erlotinib. CONCLUSIONS: The presence of EGFR mutations and EGFR FISH-positive tumors may predispose patients to achieving better outcomes on erlotinib, but may have a beneficial impact on prognosis (irrespective of treatment). Prospective, placebo-controlled studies are needed to determine the predictive value of the putative biomarkers.

AB - INTRODUCTION: Relationships between clinical outcomes and epidermal growth factor receptor (EGFR)-related tumor markers were investigated in patients with advanced non-small cell lung cancer. METHODS: Patients with stage IIIB/IV non-small cell lung cancer (0-2 prior regimens) received erlotinib (150 mg PO per day). Response and survival were evaluated, and tumor samples were assessed by immunohistochemistry (EGFR, phosphorylated mitogen-activated protein kinase, and phosphorylated AKT protein expression), fluorescence in situ hybridization (FISH; EGFR gene copy number), and DNA sequencing (EGFR, KRAS gene mutations). RESULTS: Among 311 patients, 8% had a complete/partial response; the disease control rate was 66%. Median Overall survival (OS) was 6.1 months; 1-year survival rate was 27.2%. Two of 4 patients with EGFR mutations had tumor responses, versus 2/68 with wild-type EGFR (p = 0.014). Progression-free survival (PFS) (HR = 0.31) and OS (HR = 0.33) were significantly prolonged in patients with EGFR mutations. Response rate was significantly higher in patients with EGFR FISH-positive (17%) than FISH-negative tumors (6%), and both PFS (HR = 0.58) and OS (HR = 0.63) significantly favored patients with EGFR FISH-positive tumors; median OS was 8.6 months in the EGFR FISH-positive group. None of 17 patients with a KRAS mutation had a tumor response, but the impact of KRAS mutation status on survival outcomes was of borderline statistical significance. Neither phosphorylated mitogen-activated protein kinase nor phosphorylated AKT immunohistochemistry status had a significant effect on PFS and OS with erlotinib. CONCLUSIONS: The presence of EGFR mutations and EGFR FISH-positive tumors may predispose patients to achieving better outcomes on erlotinib, but may have a beneficial impact on prognosis (irrespective of treatment). Prospective, placebo-controlled studies are needed to determine the predictive value of the putative biomarkers.

M3 - SCORING: Zeitschriftenaufsatz

VL - 3

SP - 1446

EP - 1453

JO - J THORAC ONCOL

JF - J THORAC ONCOL

SN - 1556-0864

IS - 12

M1 - 12

ER -