Audrey Goddard
University of Texas MD Anderson Cancer Center
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Journal of Clinical Oncology | 2005
David A. Eberhard; Bruce E. Johnson; Lukas C. Amler; Audrey Goddard; Sherry Heldens; Roy S. Herbst; William L. Ince; Pasi A. Jänne; Thomas Januario; David H. Johnson; Vincent A. Miller; Michael A. Ostland; David A. Ramies; Jeremy Stinson; Yu R. Zhang; Somasekar Seshagiri; Kenneth J. Hillan
PURPOSE Epidermal growth factor receptor (EGFR) mutations have been associated with tumor response to treatment with single-agent EGFR inhibitors in patients with relapsed non-small-cell lung cancer (NSCLC). The implications of EGFR mutations in patients treated with EGFR inhibitors plus first-line chemotherapy are unknown. KRAS is frequently activated in NSCLC. The relationship of KRAS mutations to outcome after EGFR inhibitor treatment has not been described. PATIENTS AND METHODS Previously untreated patients with advanced NSCLC in the phase III TRIBUTE study who were randomly assigned to carboplatin and paclitaxel with erlotinib or placebo were assessed for survival, response, and time to progression (TTP). EGFR exons 18 through 21 and KRAS exon 2 were sequenced in tumors from 274 patients. Outcomes were correlated with EGFR and KRAS mutations in retrospective subset analyses. RESULTS EGFR mutations were detected in 13% of tumors and were associated with longer survival, irrespective of treatment (P < .001). Among erlotinib-treated patients, EGFR mutations were associated with improved response rate (P < .05) and there was a trend toward an erlotinib benefit on TTP (P = .092), but not improved survival (P = .96). KRAS mutations (21% of tumors) were associated with significantly decreased TTP and survival in erlotinib plus chemotherapy-treated patients. CONCLUSION EGFR mutations may be a positive prognostic factor for survival in advanced NSCLC patients treated with chemotherapy with or without erlotinib, and may predict greater likelihood of response. Patients with KRAS-mutant NSCLC showed poorer clinical outcomes when treated with erlotinib and chemotherapy. Further studies are needed to confirm the findings of this retrospective subset analysis.
Clinical Cancer Research | 2018
Brian I. Rini; Bernard Escudier; Jean-Francois Martini; Ahmed Magheli; Christer Svedman; Margarita Lopatin; Dejan Knezevic; Audrey Goddard; Phillip G. Febbo; Rachel Li; Xun Lin; Olga Valota; Michael Staehler; Robert J. Motzer; Alain Ravaud
Purpose: Adjuvant sunitinib prolonged disease-free survival (DFS; HR, 0.76) in patients with locoregional high-risk renal cell carcinoma (RCC) in the S-TRAC trial (ClinicalTrials.gov NCT00375674). The 16-gene Recurrence Score (RS) assay was previously developed and validated to estimate risk for disease recurrence in patients with RCC after nephrectomy. This analysis further validated the prognostic value of RS assay in patients from S-TRAC and explored the association of RS results with prediction of sunitinib benefit. Patients and Methods: The analysis was prospectively designed with prespecified genes, algorithm, endpoints, and analytical methods. Primary RCC was available from 212 patients with informed consent; primary analysis focused on patients with T3 RCC. Gene expression was quantitated by RT-PCR. Time to recurrence (TTR), DFS, and renal cancer–specific survival (RCSS) were analyzed using Cox proportional hazards regression. Results: Baseline characteristics were similar between patients with and those without RS results, and between the sunitinib and placebo arms among patients with RS results. RS results predicted TTR, DFS, and RCSS in both arms, with the strongest results observed in the placebo arm. When high versus low RS groups were compared, HR for recurrence was 9.18 [95% confidence interval (CI), 2.15–39.24; P < 0.001) in the placebo arm; interaction of RS results with treatment was not significant. Conclusions: The strong prognostic performance of the 16-gene RS assay was confirmed in S-TRAC, and the RS assay is now supported by level IB evidence. RS results may help identify patients at high risk for recurrence who may derive higher absolute benefit from adjuvant therapy. Clin Cancer Res; 24(18); 4407–15. ©2018 AACR.
Archive | 2011
Steven Shak; Frederick L. Baehner; Tara Maddala; Mark Lee; Robert J. Pelham; Wayne Cowens; Diana B. Cherbavaz; Michael C. Kiefer; Michael Crager; Audrey Goddard; Joffre B. Baker
Journal of Clinical Oncology | 2005
Anne Tsao; Roy S. Herbst; Alan Sandler; Somasekar Seshagiri; I. Wistuba; Tara O. Henderson; David A. Ramies; Audrey Goddard; David H. Johnson; David A. Eberhard
Archive | 2011
Wayne Cowens; Steven Shak; Audrey Goddard; Dejan Knezevic; Joffre B. Baker; Michael C. Kiefer; Tara Maddala; Frederick L. Baehner
Journal of Clinical Oncology | 2017
Bernard Escudier; Brian I. Rini; Jean-Francois Martini; Wayne Yen-Hwa Chang; Jan Breza; Ahmed Magheli; Christer Svedman; Margarita Lopatin; Dejan Knezevic; Audrey Goddard; Patricia A. English; Rachel Li; Xun Lin; Olga Valota; Giacomo Cartenì; Michael Staehler; Robert J. Motzer; Alain Ravaud
Journal of Clinical Oncology | 2014
Bernard Escudier; Serge Koscielny; Margarita Lopatin; Christer Svedman; Virginie Verkarre; Camelia Radulescu; Yann Neuzillet; Isabelle Hemmerle; Marc Olivier Timsit; Athanasios C. Tsiatis; Michael Bonham; Dejan Knezevic; Thierry Lebret; Audrey Goddard; Mejean Arnaud
Lancet Oncology | 2015
Brian I. Rini; Audrey Goddard; Dejan Knezevic; Bernard Escudier
Journal of Clinical Oncology | 2015
Bernard Escudier; Serge Koscielny; Tara Maddala; Christer Svedman; Virginie Verkarre; Camelia Radulescu; Yann Neuzillet; Marc Olivier Timsit; Isabelle Hemmerle; Athanasios C. Tsiatis; Michael Bonham; Dejan Knezevic; Jean-Francois Martini; James Andrew Williams; Thierry Lebret; Audrey Goddard; Arnaud Mejean
Archive | 2011
Steven Shak; Frederick L. Baehner; Tara Maddala; Mark Lee; Robert J. Pelham; Wayne Cowens; Diana B. Cherbavaz; Michael C. Kiefer; Michael Crager; Audrey Goddard; Joffre B. Baker