Osimertinib As First-Line Treatment of EGFR Mutation-Positive Advanced Non-Small-Cell Lung Cancer

Purpose The AURA study ( ClinicalTrials.gov identifier: NCT01802632) included two cohorts of treatment-naïve patients to examine clinical activity and safety of osimertinib (an epidermal growth factor receptor [EGFR] -tyrosine kinase inhibitor selective for EGFR-tyrosine kinase inhibitor sensitizing...

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Vydáno v:Journal of clinical oncology Ročník 36; číslo 9; s. 841
Hlavní autoři: Ramalingam, Suresh S, Yang, James C-H, Lee, Chee Khoon, Kurata, Takayasu, Kim, Dong-Wan, John, Thomas, Nogami, Naoyuki, Ohe, Yuichiro, Mann, Helen, Rukazenkov, Yuri, Ghiorghiu, Serban, Stetson, Daniel, Markovets, Aleksandra, Barrett, J Carl, Thress, Kenneth S, Jänne, Pasi A
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States 20.03.2018
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ISSN:1527-7755, 1527-7755
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Abstract Purpose The AURA study ( ClinicalTrials.gov identifier: NCT01802632) included two cohorts of treatment-naïve patients to examine clinical activity and safety of osimertinib (an epidermal growth factor receptor [EGFR] -tyrosine kinase inhibitor selective for EGFR-tyrosine kinase inhibitor sensitizing [ EGFRm] and EGFR T790M resistance mutations) as first-line treatment of EGFR-mutated advanced non-small-cell lung cancer (NSCLC). Patients and Methods Sixty treatment-naïve patients with locally advanced or metastatic EGFRm NSCLC received osimertinib 80 or 160 mg once daily (30 patients per cohort). End points included investigator-assessed objective response rate (ORR), progression-free survival (PFS), and safety evaluation. Plasma samples were collected at or after patients experienced disease progression, as defined by Response Evaluation Criteria in Solid Tumors (RECIST), to investigate osimertinib resistance mechanisms. Results At data cutoff (November 1, 2016), median follow-up was 19.1 months. Overall ORR was 67% (95% CI, 47% to 83%) in the 80-mg group, 87% (95% CI, 69% to 96%) in the 160-mg group, and 77% (95% CI, 64% to 87%) across doses. Median PFS time was 22.1 months (95% CI, 13.7 to 30.2 months) in the 80-mg group, 19.3 months (95% CI, 13.7 to 26.0 months) in the 160-mg group, and 20.5 months (95% CI, 15.0 to 26.1 months) across doses. Of 38 patients with postprogression plasma samples, 50% had no detectable circulating tumor DNA. Nine of 19 patients had putative resistance mechanisms, including amplification of MET (n = 1); amplification of EGFR and KRAS (n = 1); MEK1, KRAS, or PIK3CA mutation (n = 1 each); EGFR C797S mutation (n = 2); JAK2 mutation (n = 1); and HER2 exon 20 insertion (n = 1). Acquired EGFR T790M was not detected. Conclusion Osimertinib demonstrated a robust ORR and prolonged PFS in treatment-naïve patients with EGFRm advanced NSCLC. There was no evidence of acquired EGFR T790M mutation in postprogression plasma samples.
AbstractList Purpose The AURA study ( ClinicalTrials.gov identifier: NCT01802632) included two cohorts of treatment-naïve patients to examine clinical activity and safety of osimertinib (an epidermal growth factor receptor [EGFR] -tyrosine kinase inhibitor selective for EGFR-tyrosine kinase inhibitor sensitizing [ EGFRm] and EGFR T790M resistance mutations) as first-line treatment of EGFR-mutated advanced non-small-cell lung cancer (NSCLC). Patients and Methods Sixty treatment-naïve patients with locally advanced or metastatic EGFRm NSCLC received osimertinib 80 or 160 mg once daily (30 patients per cohort). End points included investigator-assessed objective response rate (ORR), progression-free survival (PFS), and safety evaluation. Plasma samples were collected at or after patients experienced disease progression, as defined by Response Evaluation Criteria in Solid Tumors (RECIST), to investigate osimertinib resistance mechanisms. Results At data cutoff (November 1, 2016), median follow-up was 19.1 months. Overall ORR was 67% (95% CI, 47% to 83%) in the 80-mg group, 87% (95% CI, 69% to 96%) in the 160-mg group, and 77% (95% CI, 64% to 87%) across doses. Median PFS time was 22.1 months (95% CI, 13.7 to 30.2 months) in the 80-mg group, 19.3 months (95% CI, 13.7 to 26.0 months) in the 160-mg group, and 20.5 months (95% CI, 15.0 to 26.1 months) across doses. Of 38 patients with postprogression plasma samples, 50% had no detectable circulating tumor DNA. Nine of 19 patients had putative resistance mechanisms, including amplification of MET (n = 1); amplification of EGFR and KRAS (n = 1); MEK1, KRAS, or PIK3CA mutation (n = 1 each); EGFR C797S mutation (n = 2); JAK2 mutation (n = 1); and HER2 exon 20 insertion (n = 1). Acquired EGFR T790M was not detected. Conclusion Osimertinib demonstrated a robust ORR and prolonged PFS in treatment-naïve patients with EGFRm advanced NSCLC. There was no evidence of acquired EGFR T790M mutation in postprogression plasma samples.Purpose The AURA study ( ClinicalTrials.gov identifier: NCT01802632) included two cohorts of treatment-naïve patients to examine clinical activity and safety of osimertinib (an epidermal growth factor receptor [EGFR] -tyrosine kinase inhibitor selective for EGFR-tyrosine kinase inhibitor sensitizing [ EGFRm] and EGFR T790M resistance mutations) as first-line treatment of EGFR-mutated advanced non-small-cell lung cancer (NSCLC). Patients and Methods Sixty treatment-naïve patients with locally advanced or metastatic EGFRm NSCLC received osimertinib 80 or 160 mg once daily (30 patients per cohort). End points included investigator-assessed objective response rate (ORR), progression-free survival (PFS), and safety evaluation. Plasma samples were collected at or after patients experienced disease progression, as defined by Response Evaluation Criteria in Solid Tumors (RECIST), to investigate osimertinib resistance mechanisms. Results At data cutoff (November 1, 2016), median follow-up was 19.1 months. Overall ORR was 67% (95% CI, 47% to 83%) in the 80-mg group, 87% (95% CI, 69% to 96%) in the 160-mg group, and 77% (95% CI, 64% to 87%) across doses. Median PFS time was 22.1 months (95% CI, 13.7 to 30.2 months) in the 80-mg group, 19.3 months (95% CI, 13.7 to 26.0 months) in the 160-mg group, and 20.5 months (95% CI, 15.0 to 26.1 months) across doses. Of 38 patients with postprogression plasma samples, 50% had no detectable circulating tumor DNA. Nine of 19 patients had putative resistance mechanisms, including amplification of MET (n = 1); amplification of EGFR and KRAS (n = 1); MEK1, KRAS, or PIK3CA mutation (n = 1 each); EGFR C797S mutation (n = 2); JAK2 mutation (n = 1); and HER2 exon 20 insertion (n = 1). Acquired EGFR T790M was not detected. Conclusion Osimertinib demonstrated a robust ORR and prolonged PFS in treatment-naïve patients with EGFRm advanced NSCLC. There was no evidence of acquired EGFR T790M mutation in postprogression plasma samples.
Purpose The AURA study ( ClinicalTrials.gov identifier: NCT01802632) included two cohorts of treatment-naïve patients to examine clinical activity and safety of osimertinib (an epidermal growth factor receptor [EGFR] -tyrosine kinase inhibitor selective for EGFR-tyrosine kinase inhibitor sensitizing [ EGFRm] and EGFR T790M resistance mutations) as first-line treatment of EGFR-mutated advanced non-small-cell lung cancer (NSCLC). Patients and Methods Sixty treatment-naïve patients with locally advanced or metastatic EGFRm NSCLC received osimertinib 80 or 160 mg once daily (30 patients per cohort). End points included investigator-assessed objective response rate (ORR), progression-free survival (PFS), and safety evaluation. Plasma samples were collected at or after patients experienced disease progression, as defined by Response Evaluation Criteria in Solid Tumors (RECIST), to investigate osimertinib resistance mechanisms. Results At data cutoff (November 1, 2016), median follow-up was 19.1 months. Overall ORR was 67% (95% CI, 47% to 83%) in the 80-mg group, 87% (95% CI, 69% to 96%) in the 160-mg group, and 77% (95% CI, 64% to 87%) across doses. Median PFS time was 22.1 months (95% CI, 13.7 to 30.2 months) in the 80-mg group, 19.3 months (95% CI, 13.7 to 26.0 months) in the 160-mg group, and 20.5 months (95% CI, 15.0 to 26.1 months) across doses. Of 38 patients with postprogression plasma samples, 50% had no detectable circulating tumor DNA. Nine of 19 patients had putative resistance mechanisms, including amplification of MET (n = 1); amplification of EGFR and KRAS (n = 1); MEK1, KRAS, or PIK3CA mutation (n = 1 each); EGFR C797S mutation (n = 2); JAK2 mutation (n = 1); and HER2 exon 20 insertion (n = 1). Acquired EGFR T790M was not detected. Conclusion Osimertinib demonstrated a robust ORR and prolonged PFS in treatment-naïve patients with EGFRm advanced NSCLC. There was no evidence of acquired EGFR T790M mutation in postprogression plasma samples.
Author Ohe, Yuichiro
Kurata, Takayasu
John, Thomas
Lee, Chee Khoon
Rukazenkov, Yuri
Ramalingam, Suresh S
Mann, Helen
Stetson, Daniel
Barrett, J Carl
Ghiorghiu, Serban
Markovets, Aleksandra
Thress, Kenneth S
Jänne, Pasi A
Kim, Dong-Wan
Yang, James C-H
Nogami, Naoyuki
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  givenname: Suresh S
  surname: Ramalingam
  fullname: Ramalingam, Suresh S
  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
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  givenname: James C-H
  surname: Yang
  fullname: Yang, James C-H
  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
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  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
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– sequence: 13
  givenname: Aleksandra
  surname: Markovets
  fullname: Markovets, Aleksandra
  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
– sequence: 14
  givenname: J Carl
  surname: Barrett
  fullname: Barrett, J Carl
  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
– sequence: 15
  givenname: Kenneth S
  surname: Thress
  fullname: Thress, Kenneth S
  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
– sequence: 16
  givenname: Pasi A
  surname: Jänne
  fullname: Jänne, Pasi A
  organization: Suresh S. Ramalingam, Emory University School of Medicine, Winship Cancer Institute, Atlanta, GA; James C.-H. Yang, National Taiwan University and National Taiwan University Cancer Center, Taipei, Taiwan; Chee Khoon Lee, St George Hospital, Sydney, New South Wales; Thomas John, Olivia Newton-John Cancer Research Institute, Austin Health, Melbourne, Victoria, Australia; Takayasu Kurata, Kansai Medical University Hirakata Hospital, Osaka; Naoyuki Nogami, National Hospital Organization Shikoku Cancer Center, Matsuyama; Yuichiro Ohe, National Cancer Center Hospital East, Kashiwa-City, Japan; Dong-Wan Kim, Seoul National University Hospital, Seoul, Republic of Korea; Helen Mann, AstraZeneca, Macclesfield; Yuri Rukazenkov and Serban Ghiorghiu, AstraZeneca, Cambridge, United Kingdom; Daniel Stetson, Aleksandra Markovets, J. Carl Barrett, and Kenneth S. Thress, AstraZeneca, Waltham; and Pasi A. Jänne, Dana-Farber Cancer Institute and the Belfer Center for Applied Cancer Science, Boston, MA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/28841389$$D View this record in MEDLINE/PubMed
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References 30430025 - J Thorac Dis. 2018 Sep;10(Suppl 26):S3071-S3077
29299414 - Transl Lung Cancer Res. 2017 Dec;6(Suppl 1):S62-S66
29610752 - Ann Transl Med. 2018 Feb;6(3):62
29299413 - Transl Lung Cancer Res. 2017 Dec;6(Suppl 1):S58-S61
29611548 - Ann Transl Med. 2018 Feb;6(3):61
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Aniline Compounds
Antineoplastic Agents - therapeutic use
Carcinoma, Non-Small-Cell Lung - drug therapy
Carcinoma, Non-Small-Cell Lung - enzymology
Carcinoma, Non-Small-Cell Lung - genetics
ErbB Receptors - blood
ErbB Receptors - genetics
Female
Humans
Lung Neoplasms - drug therapy
Lung Neoplasms - enzymology
Lung Neoplasms - genetics
Male
Middle Aged
Mutation
Piperazines - therapeutic use
Progression-Free Survival
Protein Kinase Inhibitors - therapeutic use
Survival Rate
Title Osimertinib As First-Line Treatment of EGFR Mutation-Positive Advanced Non-Small-Cell Lung Cancer
URI https://www.ncbi.nlm.nih.gov/pubmed/28841389
https://www.proquest.com/docview/1932850138
Volume 36
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