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Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

966 - Potential resistance mechanisms revealed primary resistance to crizotinib in ROS1+ non-small-cell lung cancer using next generation sequencing: A multicenter study

Date

20 Oct 2018

Session

Poster display session: Biomarkers, Gynaecological cancers, Haematological malignancies, Immunotherapy of cancer, New diagnostic tools, NSCLC - early stage, locally advanced & metastatic, SCLC, Thoracic malignancies, Translational research

Presenters

Quxia Zhang

Citation

Annals of Oncology (2018) 29 (suppl_8): viii14-viii57. 10.1093/annonc/mdy269

Authors

Q. Zhang1, C. Xu1, W. Wang2, W. Zhuang3, Z. Song2, Y. Zhu4, Y. Chen1, G. Chen1, M. Fang2, T. Lv5, Y. Song5

Author affiliations

  • 1 Pathology, Fujian Cancer Hospital, 350014 - Fuzhou/CN
  • 2 Chemotherapy, Zhejiang Cancer Hospital, 310022 - Hangzhou/CN
  • 3 Medical Thoracic Oncology, Fujian Cancer Hospital, 350014 - Fuzhou/CN
  • 4 Thoracic Disease Center, Zhejiang Rongjun Hospital, 314000 - Jiaxing/CN
  • 5 Respiratory Medicine, Jinling Hospital, 210002 - Nanjing/CN
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Resources

Abstract 966

Background

Crizotinib have greatly improved the prognosis of ROS1+ lung adenocarcinoma. However, approximately 5% to 10% of patients with ROS1+ non-small-cell lung cancer (NSCLC) have primary resistance to crizotinib treatment. The underlying mechanism is unknown.

Methods

We screened 2617 patients with NSCLC for ROS1 fusion. Among them, 23 patients received crizotinib treatment, and a total of 20 patients with stage IIIb-IV ROS1+ NSCLC were undergoing tumor biopsies or blood withdrawing by the time of primary or acquiring resistance to crizotinib, in including 4 formalin-fixed paraffin-embedded (FFPE) samples, 13 serum samples and 3 serous effusions. We used targeted NGS to detect genes status of patients.

Results

Among 23 patients treated with crizotinib, 73.9% (17/23) developed acquired resistance, and 13.04% (3/23) had primary resistance. Using the specimens at the baseline, there was 1 (33.3%) patient with BCL2L11 loss (BIM deletion polymorphism), 1 (33.3%) patient with PTEN mutation, and 1 (33.3%) patient with KIT mutation. Median PFS was significantly shorter in patients with primary resistance than those with acquired resistance (2.3 vs. 14.5 months, P < 0.001).

Conclusions

BCL2L11 loss, PTEN mutation, and KIT mutation might contribute to molecular mechanisms of primary resistance to crizotinib in ROS1+ NSCLC. Further investigations are warranted to overcome these primary resistances.

Clinical trial identification

Legal entity responsible for the study

Quxia Zhang.

Funding

Has not received any funding.

Editorial Acknowledgement

Disclosure

All authors have declared no conflicts of interest.

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