Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

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

Topics

Targeted Therapy

Tumour Site

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

Resources

Login to access the resources on OncologyPRO.

If you do not have an ESMO account, please create one for free.

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.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.