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Poster Display session

517P - Circulating tumor DNA dynamics to predict response to tyrosine kinase inhibitors in patients with advanced non-small cell lung cancer: An interim report

Date

07 Dec 2024

Session

Poster Display session

Presenters

Giang Vu

Citation

Annals of Oncology (2024) 35 (suppl_4): S1580-S1594. 10.1016/annonc/annonc1694

Authors

G.H. Vu1, V. Le Thuong2, N.T. Tu1, T.M. Tran2, V.H. Nguyen1, D. Nguyen1, L. Tu1

Author affiliations

  • 1 Genetics, Medical Genetics Institute, 740100 - Ho Chi Minh City/VN
  • 2 Pulmonology Department, Ho Chi Minh City Medicine and Pharmacy University, Ho Chi Minh City/VN

Resources

This content is available to ESMO members and event participants.

Abstract 517P

Background

Recent studies suggested that ctDNA monitoring could predict response to tyrosine kinase inhibitors (TKIs) early and detect resistant mutations in patients with advanced non-small cell lung cancer (NSCLC). However, such clinical utilization is not yet evaluated in different patient populations and clinical settings.

Methods

This prospective clinical trial is designed to enroll 30 patients diagnosed with stage IIIB-IV NSCLC and indicated for EGFR-TKIs. Blood samples are collected before treatment (T0) and every 3 months during treatment (T1-8) for 2 years. ctDNA is analyzed using a tumor-informed personalized assay (K-TrackTM MET, Gene Solutions) and compared with clinical response assessment based on RECIST 1.1 criteria.

Results

This interim report analyzed preliminary data of the first 18 patients enrolled in the study and their 33 plasma samples. The subtypes of NSCLC were predominantly adenocarcinoma (77.8%) and squamous cell carcinoma (11.1%). Tumor EGFR mutations were L858R (44.4%), Del19 (50.0%), and other variants (5.6%). The pre-treatment detection rate of ctDNA at T0 was 72.2% (13/18). Among the 11 patients who achieved a partial response, ctDNA at T1 and T2 was cleared in 6 patients (54.5%), reduced in VAF but still detectable in 3 patients (27.3%), and remained negative similar to T0 in 2 patients (18.2%). In one patient experiencing disease progression, ctDNA was undetectable in all blood samples. In order to improve sensitivity of ctDNA detection, we modified the protocol to capture additional non-mutation features of ctDNA, including changes in copy number and fragment length. The adjusted ctDNA detection rate at T0 increased to 94.4% (17/18), and in the patient with disease progression, ctDNA level was indeed found rising after treatment.

Conclusions

The assay could reliably detect ctDNA in plasma samples before TKI treatment, and the clinical utilization of ctDNA monitoring to predict treatment response continues to be evaluated in the study.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Gene Solutions JSC.

Disclosure

All authors have declared no conflicts of interest.

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