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        <datestamp>2026-09-25T04:30:06Z</datestamp>
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          <dc:title>Data Sheet 1_Impact of post-resistance molecular retesting strategies on treatment timeliness and clinical outcomes in EGFR-mutant advanced NSCLC: a real-world study.docx</dc:title>
          <dc:creator>Wenting Zhang (342162)</dc:creator>
          <dc:creator>Feng Cheng (124653)</dc:creator>
          <dc:creator>Ping Lin (146330)</dc:creator>
          <dc:creator>Jinhe Xu (12010934)</dc:creator>
          <dc:creator>Ying Chen (9697)</dc:creator>
          <dc:creator>Jiaqi Meng (6111086)</dc:creator>
          <dc:creator>Xiulian Huang (25107367)</dc:creator>
          <dc:creator>Wen Wen (596162)</dc:creator>
          <dc:creator>Zhongquan Zhao (556760)</dc:creator>
          <dc:creator>Yingfang Song (25107370)</dc:creator>
          <dc:creator>Lei Zhang (38117)</dc:creator>
          <dc:creator>Zongyang Yu (6566321)</dc:creator>
          <dc:subject>Oncology and Carcinogenesis not elsewhere classified</dc:subject>
          <dc:subject>circulating tumor DNA</dc:subject>
          <dc:subject>EGFR mutation</dc:subject>
          <dc:subject>non-small cell lung cancer</dc:subject>
          <dc:subject>real-world study</dc:subject>
          <dc:subject>time to treatment initiation</dc:subject>
          <dc:description>Objective&lt;p&gt;To evaluate the association of ctDNA-based molecular retesting with treatment timeliness and clinical outcomes in patients with advanced EGFR-mutant NSCLC after first-line EGFR-TKI resistance.&lt;/p&gt;Patients and methods&lt;p&gt;We retrospectively analyzed patients with advanced EGFR-mutant NSCLC who had radiologically confirmed progression after first-line EGFR-TKIs between 2019 and 2024. Patients were classified as no retesting (n=86), tissue NGS (n=94), or ctDNA testing (n=49). Primary endpoints were second-line progression-free survival (2L-PFS) and overall survival from initiation of second-line therapy (2L-OS). Secondary endpoints included time to treatment initiation (TTI) and treatment patterns. Survival was analyzed using Kaplan–Meier and log-rank methods; Cox models were used for exploratory subgroup analyses. A 1:1:1 propensity score–matched analysis and sensitivity analyses restricted to patients who initiated second-line therapy within 28 or 30 days after progression were performed.&lt;/p&gt;Results&lt;p&gt;Among 229 patients, median TTI was shorter with ctDNA than tissue NGS (11.0 vs. 20.5 days, P &lt; 0.001). Subsequent targeted therapy was most frequently used in the ctDNA group (95.9%), followed by the tissue NGS (89.4%) and no-retesting groups (81.4%; P = 0.039). After matching, median 2L-PFS was 5.0, 9.0, and 9.0 months in the no-retesting, tissue NGS, and ctDNA groups, respectively (overall P = 0.005). Median 2L-OS was 12.0, 20.0, and 19.0 months, respectively (overall P = 0.074). No significant differences in 2L-PFS or 2L-OS were observed between ctDNA and tissue NGS, and findings were consistent in 28- and 30-day sensitivity analyses.&lt;/p&gt;Conclusions&lt;p&gt;Compared with tissue NGS, ctDNA testing was associated with shorter TTI, with no significant differences in 2L-PFS or 2L-OS. The ctDNA group had the highest observed targeted therapy use.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-25T04:30:06Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fonc.2026.1969822.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Data_Sheet_1_Impact_of_post-resistance_molecular_retesting_strategies_on_treatment_timeliness_and_clinical_outcomes_in_EGFR-mutant_advanced_NSCLC_a_real-world_study_docx/33992593</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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