Association of PD-L1 expression and clinical outcomes in ROS1-rearranged advanced non-small cell lung cancer treated with entrectinib

Introduction

Non-small cell lung cancer (NSCLC) is a leading cause of global cancer-related mortality (1), with ROS1 gene rearrangement identified as a key driver mutation. ROS1 rearrangement occurs in approximately 2% of NSCLC cases and is characterized by a higher prevalence among non-smokers and an increased incidence of brain metastases. The proto-oncogene ROS1, encoded by the ROS1 gene located at chromosome 6q22.1, belongs to the insulin receptor tyrosine kinase family. Initially discovered in glioblastoma, ROS1 rearrangement leads to the formation of fusion proteins with partner genes such as FIG, resulting in aberrant tyrosine kinase activation and subsequent tumor growth. To date, 23 distinct ROS1 fusion variants have been identified in NSCLC, with CD74-ROS1 being the most common. Targeted therapies, including crizotinib and entrectinib, have emerged as essential treatment options for patients with ROS1-rearranged NSCLC (2,3).

Entrectinib, a multi-target tyrosine kinase inhibitor (TKI), was approved by the Food and Drug Administration (FDA) in 2019 for treating NTRK fusion-positive solid tumors and ROS1 fusion NSCLC, owing to its potent antitumor activity and exceptional blood-brain barrier penetration. Updated long-term survival results from the integrated analysis of the phase I/II trials STARTRK-2, STARTRK-1, and ALKA-372-001 presented at the 2024 European Society for Medical Oncology (ESMO) Congress demonstrated that entrectinib achieved an objective response rate (ORR) of 67.2% globally, with median progression-free survival (mPFS) and overall survival (OS) of 15.8 and 46.9 months, respectively. The efficacy in the Asian population was consistent with global outcomes, and the drug also showed significant activity in patients with brain metastases (4-6). These results solidify entrectinib’s role as a first-line therapy for ROS1 fusion NSCLC.

Recent progress in NSCLC treatment has been largely driven by immune checkpoint inhibitors (ICIs) targeting programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1). Although PD-L1 expression is a critical predictor of response to ICIs, its association with the efficacy of targeted therapies remains poorly understood. Previous studies suggest that PD-L1 positivity is linked to unfavorable outcomes in epidermal growth factor receptor (EGFR)-TKI therapy (7), and crizotinib’s effectiveness in ROS1-rearranged patients may be influenced by PD-L1 expression, albeit without statistical significance (8,9). However, research investigating the relationship between PD-L1 expression and entrectinib’s efficacy in advanced ROS1-rearranged NSCLC remains limited.

This study enrolled advanced NSCLC patients with ROS1 rearrangement who were treated with entrectinib, aiming to evaluate the impact of pre-treatment PD-L1 expression on the drug’s efficacy. It is anticipated that this research will provide valuable clinical evidence to advance precision treatment strategies for patients with ROS1-rearranged NSCLC. We present this article in accordance with the STROBE reporting checklist (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0055/rc).

Methods

Patients

We conducted a retrospective cohort study of patients with ROS1-rearranged NSCLC treated at Shanghai Chest Hospital between January 2015 and December 2024. The data were collected from clinical records on medical history. Inclusion criteria comprised: (I) pathologically confirmed advanced (stage IIIB/IV) NSCLC with ROS1 fusion detected by polymerase chain reaction (PCR) or next-generation sequencing (NGS); (II) treatment with entrectinib as systemic therapy; (III) availability of baseline PD-L1 expression results; (IV) one or more measurable tumor lesions. Exclusion criteria were: (I) never received entrectinib or used it as adjuvant therapy after resection; (II) lack of ≥1 post-treatment radiological evaluation per Response Evaluation Criteria in Solid Tumors (RECIST) 1.1.

This retrospective study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Shanghai Chest Hospital Ethical Committee (No. IS25191) and individual consent for this retrospective analysis was waived.

Assessment of endpoints

All patients received entrectinib for stage IIIB/IV NSCLC (American Joint Committee on Cancer, 8th ed.). Radiologic assessments included: mandatory chest computed tomography (CT) at 8–12-week intervals, supplemental abdominal ultrasound, brain magnetic resonance imaging (MRI), or bone scintigraphy as clinically indicated. Surveillance continued until disease progression, treatment discontinuation, or last follow-up, whichever occurred first.

Best overall responses (BORs) were assessed per RECIST version 1.1. Treatment responses were categorized as complete response (CR), partial response (PR), stable disease (SD), and progressive disease (PD). The ORR was defined as the proportion of patients achieving CR or PR based on radiographic assessments. Disease control rate (DCR) was calculated as the percentage of patients demonstrating CR, PR, or SD. PFS was measured from treatment initiation until disease progression, treatment discontinuation due to intolerance, death, or last follow-up (whichever occurred first). The primary endpoints of this study were investigator-assessed ORR and PFS, with DCR as a secondary endpoint. The median follow-up duration was 14.13 months [interquartile range (IQR): 4.73–29.10 months]. Data cutoff date was June 23, 2025.

Tumor PD-L1 expression was assessed by immunohistochemistry (IHC) prior to entrectinib treatment using the Dako PD-L1 IHC 22C3 pharmDx assay. Tumor proportion score (TPS) was stratified as: <1%, 1–49%, and ≥50%.

Statistical analysis

Analyses used GraphPad Prism 9.0.0 and R (4.2.1). Continuous variables (e.g., age) were reported as median (range); categorical variables as frequency (percentage). Between-group comparisons of baseline characteristics and response rates employed the chi-square test or Fisher’s exact test, with Monte Carlo simulation for small samples. Time-to-event endpoints (PFS) were analyzed by Kaplan-Meier methodology, with survival distributions compared via log-rank test. Hazards ratio (HRs) and 95% confidence intervals (CIs) were generated from univariable Cox proportional hazards models. The threshold for statistical significance was a two-sided P value <0.05. No imputation was performed for missing data.

Results

Patient demographics and clinical characteristics

A total of 37 patients with ROS1-rearranged NSCLC who met the study criteria were included in the final analysis at Shanghai Chest Hospital between November 2010 and December 2024 (Figure 1). The cohort had a median age of 57 years and comprised 19 males (51.4%) and 18 females (48.6%). Histologically, adenocarcinoma predominated (34 cases, 91.9%), with one case of squamous cell carcinoma (2.7%) and two cases of undifferentiated NSCLC subtypes (5.4%). All patients presented with advanced or locally advanced disease; the majority (34 cases, 91.9%) had Stage IV cancer. Distant metastases occurred in 26 patients (70.3%), including 13 cases (35.1%) with brain metastases. Baseline characteristics are detailed in Table 1.

Figure 1 CONSORT diagram. NSCLC, non-small cell lung cancer; PD-L1, programmed death-ligand 1.

ROS1 fusion status was assessed by NGS in 26 patients (70.3%) and by PCR in 11 patients (29.7%). Eight distinct fusion partners were identified through NGS. CD74-ROS1 was most prevalent (12 cases, 46.2% of NGS-tested patients). Other fusions included: EZR-ROS1 (5 cases, 19.2%), SLC34A2-ROS1 (2 cases, 7.7%), SDC4-ROS1 (2 cases, 7.7%), and single cases of TMEM106B-ROS1, TPM3-ROS1, DCBLD1-ROS1, and CMAHP-ROS1 (each 3.8%). One NGS case (3.8%) demonstrated an unspecified ROS1 mutation (Figure 2). Among the 26 patients with available NGS data, 22 (84.6%) were identified as harboring at least one concurrent genomic alteration. The most prevalent comutation was TP53 (n=12, 46.2%), with various mutation types including missense, nonsense, and splice-region variants. Other recurrently altered pathways included the Wnt/β-catenin signaling [adenomatous polyposis coli (APC), n=6, 23.1%; CTNNB1, n=1, 3.8%], the Notch pathway (NOTCH1, n=3, 11.5%), and the Hedgehog pathway (PTCH1, n=3, 11.5%; SMO, n=2, 7.7%). Notably, we identified several genomic markers associated with potential resistance to systemic therapies, such as STK11 (n=2, 7.7%) and CDKN2A (n=2, 7.7%) loss-of-function mutations, as well as copy number amplifications of KRAS, EGFR, and CDK4 in isolated cases. These findings underscore the complex molecular landscape beyond the ROS1 rearrangement in this cohort.

Figure 2 Frequency of ROS1 variants (n=26).

Correlation between PD-L1 expression and clinical outcome

PD-L1 expression was analyzed in all 37 patients. Based on the TPS, patients were stratified into three groups: PD-L1 negative (TPS <1%) in 16 patients (43.2%), PD-L1 low expression (TPS 1–49%) in 10 patients (27.0%), and PD-L1 high expression (TPS ≥50%) in 11 patients (29.7%, Table 1).

A total of 16 patients received entrectinib as first-line therapy. Among these patients, the ORR was 68.8% (11/16), with a DCR of 87.5% (14/16) (Figure 3A). The ORR was 60.0% (3/5) in PD-L1-negative patients versus 72.7% (8/11) in PD-L1-positive patients. Statistical similarity was observed across groups. When stratified by PD-L1 TPS, the ORRs were 60.0% (3/5) in the TPS <1% group, 50.0% (2/4) in the TPS 1–49% group, and 85.7% (6/7) in the TPS ≥50% group (P=0.41, Figure 3A).

Figure 3 Correlation between PD-L1 expression and clinical outcome. (A) ORR by PD-L1 expression status in first-line patients; (B) Kaplan-Meier curves for PFS stratified by PD-L1 expression in first-line treatment; (C) ORR by PD-L1 expression status in second-line or later therapy patients; (D) Kaplan-Meier curves for PFS with different PD-L1 status of patients with second-line or later therapy. ORR, objective response rate; PD, progression disease; PD-L1, programmed death-ligand 1; PFS, progression-free survival; PR, partial response; SD, stable disease; TPS, tumor proportion score.

The final follow-up was completed on June 23, 2025. At data cutoff, disease progression had occurred in 8 of 16 patients (50.0%) who received entrectinib as first-line therapy. Given that the majority of patients had not reached the mortality endpoint within the 2-year observation period, OS analysis was not performed to avoid generating potentially unreliable estimates. The mPFS for these patients was 16.9 months [95% CI: 4.9–not estimable (NE)]. There was no significant difference in mPFS between PD-L1-negative and PD-L1-positive groups (n=5; mPFS =16.9 months, 95% CI: NE–NE versus n=11; mPFS =9.53 months, 95% CI: 4.73–NE; P=0.35). The mPFS of patients in TPS <1%, TPS 1–49%, and TPS ≥50% was 16.9 months (95% CI: 4.9–NE), not reached (95% CI: 4.9–NE) and 5.07 months (95% CI: 2.83–NE), respectively (P=0.31, Figure 3B).

There are 21 patients who received entrectinib as second-line or later therapy, whose ORR was 38.2% (8/21), with a DCR of 90.5% (19/21). The ORR were comparable across TPS subgroups: 36.4% (TPS <1%, 4/11), 33.3% (TPS 1–49%, 2/6), and 50.0% (TPS ≥50%, 2/4; P=0.86). PD-L1 expression status did not significantly influence response rates, with 36.4% ORR in PD-L1-negative patients compared to 40.0% in PD-L1-positive patients (P>0.99, Figure 3C). In this cohort (n=21), disease progression occurred in 16 cases (76.2%). The mPFS was 7.33 months (95% CI: 3.87–NE). PD-L1-positive patients exhibited a mPFS of 9.6 months (95% CI: 3.13–NE), while their PD-L1-negative counterparts demonstrated 5.33 months (95% CI: 4.37–NE). Comparison showed no significant difference (P=0.65). The mPFS of TPS <1% (n=11; 5.33 months, 95% CI: 4.37–NE) and TPS 1–49% (n=6; 7.87 months, 95% CI: 2.83–NE) were found to be similar (P=0.84). However, PD-L1 high expression group (TPS ≥50%) showed a trend toward longer survival (n=4; mPFS =15.93 months, 95% CI: 3.13–NE) compared to PD-L1-negative patients (n=11; mPFS =5.33 months, 95% CI: 4.37–NE), though this difference did not reach statistical significance (P=0.39, Figure 3D). Regarding subsequent therapies after entrectinib resistance, most patients transitioned to platinum-based chemotherapy combined with bevacizumab (n=10). Only two patients received ICIs; however, treatment was discontinued after a single cycle due to deteriorating performance status, precluding any radiological response assessment

Correlation between different ROS1 fusion variants and clinical outcome

The mPFS was comparable between the CD74-ROS1 fusion-positive cohort (11.87 months; 95% CI 5.33–NE) and non-CD74-ROS1 fusion group (9.53 months; 95% CI: 3.87–NE), with no statistically significant intergroup difference (P=0.51, Figure 4A). The complete results of all univariable survival analyses are comprehensively presented in Figure 4B.

Figure 4 Survival analyses of different ROS1 fusion variants and univariate analysis. (A) Progression-free survival of patients with CD74-ROS1 and non-CD74-ROS1; (B) univariate analysis evaluating the association with the progression-free survival of patients treated with entrectinib. CI, confidence interval; HR, hazard ratio; PD-L1, programmed death-ligand 1; TPS, tumor proportion score.

Brain metastases

In this cohort, 13 patients had baseline brain metastases, with 9 undergoing NGS profiling. The detected ROS1 fusion variants included CD74-ROS1 (n=4), EZR-ROS1 (n=2), TMEM106B-ROS1 (n=1), SLC34A2-ROS1 (n=1), and CMAHP-ROS1 (n=1). Among these 13 patients, only 3 exhibited intracranial progression. Additionally, 3 patients without baseline brain metastases developed new intracranial lesions upon disease progression, of whom only 1 underwent NGS testing and was found to harbor CD74-ROS1 fusion.

Discussion

This study evaluated the correlation between PD-L1 expression and clinical efficacy of entrectinib in treatment-naïve and pretreated patients with advanced ROS1-rearranged NSCLC. Although in our cohort, the PD-L1 positivity rate in ROS1-rearranged patients was 58.3%, no significant association was observed between PD-L1 expression levels and short-term outcomes (including ORR, DCR, or PFS) following entrectinib treatment.

Entrectinib showed high disease control across both cohorts, with objective DCR of 86.7% in the first-line setting and 90.5% in second-line or later therapy. The efficacy outcomes observed in our real-world cohort were generally consistent with those reported in pivotal clinical trials (ALKA-372-001, STARTRK-1, and STARTRK-2), which established a mPFS ranging from 11.8 to 26.3 months (10). Importantly, our analysis demonstrated comparable survival outcomes in routine clinical practice, with first-line treated patients achieving an mPFS of 16.90 months (95% CI: 16.90–NE), closely mirroring the clinical trial data. Notably, the therapeutic benefit was maintained in second-line or later therapy, albeit with expected attenuation of effect size. The second-line or later therapy subgroup exhibited an mPFS of 7.33 months (95% CI: 3.87–NE), reflecting the recognized pattern of reduced efficacy with successive lines of therapy in precision oncology paradigms.

Oncogenic driver genes regulate PD-L1 expression through specific signaling pathways. In EGFR-mutant NSCLC, activation of PI3K-Akt, MAPK, and NF-κB pathways mediates PD-L1 upregulation (11). In ROS1 fusion tumors, fusion proteins induce PD-L1 expression via ROS1-SHP2 or MEK-ERK cascades (12,13). Our findings suggest that the strong positivity (TPS ≥50%) rate in ROS1-rearranged patients is 29.7%—higher than in EGFR-mutant NSCLC patients (11.0–22.6%) (14,15). This observation is consistent with previous studies by Huang et al. (16) and Remon et al. (17), suggesting that oncogenic pathways may influence PD-L1 expression levels.

The predictive value of PD-L1 expression for TKI efficacy warrants attention. A study of 126 osimertinib-treated patients revealed significantly shorter mPFS in the high PD-L1 expression group (3.8 months) versus the low-expression (6.0 months) and negative groups (9.5 months) (18). Another study (N=117) confirmed PD-L1 positivity as an independent risk factor for reduced PFS with EGFR-TKIs (19), potentially attributable to PD-L1-mediated immunosuppressive microenvironments impairing T-cell function (20). In ALK-rearranged patients, 2024 American Society of Clinical Oncology (ASCO) data demonstrated significantly longer mPFS (though not OS) in low versus high PD-L1 expressors (21). Consistent with previous findings, Zhang et al. and Xu et al. reported that PD-L1 expression may serve as a negative prognostic biomarker for PFS in ROS1-positive NSCLC patients receiving first-line crizotinib therapy, although the association did not reach statistical significance (8,9). In contrast, our cohort study did not observe a significant association between PD-L1 expression and the clinical outcomes of entrectinib, which may indicate a more complex relationship between TKI efficacy and the tumor microenvironment.

Previous studies have reported inconsistent findings regarding PFS between CD74-ROS1 and non-CD74-ROS1 fusion cohorts. Li et al. (22) demonstrated that patients harboring CD74-ROS1 fusions exhibited significantly shorter PFS compared to those with other ROS1 fusion variants(17.63 vs. 12.63 months, P=0.048). However, Xu et al. (23) conversely observed that CD74 fusion carriers achieved markedly prolonged median PFS when treated with first-line crizotinib (20.1 vs. 12.0 months; P=0.046). In their seminal 2023 publication, Li et al. (24) established a novel molecular classification system for ROS1 fusions, stratifying them into long and short transcript variants. Their comprehensive analysis demonstrated that the long ROS1 fusion cohort exhibited a clinically significant reduction in mPFS relative to patients with short fusion isoforms (8.0 vs. 24.0 months, P=0.006). In our patient cohort, no statistically significant intergroup differences were observed.

Nonetheless, several limitations of this study should be acknowledged. Primarily, as a retrospective analysis, some patients did not undergo NGS, resulting in unknown ROS1 fusion status. In addition, due to the low incidence of ROS1 fusions in NSCLC and limited entrectinib use at our center, the sample size was small, which may impact the generalizability of findings. Furthermore, as entrectinib was not approved in China until July 2022, the follow-up duration was relatively short, with a subset of patients remaining on treatment, resulting in a substantial proportion of censored data. This may introduce non-negligible selection bias and compromise the precision of survival rate estimation. Additionally, due to the immaturity of OS data (maturity rate <30%), these endpoints were excluded from the final analysis. Given the limited number of patients who received subsequent chemotherapy and the absence of chemo-immunotherapy in this cohort, the efficacy of immune-based therapies stratified by PD-L1 expression could not be evaluated.

Conclusions

In summary, this study did not find evidence that baseline PD-L1 expression significantly influenced the efficacy of entrectinib in patients with advanced ROS1-rearranged NSCLC. Clinical benefit (ORR, DCR, and PFS) was observed across treatment lines (first-line and second-line or later), although these findings should be interpreted cautiously given the limited sample size.

Acknowledgments

We would like to thank all of the investigators for their involvement in this study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0055/rc

Data Sharing Statement: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0055/dss

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0055/prf

Funding: This work was supported by Noncommunicable Chronic Diseases-National Science and Technology Major Project (Nos. 2023ZD0501900 & 2023ZD0501905), National Natural Science Foundation of China (No. 82473288), Shanghai Municipal Health Commission (No. 2022XD029), Beijing Xisike Clinical Oncology Research Foundation [No. Y-2024AZ(EGFR)ZD-0260], Yangtze River Delta Joint Sci-tech Innovation and Research Projects (No. 2023CSJZN0600), Project of the Shanghai Key Laboratory of Biological Therapy for Thoracic Tumors (No. 2025SZ1705) and Shanghai Hospital Development Center Project (No. SHDC2024CRI066).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0055/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. This retrospective study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Shanghai Chest Hospital Ethical Committee (No. IS25191) and individual consent for this retrospective analysis was waived.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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