PD-L1 expression across molecular driver subsets in non-small cell lung carcinoma: a 299-case real-world thoracic oncology cohort.
4 affiliations
- 1Department of Pathology, Kayseri City Hospital, Şeker Mah. Muhsin Yazıcıoğlu Bulvarı No. 77, Kocasinan, Kayseri, 38080, Turkey. [email protected].
- 2Department of Pathology, Kayseri City Hospital, Şeker Mah. Muhsin Yazıcıoğlu Bulvarı No. 77, Kocasinan, Kayseri, 38080, Turkey.
- 3Department of Medical Oncology, Kayseri City Hospital, Kayseri, Turkey.
- 4Department of Thoracic Surgery, Kayseri City Hospital, Kayseri, Turkey.
Abstract
Introduction
PD-L1 immunohistochemistry and molecular driver testing are complementary components of non-small cell lung carcinoma (NSCLC) evaluation. We examined the distribution of PD-L1 tumor proportion score (TPS) across routinely detected molecular driver subsets in a consecutive real-world thoracic oncology cohort.Methods
We retrospectively reviewed 299 consecutive NSCLC cases that underwent clinical targeted next-generation sequencing (NGS) between 2023 and 2025. Archived VENTANA SP263-stained PD-L1 slides were re-reviewed by two pathologists and categorized as TPS < 1%, 1-49%, or > = 50%. Driver-association analyses were restricted to PD-L1-tested tumors with an evaluable, mutually exclusive primary driver category; cases with indeterminate DNA-driver status were excluded. Prespecified KRAS and EGFR contrasts used reproducible 2 × 2 methods, with univariable Firth regression as a sparse-cell sensitivity analysis.Results
PD-L1 results were available for 237 tumors. TPS was < 1% in 63 cases (26.6%), 1-49% in 108 cases (45.6%), and > = 50% in 66 cases (27.8%). Among 223 PD-L1-tested tumors with an evaluable, mutually exclusive primary driver category, KRAS-mutant tumors were more frequently PD-L1 high than the other evaluable categories (24/54 [44.4%] vs. 35/169 [20.7%]; OR, 3.06; 95% CI, 1.59-5.89; p = 0.001). EGFR-mutant tumors showed a lower PD-L1-high frequency, but this observation was based on only two PD-L1-high events (2/26 [7.7%] vs. 57/197 [28.9%]; OR, 0.20; 95% CI, 0.05-0.89; p = 0.019). Eleven cases with indeterminate DNA-driver status were excluded from driver-frequency and association analyses.Conclusion
PD-L1 high expression was enriched among KRAS-mutant NSCLC in this diagnostic cohort, whereas EGFR-mutant tumors showed a directionally lower but sparse-data-limited PD-L1-high pattern. These findings support integrated interpretation of PD-L1 and molecular driver results in routine practice, but they should be viewed as biomarker-distribution evidence rather than proof of immunotherapy benefit or prognosis.
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BibTeX
@article{tasdemir2026pdl1,
title = {{PD-L1 expression across molecular driver subsets in non-small cell lung carcinoma: a 299-case real-world thoracic oncology cohort.}},
author = {Arzu Taşdemir and Hatice Karaman and Nihal Kiremit and Murat Levent Güneş and Ender Doğan and İbrahim Ethem Özsoy},
journal = {BMC cancer},
year = {2026},
month = jul,
doi = {10.1186/s12885-026-16599-7},
url = {https://europepmc.org/article/MED/42963764},
note = {CC BY},
}
RIS
TY - JOUR
TI - PD-L1 expression across molecular driver subsets in non-small cell lung carcinoma: a 299-case real-world thoracic oncology cohort.
AU - Arzu Taşdemir
AU - Hatice Karaman
AU - Nihal Kiremit
AU - Murat Levent Güneş
AU - Ender Doğan
AU - İbrahim Ethem Özsoy
PY - 2026
DA - 2026/07/30
JO - BMC cancer
DO - 10.1186/s12885-026-16599-7
UR - https://europepmc.org/article/MED/42963764
AB - Introduction PD-L1 immunohistochemistry and molecular driver testing are complementary components of non-small cell lung carcinoma (NSCLC) evaluation. We examined the distribution of PD-L1 tumor proportion score (TPS) across routinely detected molecular driver subsets in a consecutive real-world thoracic oncology cohort.Methods We retrospectively reviewed 299 consecutive NSCLC cases that underwent clinical targeted next-generation sequencing (NGS) between 2023 and 2025. Archived VENTANA SP263-stained PD-L1 slides were re-reviewed by two pathologists and categorized as TPS < 1%, 1-49%, or > = 50%. Driver-association analyses were restricted to PD-L1-tested tumors with an evaluable, mutually exclusive primary driver category; cases with indeterminate DNA-driver status were excluded. Prespecified KRAS and EGFR contrasts used reproducible 2 × 2 methods, with univariable Firth regression as a sparse-cell sensitivity analysis.Results PD-L1 results were available for 237 tumors. TPS was < 1% in 63 cases (26.6%), 1-49% in 108 cases (45.6%), and > = 50% in 66 cases (27.8%). Among 223 PD-L1-tested tumors with an evaluable, mutually exclusive primary driver category, KRAS-mutant tumors were more frequently PD-L1 high than the other evaluable categories (24/54 [44.4%] vs. 35/169 [20.7%]; OR, 3.06; 95% CI, 1.59-5.89; p = 0.001). EGFR-mutant tumors showed a lower PD-L1-high frequency, but this observation was based on only two PD-L1-high events (2/26 [7.7%] vs. 57/197 [28.9%]; OR, 0.20; 95% CI, 0.05-0.89; p = 0.019). Eleven cases with indeterminate DNA-driver status were excluded from driver-frequency and association analyses.Conclusion PD-L1 high expression was enriched among KRAS-mutant NSCLC in this diagnostic cohort, whereas EGFR-mutant tumors showed a directionally lower but sparse-data-limited PD-L1-high pattern. These findings support integrated interpretation of PD-L1 and molecular driver results in routine practice, but they should be viewed as biomarker-distribution evidence rather than proof of immunotherapy benefit or prognosis.
SN - 1471-2407
ER -