ArticleFrontiers in oncology2026
CD73 expression as a resistance mechanism in advanced
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02504346 (AZD9291, an Irreversible EGFR-TKI, in Relapsed EGFR-mutated Non-small Cell Lung Cancer Patients Previously Treated With an EGFR-TKI, Coupled to Extensive Translational Studies), which is not on this map. Not yet cited in PubMed.
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AZD9291, an Irreversible EGFR-TKI, in Relapsed EGFR-mutated Non-small Cell Lung Cancer Patients Previously Treated With an EGFR-TKI, Coupled to Extensive Translational Studies
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10 authors.
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Abstract
Introduction: The ectoenzyme CD73 induces an immune-evasive tumor microenvironment and has been proposed to be modulated by EGFR-TKI treatment. In this exploratory study, we analyzed CD73 expression and related immune markers during sequenced EGFR-TKI treatment, including osimertinib, to identify potential biomarkers for CD73-based therapeutic opportunities in EGFR-resistant tumors. Methods: Tumor specimens from patients included in a clinical trial (NCT02504346) evaluating osimertinib in Results: Samples from 51 patients were evaluable. Upon progression after first line EGFR-TKI, 25 patients had T790M-postive disease, 18 cases were negative and 8 had unknown T790M-status. CD73 and HLA-E were significantly higher expressed in epithelium, while CD39 and NKp46 showed higher expression in the stroma of the tumors. There was no significant difference in expression pattern for any marker from diagnosis to progression after first line EGFR-treatment, but tumors with non-T790M-resistance to first- or second-generation TKIs had a significantly higher level of CD73 than T790M-positive tumors before commencing osimertinib. Paired tissue samples pre- and post-osimertinib were available in only four cases, of which three cases showed increased expression of HLA-E and NKp46 after osimertinib, while 2 cases had an increase in CD73 expression. Conclusion: We demonstrated differential expression patterns among the immune markers and higher levels of CD73 in cases with non-T790M-resistance to EGFR-TKIs. Although a limited number of cases were included in these analyses, the results might point to a potential role of immune markers inducing an immunosuppressive environment and thereby contribute to development of resistance to TKIs, which in turn could have future therapeutic implications.
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