TY - JOUR
T1 - Adequacy of endosonography-derived samples from peribronchial or periesophageal intrapulmonary lesions for the molecular profiling of lung cancer
AU - Livi, Vanina
AU - Ardizzoni, Andrea
AU - Cancellieri, Alessandra
AU - Natali, Filippo
AU - Ferrari, Marco
AU - Paioli, Daniela
AU - De Biase, Dario
AU - Capizzi, Elisa
AU - Tallini, Giovanni
AU - Fiorentino, Michelangelo
AU - Trisolini, Rocco
PY - 2019
Y1 - 2019
N2 - Introduction and Objectives Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from intrapulmonary lesions for cancer genotyping and programmed-death ligand 1 (PD-L1) testing. Methods A prospectively collected database regarding 99 consecutive patients undergoing endosonography for the diagnosis of an intrapulmonary lesion was retrospectively reviewed. Genotyping +/- PD-L1 testing was carried out in the 53 patients with advanced lung cancer and was classified as complete if all clinically indicated tests could be performed, incomplete if at least one test could not be carried out, and unsuccessful if the sample was unsuitable for molecular analysis. Results All clinically indicated biomarkers could be tested in 44 (83%) patients, whereas the molecular profiling was classified as incomplete in 6 (11.3%), and unsuccessful in 3 (5.7%). Thirty-seven genetic alterations (KRAS mutation, 17; EGFR mutation, 17; ALK rearrangement, 3) and 2 cases of PD-L1 expression >50% were found in 31 (58%) patients. EGFR was successfully analysed in 94.1% of cases, KRAS in 93.9%, ALK in 89%, ROS1 in 90% and PD-L1 in 63.1%. Conclusion Endosonography-derived samples from intrapulmonary lesions were suitable for a thorough molecular profiling in most patients. The few cases of incomplete accomplishment of the testing algorithm were related to the failure of PD-L1 analysis due to the exhaustion of the sample or the lack of sufficient tumour cells in the paraffin-embedded material.
AB - Introduction and Objectives Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from intrapulmonary lesions for cancer genotyping and programmed-death ligand 1 (PD-L1) testing. Methods A prospectively collected database regarding 99 consecutive patients undergoing endosonography for the diagnosis of an intrapulmonary lesion was retrospectively reviewed. Genotyping +/- PD-L1 testing was carried out in the 53 patients with advanced lung cancer and was classified as complete if all clinically indicated tests could be performed, incomplete if at least one test could not be carried out, and unsuccessful if the sample was unsuitable for molecular analysis. Results All clinically indicated biomarkers could be tested in 44 (83%) patients, whereas the molecular profiling was classified as incomplete in 6 (11.3%), and unsuccessful in 3 (5.7%). Thirty-seven genetic alterations (KRAS mutation, 17; EGFR mutation, 17; ALK rearrangement, 3) and 2 cases of PD-L1 expression >50% were found in 31 (58%) patients. EGFR was successfully analysed in 94.1% of cases, KRAS in 93.9%, ALK in 89%, ROS1 in 90% and PD-L1 in 63.1%. Conclusion Endosonography-derived samples from intrapulmonary lesions were suitable for a thorough molecular profiling in most patients. The few cases of incomplete accomplishment of the testing algorithm were related to the failure of PD-L1 analysis due to the exhaustion of the sample or the lack of sufficient tumour cells in the paraffin-embedded material.
KW - anaplastic lymphoma kinase
KW - endobronchial ultrasound
KW - rapid onsite evaluation
KW - programmed-death ligand 1
KW - epidermal growth factor receptor
KW - anaplastic lymphoma kinase
KW - endobronchial ultrasound
KW - rapid onsite evaluation
KW - programmed-death ligand 1
KW - epidermal growth factor receptor
UR - http://hdl.handle.net/10807/282357
U2 - 10.1111/crj.13063
DO - 10.1111/crj.13063
M3 - Article
SN - 1752-6981
VL - 13
SP - 590
EP - 597
JO - THE CLINICAL RESPIRATORY JOURNAL
JF - THE CLINICAL RESPIRATORY JOURNAL
ER -