Clinical Utility and Outcomes Impact of Crystal Digital PCR of Sensitizing and Resistance EGFR Mutations in Patients With Advanced Non-Small Cell Lung Cancer.


Journal

Clinical lung cancer
ISSN: 1938-0690
Titre abrégé: Clin Lung Cancer
Pays: United States
ID NLM: 100893225

Informations de publication

Date de publication:
09 2022
Historique:
received: 06 01 2022
revised: 05 04 2022
accepted: 02 05 2022
pubmed: 7 6 2022
medline: 9 9 2022
entrez: 6 6 2022
Statut: ppublish

Résumé

EGFRm represent 15% of advanced NSCLC in European patients. LB for molecular profiling offers a non-invasive alternative to tissue. cdPCR is a high-sensitive and low-cost LB to detect molecular alterations. We aimed to describe cdPCR clinical utility for EGFRm detection in advanced NSCLC. Prospective blood sample collection in patients with advanced NSCLC harbouring EGFRm either at diagnosis, under response or at PD between January 16 and September 20 at Gustave Roussy. LB was performed by cdPCR (Stilla): sensitizing (exon19; exon21 [p.L858R]) and exon 20 p.T790M resistance EGFRm. We defined high tumour burden (high-TB) as >2 metastatic sites. We analysed EGFRm detection by cdPCR and its correlation with progression-free and overall survival (PFS, OS). A total of 252 blood samples were collected in 140 patients. At baseline (n=25), sensitizing EGFRm were detected in 64% of samples, 88% in patients with high-TB (n=8) and 40% among those with intracranial/intrathoracic isolated lesions (n=5). At PD to tyrosine-kinase inhibitors (TKI) (n=117), detection rate (sensitizing EGFRm) was 56%; 30% in patients with intracranial/thoracic isolated lesions (n=37) vs. 67% in those with high-TB (n=63). At PD to first/second generation TKI (n=81), the p.T790M mutation was found in 22% (18/81); detection rate was 9% for intracranial/thoracic (n=23) vs. 32% for high-TB (n=41) cases. The clearance of EGFRm allelic frequency was correlated with radiological response. The absence of EGFRm detection at TKI-failure was associated with longer OS (39.1 vs. 18.4 months; P=.02). cdPCR is a sensitive LB for sensitizing and resistance EGFRm detection. cdPCR positivity was more likely observed in systemic PD cases with high-TB. It is a low-cost EGFRm detecting approach to guide treatment in NSCLC, however metastatic profile should be taken into account.

Sections du résumé

BACKGROUND
EGFRm represent 15% of advanced NSCLC in European patients. LB for molecular profiling offers a non-invasive alternative to tissue. cdPCR is a high-sensitive and low-cost LB to detect molecular alterations. We aimed to describe cdPCR clinical utility for EGFRm detection in advanced NSCLC.
METHODS
Prospective blood sample collection in patients with advanced NSCLC harbouring EGFRm either at diagnosis, under response or at PD between January 16 and September 20 at Gustave Roussy. LB was performed by cdPCR (Stilla): sensitizing (exon19; exon21 [p.L858R]) and exon 20 p.T790M resistance EGFRm. We defined high tumour burden (high-TB) as >2 metastatic sites. We analysed EGFRm detection by cdPCR and its correlation with progression-free and overall survival (PFS, OS).
RESULTS
A total of 252 blood samples were collected in 140 patients. At baseline (n=25), sensitizing EGFRm were detected in 64% of samples, 88% in patients with high-TB (n=8) and 40% among those with intracranial/intrathoracic isolated lesions (n=5). At PD to tyrosine-kinase inhibitors (TKI) (n=117), detection rate (sensitizing EGFRm) was 56%; 30% in patients with intracranial/thoracic isolated lesions (n=37) vs. 67% in those with high-TB (n=63). At PD to first/second generation TKI (n=81), the p.T790M mutation was found in 22% (18/81); detection rate was 9% for intracranial/thoracic (n=23) vs. 32% for high-TB (n=41) cases. The clearance of EGFRm allelic frequency was correlated with radiological response. The absence of EGFRm detection at TKI-failure was associated with longer OS (39.1 vs. 18.4 months; P=.02).
CONCLUSIONS
cdPCR is a sensitive LB for sensitizing and resistance EGFRm detection. cdPCR positivity was more likely observed in systemic PD cases with high-TB. It is a low-cost EGFRm detecting approach to guide treatment in NSCLC, however metastatic profile should be taken into account.

Identifiants

pubmed: 35660356
pii: S1525-7304(22)00105-X
doi: 10.1016/j.cllc.2022.05.010
pii:
doi:

Substances chimiques

Protein Kinase Inhibitors 0
EGFR protein, human EC 2.7.10.1
ErbB Receptors EC 2.7.10.1

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e377-e383

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Auteurs

Mariona Riudavets (M)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Virginie Lamberts (V)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Damien Vasseur (D)

Medical Biology and Pathology Department, BMO unit from AMMICa UMS3655/US23, Gustave Roussy, Villejuif, France.

Edouard Auclin (E)

Medical and Thoracic Oncology Department, Hôpital Européen Georges Pompidou, Paris, France.

Mihaela Aldea (M)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Cécile Jovelet (C)

Medical Biology and Pathology Department, BMO unit from AMMICa UMS3655/US23, Gustave Roussy, Villejuif, France.

Charles Naltet (C)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Pernelle Lavaud (P)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Anas Gazzah (A)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Frank Aboubakar (F)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Miriam Dorta (M)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Jordi Remon (J)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Etienne Rouleau (E)

Medical Biology and Pathology Department, BMO unit from AMMICa UMS3655/US23, Gustave Roussy, Villejuif, France.

Maud Ngocamus (M)

Early Drug Development Department, Institut Gustave Roussy, Villejuif, France.

Claudio Nicotra (C)

Early Drug Development Department, Institut Gustave Roussy, Villejuif, France.

Ludovic Lacroix (L)

Medical Biology and Pathology Department, BMO unit from AMMICa UMS3655/US23, Gustave Roussy, Villejuif, France.

Benjamin Besse (B)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

Laura Mezquita (L)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France; Medical Oncology Department, Hospital Clínic, Barcelona, Spain; Laboratory of Translational Genomics and Targeted therapies in solid tumors, Barcelona, Spain. Electronic address: lmezquita@clinic.cat.

David Planchard (D)

Medical Oncology Department, Institut Gustave Roussy, Villejuif, France.

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Classifications MeSH