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In vivo monitoring of the therapeutic efficacy of a CXCR1/2 inhibitor with 18F-FDG PET/CT imaging in experimental head and neck carcinoma: A feasibility study

The chemokine receptors CXCR1/2 play a key role in the aggressiveness of several types of cancers including head and neck squamous cell carcinomas (HNSCCs). In HNSCCs, CXCR1/2 signaling promotes cell proliferation and angiogenesis leading to tumor growth and metastasis. The competitive inhibitor of...

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Detalles Bibliográficos
Autores principales: Montemagno, Christopher, Serrano, Benjamin, Durivault, Jérôme, Nataf, Valérie, Mocquot, François, Amblard, Régis, Vial, Valérie, Ronco, Cyril, Benhida, Rachid, Dufies, Maeva, Faraggi, Marc, Pagès, Gilles
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8374394/
https://www.ncbi.nlm.nih.gov/pubmed/34430714
http://dx.doi.org/10.1016/j.bbrep.2021.101098
Descripción
Sumario:The chemokine receptors CXCR1/2 play a key role in the aggressiveness of several types of cancers including head and neck squamous cell carcinomas (HNSCCs). In HNSCCs, CXCR1/2 signaling promotes cell proliferation and angiogenesis leading to tumor growth and metastasis. The competitive inhibitor of CXCR1/2, C29, inhibits the growth of experimental HNSCCs in mice. However, a non-invasive tool to monitor treatment response is essential to implement the use of C29 in clinical practices. (18)F-FDG PET/CT is a gold-standard tool for the staging and the post-therapy follow-up of HNSCCs patients. Our study aimed to perform the first in vivo monitoring of C29 efficacy by non-invasive (18)F-FDG PET/CT imaging. Mice bearing experimental HNSCCs (CAL33) were injected with (18)F-FDG (T0) and thereafter treated (n = 7 mice, 9 tumors, 50 mg/kg by gavage) or not (n = 7 mice, 10 tumors) with C29 for 4 consecutive days. Final (18)F-FDG-tumor uptake was determined at day 4 (TF). The average relative change (TF-T0) in (18)F-FDG tumor uptake was +25.85 ± 10.93 % in the control group vs −5.72 ± 10.07 % in the C29-treated group (p < 0.01). These results were consistent with the decrease of the tumor burden and with the decrease of tumor proliferating Ki67+ cells. These results paved the way for the use of (18)F-FDG to monitor tumor response following C29 treatment.