PO.ET03.05 · 实验与分子治疗

Neuregulin-1(NRG1 ) -directed therapies induce alkaline phosphatase placental (ALPP) expression in NRG1 -fusion positive cancers: Preclinical data and therapeutic perspective

海报缩略图:Neuregulin-1(NRG1 ) -directed therapies induce alkaline phosphatase placental (ALPP) expression in NRG1 -fusion positive cancers: Preclinical data and therapeutic perspective
编号 7048 展板 27 时间 4/22 09:00–12:00 区域 Section 11 主讲 Manon Barre
分会场 Drug Resistance 2: Tyrosine Kinase Inhibitors
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作者与单位

Manon Barre1, Clarisse Thiollier-Schmitt1, Marie Issenmann1, Célia Cortay1, Emeline Cros-Perrial1, Sandra Ortiz-Cuaran1, Nicolas Gadot2, Elodie Voilin2, Sylvie Lantuejoul3, Anthony Ferrari4, Eric Cumunel4, Charles Dumontet1, Lars Petter Jordheim1, Michael Duruisseaux5

1Cancer Research Center of Lyon (CRCL), Lyon, France,2Research pathology platform East, Cancer Research Center of Lyon (CRCL), Lyon, France,3UNICANCER Centre Léon Bérard, Lyon, France,4Gilles Thomas bioinformatics platform, Cancer Research Center of Lyon (CRCL), Lyon, France,5Hospices Civils de Lyon, Bron, France

摘要 Abstract

Background: NRG1- fusion positive ( NRG1 +) cancers define a new molecular subtype of solid tumors. NRG1 chimeric proteins signal through ERRB3/ERRB2 dimerization, activating PI3K/AKT and MAPK signalling pathways, promoting pro-tumoral properties. NRG1 + cancers targeting relies on bispecific anti-ERBB2/ERBB3 antibodies such as zenocutuzumab (zeno) or ERBB2 inhibitors such as afatinib (afa). These therapies have limited clinical efficacy, suggesting that the biology of the NRG1/ERBB3 pathway is not totally understood. Our objective is to understand the mechanisms of resistance to NRG1-directed therapies in NRG1 + cancers. Material and Methods: We have generated afa-resistant models by continuous exposure to increasing concentrations of afa, using MDA-MB-175 cells. They grew in presence of 256 nM afatinib. Afa-sensitivity was assessed by Prestoblue test. MDA-MB-175 cells exhibit an endogenous PPP6R3-TENM4-NRG1 fusion and are sensitive to afa, zeno and other NRG1-directed therapy. Bulk RNA sequencing data from afa-naive and afa-resistant MDA-MB-175 were subjected to unsupervised and comparative analysis. Characterization of these models was completed by quantitative RT-PCR and western blotting. Results: Five afa-resistant MDA-MB-175 models were generated, showing 10-to-100-fold increase in IC50 as compared to sensitive cells. RNA-seq data unsupervised analysis showed that afa-resistant (n=5) and afa-naive (n=5) MDA-MB-175 formed two distinct clusters. ALPP was one of the ten most differentially expressed genes in afa-resistant models (log2FoldChange = 8.1, p = 2.46.10 -20 ) and the only one with a confirmed lack of expression in afa-naive and expression in afa-resistant MDA-MB-175 at the RNA and protein levels. In afa-resistant models, ALPP expression disappeared after 2-8 weeks when cultured without afa. In afa-naive and afa-resistant MDA-MB-175, an increase of ALPP expression was observed after one or two days of afa exposure. Investigation of NRG1-ERBB3 pathway in afa-resistant models showed a decrease of phospho-ERBB3 and phospho-ERK with no variation of total ERBB3 and ERK. Conclusion: Afa induced early ALPP expression in NRG1 + MDA-MB-175 cells, and afa-resistance was associated with high ALPP expression and a decrease of ERBB3 and ERK phosphorylation. Validation of ALPP as a relevant target is ongoing using ALPP KO and overexpressing NRG1+ models, including NRG1+ engineered preclinical models and NRG1+ patient-derived models from patients exposed to NRG1-directed therapies. Zeno and zongertinib impact on ALPP expression in preclinical models as well as ALPP expression in a cohort of NRG1 + non-small cell lung cancer and pancreatic ductal adenocarcinoma is ongoing. Overall, ALPP may represent an attractive target in NRG1+ cancers that may prevent resistance to NRG1-directed therapies.
利益披露 Disclosure
M. Barre, None.. C. Thiollier-Schmitt, None.. M. Issenmann, None.. C. Cortay, None.. E. Cros-Perrial, None.. S. Ortiz-Cuaran, None.. N. Gadot, None.. E. Voilin, None.. A. Ferrari, None.. E. Cumunel, None.. C. Dumontet, None.. L. Jordheim, None. M. Duruisseaux, Pfizer g., Board of Directors, non-salaried role), ), Other, Remuneration for participation in scientific meetings. Merus ). Takeda g., Board of Directors, non-salaried role), ). Guardant g., Board of Directors, non-salaried role), ), Other, Remuneration for participation in scientific meetings. Eli Lilly ). Boehringer Ingelheim g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. Astra Zeneca g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. Roche g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. BMS g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. Abbvie g., Board of Directors, non-salaried role). MSD g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. Novartis g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. GSK g., Board of Directors, non-salaried role). Sanofi g., Board of Directors, non-salaried role). Amgen g., Board of Directors, non-salaried role), Other, Remuneration for participation in scientific meetings. Regeneron g., Board of Directors, non-salaried role). Revolution medecine g., Board of Directors, non-salaried role). Novocure g., Board of Directors, non-salaried role).

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