34P - High chemopreventive and therapeutic efficacy of Id1 Inhibition in KRAS-mutant (KM) adenocarcinoma (AD) non-small cell lung cancer (NSCLC)

Date 11 September 2017
Event ESMO 2017 Congress
Session Poster display session
Topics Basic Science
Lung and other Thoracic Tumours
Presenter Marta Roman Moreno
Citation Annals of Oncology (2017) 28 (suppl_5): v1-v21. 10.1093/annonc/mdx361
Authors M. Roman Moreno1, S. Vicent2, I. Lopez2, I. Baraibar Argota1, E. Fraile2, I. Gil Bazo1
  • 1Medical Oncology, Clinica Universitaria de Navarra, 31008 - Pamplona/ES
  • 2Tumores Solidos Y Biomarcadores, CENTRO DE INVESTIGACION MEDICA APLICADA (CIMA), 31008 - PAMPLONA/ES

Abstract

Background

Id1 is an independent prognostic factor in NSCLC-AD. Id1 silencing impairs cell viability and migration of NSCLC-AD cell lines. KRAS is the most frequently mutant gene in NSCLC with no specific therapies clinically available. Here we evaluate Id1 as a potential chemopreventive and therapeutic target in a humanized mouse model of KM NSCLC-AD.

Methods

Several human lung AD cell lines with known mutations (H1792-604, H2009, H358, H1568, H1437, H1703 and H2126) were selected for Id1 silencing using inducible short hairpin RNA (shRNA). Humanized AD xenograft mouse models were generated by subcutaneous injection of H1792-604 and H2009 cell lines (Id1 silenced or Id1 wild type) in flanks of immunodeficient mice. Id1 silencing was activated at the time of tumor cell inoculation (chemoprevention assay) or once the tumors were established (therapeutic assay).

Results

Id1 inhibition was achieved in all selected cell lines compared to their controls. In vivo, in the chemoprevention assay we observed a significant decrease in tumor volume in mice injected with Id1 silenced H1792-604 cells (60% ± 32.39) compared to the control group (356.29% ± 115.32) (p 

Conclusions

These findings encourage further evaluation of Id1 as a potential therapeutic target in KM NSCLC-AD patients.

Clinical trial identification

Legal entity responsible for the study

Clínica Universidad de Navarra

Funding

Clínica Universidad de Navarra

Disclosure

All authors have declared no conflicts of interest.