Toll-like Receptor 9 Agonist IMO Cooperates with Cetuximab in K - Ras Mutant Colorectal and Pancreatic Cancers
Published version of a preprint
Abstract
Purpose: K-Ras somatic mutations are a strong predictive biomarker for resistance to epidermal growth factor receptor (EGFR) inhibitors in patients with colorectal and pancreatic cancer. We previously showed that the novel Toll-like receptor 9 (TLR9) agonist immunomodulatory oligonucleotide (IMO) has a strong in vivo activity in colorectal cancer models by interfering with EGFR-related signaling and synergizing with the anti-EGFR monoclonal antibody cetuximab. Experimental Design: In the present study, we investigated, both in vitro and in vivo, the antitumor effect of IMO alone or in combination with cetuximab in subcutaneous colon and orthotopic pancreatic cancer models harboring K-Ras mutations and resistance to EGFR inhibitors. Results: We showed that IMO was able to significantly restore the sensitivity of K-Ras mutant cancer cells to cetuximab, producing a marked inhibition of cell survival and a complete suppression of mitogen—activated protein kinase phosphorylation, when used in combination with cetuximab. IMO interfered with EGFR-dependent signaling, modulating the functional interaction between TLR9 and EGFR. In vivo, IMO plus cetuximab combination caused a potent and long-lasting cooperative antitumor activity in LS174T colorectal cancer and in orthotopic AsPC1 pancreatic cancer. The capability of IMO to restore cetuximab sensitivity was further confirmed by using K-Ras mutant colorectal cancer cell models obtained through homologous recombination technology. Conclusions: We showed that IMO markedly inhibits growth of K-Ras mutant colon and pancreatic cancers in vitro and in nude mice and cooperates with cetuximab via multiple mechanisms of action. Therefore, we propose IMO plus cetuximab as a therapeutic strategy for K-Ras wild-type as well for K-Ras mutant, cetuximab-resistant colorectal and pancreatic cancers. Clin Cancer Res; 17(20); 6531–41. ©2011 AACR.
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IMO was proven to synergistically inhibit tumour growth by improving the ADCC activity of cetuximab in a cetuximab-resistant colorectal cancer line and a mouse model regardless of KRAS genotype.
“IMO is a novel second-generation, modified, immunomodulatory TLR9 agonist and was proven to synergistically inhibit tumour growth by improving the ADCC activity of cetuximab in a cetuximab-resistant colorectal cancer line and a mouse model regardless of KRAS genotype [55, 56].”
From Resistance to anti-EGFR therapies in metastatic colorectal cancer: underlying mechanisms and reversal strategies (2021) · cites this paper as [56]
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Lim, K. (2013) · Springer eBooks · doi:10.1007/978-1-4614-6613-0_70-2
Corrò, C., Carvalho, J. V. M., Rapti, M., Angelino, P., Tihy, M., Bakaric, A., Puppa, G., Wirahpati, P., Durham, A., Ris, F., et al. (2025) · SSRN Electronic Journal · doi:10.2139/ssrn.5066297
叶, 唐. (2025) · Advances in Clinical Medicine · doi:10.12677/acm.2025.15123695
Wang, E., Li, Y., Yan, S., Fahy, I., Lay, R., Nguyen, P., Shi, L., & Gomez‐Godinez, V. (2026) · Journal of Biomedical Engineering and Biosciences · doi:10.11159/jbeb.2026.011
- Authors
- Rosa, R., Melisi, D., Damiano, V., Bianco, R., Garofalo, S., Gelardi, T., Agrawal, S., Di Nicolantonio, F., Scarpa, A., Bardelli, A., & Tortora, G.
- Affiliations
- University of Verona (IT)
- Authors' Affiliations: 1Dipartmento di Endocrinologia ed Oncologia Molecolare e Clinica, Università di Napoli “Federico II”; 2Unità di Farmacologia Sperimentale, Istituto Nazionale per lo Studio e la Cura dei Tumori-Fondazione “G. Pascale,” Naples, Italy; Departments of 3Surgical Oncology and 4Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas; 5Oncologia Medica, 6Dipartimento di Patologia e Diagnostica, Università di Verona; 7ARC-NET, Center for Applied Research in Cancer, Verona, Italy; 8Idera Pharmaceuticals, Cambridge, Massachusetts; 9Institute for Cancer Research and Treatment, Università di Torino, Torino; and 10FIRC Institute of Molecular Oncology, Milan, Italy
- ORCID
- Venue
- Clinical Cancer Research
- Published
- 2011-10-14
- Volume
- 17
- Issue
- 20
- Pages
- 6531-6541
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2166586819
- Cited by
- 54
- References
- 38
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 3 · 2022: 1 · 2021: 7 · 2020: 4 · 2018: 2 · 2017: 3 · 2016: 3 · 2015: 5 · 2014: 10 · 2013: 6 · 2012: 5
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System University of Turin (University of Turin) (submittedVersion)
- Funders
- Regione Campania
- Associazione Italiana per la Ricerca sul Cancro
- Topics
- Health Sciences › Medicine › Oncology › Colorectal Cancer Treatments and Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- Toll-like receptor 9 agonist, cetuximab, KRAS mutation, EGFR inhibitor resistance, colorectal cancer, pancreatic cancer, combination therapy, EGFR signaling, MAPK phosphorylation, antitumor immunity
- MeSH terms
- Cetuximab, Animals, Antibodies, Monoclonal, Antineoplastic Combined Chemotherapy Protocols, Humans, Mice, Nude, Mutation, Oligonucleotides, Pancreatic Neoplasms, Random Allocation, Genes, ras, Colorectal Neoplasms, Drug Resistance, Neoplasm, Xenograft Model Antitumor Assays, Cell Line, Tumor, Toll-Like Receptor 9, Mice, Antibodies, Monoclonal, Humanized
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