TLR2 activation promotes tumour growth and associates with patient survival and chemotherapy response in pancreatic ductal adenocarcinoma
Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, and is plagued by a paucity of targeted treatment options and tumour resistance to chemotherapeutics. The causal link between chronic inflammation and PDAC suggests that molecular regulators of the immune system promote disease...
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| Veröffentlicht in: | Oncogene Jg. 40; H. 41; S. 6007 - 6022 |
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| Sprache: | Englisch |
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Nature Publishing Group UK
14.10.2021
Nature Publishing Group |
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| ISSN: | 0950-9232, 1476-5594, 1476-5594 |
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| Abstract | Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, and is plagued by a paucity of targeted treatment options and tumour resistance to chemotherapeutics. The causal link between chronic inflammation and PDAC suggests that molecular regulators of the immune system promote disease pathogenesis and/or therapeutic resistance, yet their identity is unclear. Here, we couple endoscopic ultrasound-guided fine-needle aspiration, which captures tumour biopsies from all stages, with whole transcriptome profiling of PDAC patient primary tumours to reveal enrichment of the innate immune Toll-like receptor 2 (TLR2) molecular pathway. Augmented TLR2 expression associated with a 4-gene “TLR2 activation” signature, and was prognostic for survival and predictive for gemcitabine-based chemoresistance. Furthermore, antibody-mediated anti-TLR2 therapy suppressed the growth of human PDAC tumour xenografts, independent of a functional immune system. Our results support TLR2-based therapeutic targeting for precision medicine in PDAC, with further clinical utility that TLR2 activation is prognostic and predictive for chemoresponsiveness. |
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| AbstractList | Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, and is plagued by a paucity of targeted treatment options and tumour resistance to chemotherapeutics. The causal link between chronic inflammation and PDAC suggests that molecular regulators of the immune system promote disease pathogenesis and/or therapeutic resistance, yet their identity is unclear. Here, we couple endoscopic ultrasound-guided fine-needle aspiration, which captures tumour biopsies from all stages, with whole transcriptome profiling of PDAC patient primary tumours to reveal enrichment of the innate immune Toll-like receptor 2 (TLR2) molecular pathway. Augmented TLR2 expression associated with a 4-gene "TLR2 activation" signature, and was prognostic for survival and predictive for gemcitabine-based chemoresistance. Furthermore, antibody-mediated anti-TLR2 therapy suppressed the growth of human PDAC tumour xenografts, independent of a functional immune system. Our results support TLR2-based therapeutic targeting for precision medicine in PDAC, with further clinical utility that TLR2 activation is prognostic and predictive for chemoresponsiveness. Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, and is plagued by a paucity of targeted treatment options and tumour resistance to chemotherapeutics. The causal link between chronic inflammation and PDAC suggests that molecular regulators of the immune system promote disease pathogenesis and/or therapeutic resistance, yet their identity is unclear. Here, we couple endoscopic ultrasound-guided fine-needle aspiration, which captures tumour biopsies from all stages, with whole transcriptome profiling of PDAC patient primary tumours to reveal enrichment of the innate immune Toll-like receptor 2 (TLR2) molecular pathway. Augmented TLR2 expression associated with a 4-gene "TLR2 activation" signature, and was prognostic for survival and predictive for gemcitabine-based chemoresistance. Furthermore, antibody-mediated anti-TLR2 therapy suppressed the growth of human PDAC tumour xenografts, independent of a functional immune system. Our results support TLR2-based therapeutic targeting for precision medicine in PDAC, with further clinical utility that TLR2 activation is prognostic and predictive for chemoresponsiveness.Pancreatic ductal adenocarcinoma (PDAC) has an extremely poor prognosis, and is plagued by a paucity of targeted treatment options and tumour resistance to chemotherapeutics. The causal link between chronic inflammation and PDAC suggests that molecular regulators of the immune system promote disease pathogenesis and/or therapeutic resistance, yet their identity is unclear. Here, we couple endoscopic ultrasound-guided fine-needle aspiration, which captures tumour biopsies from all stages, with whole transcriptome profiling of PDAC patient primary tumours to reveal enrichment of the innate immune Toll-like receptor 2 (TLR2) molecular pathway. Augmented TLR2 expression associated with a 4-gene "TLR2 activation" signature, and was prognostic for survival and predictive for gemcitabine-based chemoresistance. Furthermore, antibody-mediated anti-TLR2 therapy suppressed the growth of human PDAC tumour xenografts, independent of a functional immune system. Our results support TLR2-based therapeutic targeting for precision medicine in PDAC, with further clinical utility that TLR2 activation is prognostic and predictive for chemoresponsiveness. |
| Audience | Academic |
| Author | Jenkins, Brendan J. Pajic, Marina West, Alison C. Lundy, Joanne Hertzog, Paul J. McLeod, Louise Gao, Hugh Yu, Liang Porazinski, Sean Gearing, Linden J. Deswaerte, Virginie Croagh, Daniel |
| Author_xml | – sequence: 1 givenname: Joanne surname: Lundy fullname: Lundy, Joanne organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 2 givenname: Linden J. orcidid: 0000-0003-3508-3056 surname: Gearing fullname: Gearing, Linden J. organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 3 givenname: Hugh surname: Gao fullname: Gao, Hugh organization: Department of Surgery (School of Clinical Sciences at Monash Health), Monash University – sequence: 4 givenname: Alison C. surname: West fullname: West, Alison C. organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 5 givenname: Louise surname: McLeod fullname: McLeod, Louise organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 6 givenname: Virginie surname: Deswaerte fullname: Deswaerte, Virginie organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 7 givenname: Liang surname: Yu fullname: Yu, Liang organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 8 givenname: Sean surname: Porazinski fullname: Porazinski, Sean organization: The Kinghorn Cancer Centre, Garvan Institute of Medical Research, St Vincent’s Clinical School, Faculty of Medicine, University of New South Wales – sequence: 9 givenname: Marina surname: Pajic fullname: Pajic, Marina organization: The Kinghorn Cancer Centre, Garvan Institute of Medical Research, St Vincent’s Clinical School, Faculty of Medicine, University of New South Wales – sequence: 10 givenname: Paul J. surname: Hertzog fullname: Hertzog, Paul J. organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University – sequence: 11 givenname: Daniel surname: Croagh fullname: Croagh, Daniel organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Surgery (School of Clinical Sciences at Monash Health), Monash University – sequence: 12 givenname: Brendan J. orcidid: 0000-0002-7552-4656 surname: Jenkins fullname: Jenkins, Brendan J. email: Brendan.Jenkins@hudson.org.au organization: Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Department of Molecular and Translational Science, Faculty of Medicine, Nursing and Health Sciences, Monash University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34400766$$D View this record in MEDLINE/PubMed |
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| CitedBy_id | crossref_primary_10_3390_ijms25010456 crossref_primary_10_1016_j_seminoncol_2025_152344 crossref_primary_10_3390_molecules27041209 crossref_primary_10_3390_cancers14122923 crossref_primary_10_3390_molecules27103076 crossref_primary_10_3389_fimmu_2023_1127828 crossref_primary_10_1016_j_heliyon_2024_e26984 crossref_primary_10_1038_s41392_025_02264_1 crossref_primary_10_1002_anse_202500014 crossref_primary_10_1016_j_intimp_2022_109168 crossref_primary_10_1038_s41568_022_00462_5 |
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| Title | TLR2 activation promotes tumour growth and associates with patient survival and chemotherapy response in pancreatic ductal adenocarcinoma |
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