Mechanisms of resistance to immune checkpoint inhibitors
Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are rapidly transforming the practice of medical oncology. Whereas cytotoxic chemotherapy and small molecule inhibitors (‘targeted therapies’) largely...
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| Veröffentlicht in: | British journal of cancer Jg. 118; H. 1; S. 9 - 16 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Journal Article |
| Sprache: | Englisch |
| Veröffentlicht: |
London
Nature Publishing Group UK
01.01.2018
Nature Publishing Group |
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| ISSN: | 0007-0920, 1532-1827, 1532-1827 |
| Online-Zugang: | Volltext |
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| Abstract | Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are rapidly transforming the practice of medical oncology. Whereas cytotoxic chemotherapy and small molecule inhibitors (‘targeted therapies’) largely act on cancer cells directly, immune checkpoint inhibitors reinvigorate anti-tumour immune responses by disrupting co-inhibitory T-cell signalling. While resistance routinely develops in patients treated with conventional cancer therapies and targeted therapies, durable responses suggestive of long-lasting immunologic memory are commonly seen in large subsets of patients treated with ICI. However, initial response appears to be a binary event, with most non-responders to single-agent ICI therapy progressing at a rate consistent with the natural history of disease. In addition, late relapses are now emerging with longer follow-up of clinical trial populations, suggesting the emergence of acquired resistance. As robust biomarkers to predict clinical response and/or resistance remain elusive, the mechanisms underlying innate (primary) and acquired (secondary) resistance are largely inferred from pre-clinical studies and correlative clinical data. Improved understanding of molecular and immunologic mechanisms of ICI response (and resistance) may not only identify novel predictive and/or prognostic biomarkers, but also ultimately guide optimal combination/sequencing of ICI therapy in the clinic. Here we review the emerging clinical and pre-clinical data identifying novel mechanisms of innate and acquired resistance to immune checkpoint inhibition. |
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| AbstractList | Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are rapidly transforming the practice of medical oncology. Whereas cytotoxic chemotherapy and small molecule inhibitors ('targeted therapies') largely act on cancer cells directly, immune checkpoint inhibitors reinvigorate anti-tumour immune responses by disrupting co-inhibitory T-cell signalling. While resistance routinely develops in patients treated with conventional cancer therapies and targeted therapies, durable responses suggestive of long-lasting immunologic memory are commonly seen in large subsets of patients treated with ICI. However, initial response appears to be a binary event, with most non-responders to single-agent ICI therapy progressing at a rate consistent with the natural history of disease. In addition, late relapses are now emerging with longer follow-up of clinical trial populations, suggesting the emergence of acquired resistance. As robust biomarkers to predict clinical response and/or resistance remain elusive, the mechanisms underlying innate (primary) and acquired (secondary) resistance are largely inferred from pre-clinical studies and correlative clinical data. Improved understanding of molecular and immunologic mechanisms of ICI response (and resistance) may not only identify novel predictive and/or prognostic biomarkers, but also ultimately guide optimal combination/sequencing of ICI therapy in the clinic. Here we review the emerging clinical and pre-clinical data identifying novel mechanisms of innate and acquired resistance to immune checkpoint inhibition. Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are rapidly transforming the practice of medical oncology. Whereas cytotoxic chemotherapy and small molecule inhibitors ('targeted therapies') largely act on cancer cells directly, immune checkpoint inhibitors reinvigorate anti-tumour immune responses by disrupting co-inhibitory T-cell signalling. While resistance routinely develops in patients treated with conventional cancer therapies and targeted therapies, durable responses suggestive of long-lasting immunologic memory are commonly seen in large subsets of patients treated with ICI. However, initial response appears to be a binary event, with most non-responders to single-agent ICI therapy progressing at a rate consistent with the natural history of disease. In addition, late relapses are now emerging with longer follow-up of clinical trial populations, suggesting the emergence of acquired resistance. As robust biomarkers to predict clinical response and/or resistance remain elusive, the mechanisms underlying innate (primary) and acquired (secondary) resistance are largely inferred from pre-clinical studies and correlative clinical data. Improved understanding of molecular and immunologic mechanisms of ICI response (and resistance) may not only identify novel predictive and/or prognostic biomarkers, but also ultimately guide optimal combination/sequencing of ICI therapy in the clinic. Here we review the emerging clinical and pre-clinical data identifying novel mechanisms of innate and acquired resistance to immune checkpoint inhibition.Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are rapidly transforming the practice of medical oncology. Whereas cytotoxic chemotherapy and small molecule inhibitors ('targeted therapies') largely act on cancer cells directly, immune checkpoint inhibitors reinvigorate anti-tumour immune responses by disrupting co-inhibitory T-cell signalling. While resistance routinely develops in patients treated with conventional cancer therapies and targeted therapies, durable responses suggestive of long-lasting immunologic memory are commonly seen in large subsets of patients treated with ICI. However, initial response appears to be a binary event, with most non-responders to single-agent ICI therapy progressing at a rate consistent with the natural history of disease. In addition, late relapses are now emerging with longer follow-up of clinical trial populations, suggesting the emergence of acquired resistance. As robust biomarkers to predict clinical response and/or resistance remain elusive, the mechanisms underlying innate (primary) and acquired (secondary) resistance are largely inferred from pre-clinical studies and correlative clinical data. Improved understanding of molecular and immunologic mechanisms of ICI response (and resistance) may not only identify novel predictive and/or prognostic biomarkers, but also ultimately guide optimal combination/sequencing of ICI therapy in the clinic. Here we review the emerging clinical and pre-clinical data identifying novel mechanisms of innate and acquired resistance to immune checkpoint inhibition. |
| Author | Barbie, David A Flaherty, Keith T Jenkins, Russell W |
| Author_xml | – sequence: 1 givenname: Russell W surname: Jenkins fullname: Jenkins, Russell W organization: Division of Medical Oncology, Massachusetts General Hospital Cancer Center, Harvard Medical School, Department of Medical Oncology, Dana-Farber Cancer Institute – sequence: 2 givenname: David A surname: Barbie fullname: Barbie, David A organization: Department of Medical Oncology, Dana-Farber Cancer Institute – sequence: 3 givenname: Keith T surname: Flaherty fullname: Flaherty, Keith T email: KFLAHERTY@mgh.harvard.edu organization: Division of Medical Oncology, Massachusetts General Hospital Cancer Center, Harvard Medical School |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/29319049$$D View this record in MEDLINE/PubMed |
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| PublicationDate | 20180100 |
| PublicationDateYYYYMMDD | 2018-01-01 |
| PublicationDate_xml | – month: 1 year: 2018 text: 20180100 |
| PublicationDecade | 2010 |
| PublicationPlace | London |
| PublicationPlace_xml | – name: London – name: England |
| PublicationTitle | British journal of cancer |
| PublicationTitleAbbrev | Br J Cancer |
| PublicationTitleAlternate | Br J Cancer |
| PublicationYear | 2018 |
| Publisher | Nature Publishing Group UK Nature Publishing Group |
| Publisher_xml | – name: Nature Publishing Group UK – name: Nature Publishing Group |
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Arlauckas (BFbjc2017434_CR3) 2017; 9 P Sharma (BFbjc2017434_CR69) 2017; 168 TN Schumacher (BFbjc2017434_CR67) 2015; 348 KM Mahoney (BFbjc2017434_CR41) 2015; 14 D Schadendorf (BFbjc2017434_CR66) 2015; 33 M Reck (BFbjc2017434_CR58) 2016; 375 W Peng (BFbjc2017434_CR53) 2016; 6 MS Rooney (BFbjc2017434_CR62) 2015; 160 SM Ansell (BFbjc2017434_CR2) 2015; 372 DS Thommen (BFbjc2017434_CR77) 2015; 3 D Roulois (BFbjc2017434_CR63) 2015; 162 MA Paley (BFbjc2017434_CR49) 2012; 338 KB Chiappinelli (BFbjc2017434_CR9) 2015; 162 SF Ngiow (BFbjc2017434_CR46) 2015; 75 DT Le (BFbjc2017434_CR38) 2017; 357 SD Blackburn (BFbjc2017434_CR5) 2008; 105 AI Daud (BFbjc2017434_CR10) 2016; 126 AC Huang (BFbjc2017434_CR23) 2017; 545 W Hugo (BFbjc2017434_CR25) 2016; 165 JM Zaretsky (BFbjc2017434_CR83) 2016; 375 DJ Konieczkowski (BFbjc2017434_CR32) 2014; 4 R He (BFbjc2017434_CR19) 2016; 537 RT Manguso (BFbjc2017434_CR42) 2017; 547 TR Simpson (BFbjc2017434_CR71) 2013; 210 JL Benci (BFbjc2017434_CR4) 2016; 167 S Koyama (BFbjc2017434_CR33) 2016; 76 NP Restifo (BFbjc2017434_CR59) 2016; 16 L Zitvogel (BFbjc2017434_CR84) 2016; 16 MA Postow (BFbjc2017434_CR57) 2015; 372 A Ribas (BFbjc2017434_CR60) 2016; 315 K Kim (BFbjc2017434_CR30) 2014; 111 M Platten (BFbjc2017434_CR56) 2014; 5 U Sahin (BFbjc2017434_CR64) 2017; 547 SC Wei (BFbjc2017434_CR81) 2017; 170 SL Highfill (BFbjc2017434_CR21) 2014; 6 C Hirt (BFbjc2017434_CR22) 2014; 79-80 W Hugo (BFbjc2017434_CR24) 2015; 162 JS O'Donnell (BFbjc2017434_CR47) 2017; 52 AA Friedman (BFbjc2017434_CR12) 2015; 15 ME Keir (BFbjc2017434_CR29) 2008; 26 HM Kluger (BFbjc2017434_CR31) 2017; 23 JM Pitt (BFbjc2017434_CR55) 2016; 44 E Heninger (BFbjc2017434_CR20) 2015; 6 MS Lawrence (BFbjc2017434_CR37) 2013; 499 PA Ott (BFbjc2017434_CR48) 2017; 547 S Goel (BFbjc2017434_CR15) 2017; 548 V Anagnostou (BFbjc2017434_CR1) 2016; 7 SJ Im (BFbjc2017434_CR26) 2016; 537 DR Sen (BFbjc2017434_CR68) 2016; 354 S Spranger (BFbjc2017434_CR75) 2013; 5 J Larkin (BFbjc2017434_CR35) 2015; 373 KE Pauken (BFbjc2017434_CR51) 2016; 354 JT Harty (BFbjc2017434_CR18) 2008; 8 TF Gajewski (BFbjc2017434_CR13) 2013; 14 VR Juneja (BFbjc2017434_CR28) 2017; 214 K Takeda (BFbjc2017434_CR76) 2017; 8 PL Chen (BFbjc2017434_CR8) 2016; 6 S George (BFbjc2017434_CR14) 2017; 46 M Philip (BFbjc2017434_CR54) 2017; 545 EM Van Allen (BFbjc2017434_CR80) 2015; 350 J Lau (BFbjc2017434_CR36) 2017; 8 A Buque (BFbjc2017434_CR7) 2015; 4 N McGranahan (BFbjc2017434_CR44) 2016; 351 SL Topalian (BFbjc2017434_CR78) 2015; 27 SR Woo (BFbjc2017434_CR82) 2012; 72 V Bronte (BFbjc2017434_CR6) 2005; 201 DS Shin (BFbjc2017434_CR70) 2017; 7 FM Marincola (BFbjc2017434_CR43) 2000; 74 K Sakuishi (BFbjc2017434_CR65) 2010; 207 JA Joyce (BFbjc2017434_CR27) 2015; 348 MM Gubin (BFbjc2017434_CR16) 2014; 515 S Koyama (BFbjc2017434_CR34) 2016; 7 DT Le (BFbjc2017434_CR39) 2015; 372 A Ribas (BFbjc2017434_CR61) 2016; 4 S Spranger (BFbjc2017434_CR73) 2015; 523 MJ Smyth (BFbjc2017434_CR72) 2016; 13 DL Farber (BFbjc2017434_CR11) 2014; 14 G Mondanelli (BFbjc2017434_CR45) 2017; 46 C Guillerey (BFbjc2017434_CR17) 2016; 17 YA Leong (BFbjc2017434_CR40) 2016; 17 S Spranger (BFbjc2017434_CR74) 2013; 1 |
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| Snippet | Immune checkpoint inhibitors (ICI) targeting CTLA-4 and the PD-1/PD-L1 axis have shown unprecedented clinical activity in several types of cancer and are... |
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| SubjectTerms | 631/67/1059/2325 692/4028/67/1059/2325 Animals Biomarkers Biomedical and Life Sciences Biomedicine Cancer Cancer Research Chemotherapy CTLA-4 protein Cytotoxicity Drug Resistance Drug Resistance, Neoplasm Epidemiology Humans Immune checkpoint inhibitors Immune response Immunologic Factors - pharmacology Immunologic Factors - therapeutic use Immunotherapy Lymphocytes T Molecular Medicine Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - immunology Oncology PD-1 protein PD-L1 protein Review Signal Transduction - drug effects T-Lymphocytes - drug effects Tumors |
| Title | Mechanisms of resistance to immune checkpoint inhibitors |
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