De-novo and acquired resistance to immune checkpoint targeting
Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Syn, Nicholas L [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: My - Citovsky, Vitaly ELSEVIER, 2019, London |
|---|---|
| Übergeordnetes Werk: |
volume:18 ; year:2017 ; number:12 ; pages:731-741 ; extent:11 |
| Links: |
|---|
| DOI / URN: |
10.1016/S1470-2045(17)30607-1 |
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ELV041264630 |
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| 520 | |a Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. | ||
| 520 | |a Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. | ||
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10.1016/S1470-2045(17)30607-1 doi GBV00000000000087A.pica (DE-627)ELV041264630 (ELSEVIER)S1470-2045(17)30607-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Syn, Nicholas L verfasserin aut De-novo and acquired resistance to immune checkpoint targeting 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. Teng, Michele W L oth Mok, Tony S K oth Soo, Ross A oth Enthalten in The Lancet Publ. Group Citovsky, Vitaly ELSEVIER My 2019 London (DE-627)ELV003173852 volume:18 year:2017 number:12 pages:731-741 extent:11 https://doi.org/10.1016/S1470-2045(17)30607-1 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 18 2017 12 731-741 11 18.2017, 12, e731-, (11 S.) 045F 610 |
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10.1016/S1470-2045(17)30607-1 doi GBV00000000000087A.pica (DE-627)ELV041264630 (ELSEVIER)S1470-2045(17)30607-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Syn, Nicholas L verfasserin aut De-novo and acquired resistance to immune checkpoint targeting 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. Teng, Michele W L oth Mok, Tony S K oth Soo, Ross A oth Enthalten in The Lancet Publ. Group Citovsky, Vitaly ELSEVIER My 2019 London (DE-627)ELV003173852 volume:18 year:2017 number:12 pages:731-741 extent:11 https://doi.org/10.1016/S1470-2045(17)30607-1 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 18 2017 12 731-741 11 18.2017, 12, e731-, (11 S.) 045F 610 |
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10.1016/S1470-2045(17)30607-1 doi GBV00000000000087A.pica (DE-627)ELV041264630 (ELSEVIER)S1470-2045(17)30607-1 DE-627 ger DE-627 rakwb eng 610 610 DE-600 570 VZ BIODIV DE-30 fid 35.70 bkl 42.12 bkl Syn, Nicholas L verfasserin aut De-novo and acquired resistance to immune checkpoint targeting 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. Teng, Michele W L oth Mok, Tony S K oth Soo, Ross A oth Enthalten in The Lancet Publ. Group Citovsky, Vitaly ELSEVIER My 2019 London (DE-627)ELV003173852 volume:18 year:2017 number:12 pages:731-741 extent:11 https://doi.org/10.1016/S1470-2045(17)30607-1 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA 35.70 Biochemie: Allgemeines VZ 42.12 Biophysik VZ AR 18 2017 12 731-741 11 18.2017, 12, e731-, (11 S.) 045F 610 |
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de-novo and acquired resistance to immune checkpoint targeting |
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De-novo and acquired resistance to immune checkpoint targeting |
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Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. |
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Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. |
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Use of immune checkpoint inhibitors targeting the programmed cell death protein-1/programmed cell death-ligand 1 and cytotoxic T lymphocyte-associated protein-4 axes has yielded impressive results in some clinical trials. However, only a subset of patients initially respond to these inhibitors, and increasing clinical evidence indicates that a substantial proportion of initial responders ultimately relapse with lethal, drug-resistant disease months or years later. Studies that have used massively parallel sequencing have shed light on the rich functional landscape of mutations that endow tumour cells with the ability to evade T-cell-mediated immunosurveillance. Cancer genomes bear signatures of clonal evolution and selection, particularly implicating acquired defects in interferon receptor signalling and antigen presentation. In this Review, we discuss the biological processes that operate in the formation of so-called immunoresistant niches, and describe the latest progress in the development of combination strategies to reinstate immunosurveillance in immune-refractory tumours. |
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