Cancer Stem Cells—Origins and Biomarkers: Perspectives for Targeted Personalized Therapies
The use of biomarkers in diagnosis, therapy and prognosis has gained increasing interest over the last decades. In particular, the analysis of biomarkers in cancer patients within the pre- and post-therapeutic period is required to identify several types of cells, which carry a risk for a disease pr...
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| Veröffentlicht in: | Frontiers in immunology Jg. 11; S. 1280 |
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| Hauptverfasser: | , , , , , , , , , |
| Format: | Journal Article |
| Sprache: | Englisch |
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Switzerland
Frontiers Media S.A
07.08.2020
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| ISSN: | 1664-3224, 1664-3224 |
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| Abstract | The use of biomarkers in diagnosis, therapy and prognosis has gained increasing interest over the last decades. In particular, the analysis of biomarkers in cancer patients within the pre- and post-therapeutic period is required to identify several types of cells, which carry a risk for a disease progression and subsequent post-therapeutic relapse. Cancer stem cells (CSCs) are a subpopulation of tumor cells that can drive tumor initiation and can cause relapses. At the time point of tumor initiation, CSCs originate from either differentiated cells or adult tissue resident stem cells. Due to their importance, several biomarkers that characterize CSCs have been identified and correlated to diagnosis, therapy and prognosis. However, CSCs have been shown to display a high plasticity, which changes their phenotypic and functional appearance. Such changes are induced by chemo- and radiotherapeutics as well as senescent tumor cells, which cause alterations in the tumor microenvironment. Induction of senescence causes tumor shrinkage by modulating an anti-tumorigenic environment in which tumor cells undergo growth arrest and immune cells are attracted. Besides these positive effects after therapy, senescence can also have negative effects displayed post-therapeutically. These unfavorable effects can directly promote cancer stemness by increasing CSC plasticity phenotypes, by activating stemness pathways in non-CSCs, as well as by promoting senescence escape and subsequent activation of stemness pathways. At the end, all these effects can lead to tumor relapse and metastasis. This review provides an overview of the most frequently used CSC markers and their implementation as biomarkers by focussing on deadliest solid (lung, stomach, liver, breast and colorectal cancers) and hematological (acute myeloid leukemia, chronic myeloid leukemia) cancers. Furthermore, it gives examples on how the CSC markers might be influenced by therapeutics, such as chemo- and radiotherapy, and the tumor microenvironment. It points out, that it is crucial to identify and monitor residual CSCs, senescent tumor cells, and the pro-tumorigenic senescence-associated secretory phenotype in a therapy follow-up using specific biomarkers. As a future perspective, a targeted immune-mediated strategy using chimeric antigen receptor based approaches for the removal of remaining chemotherapy-resistant cells as well as CSCs in a personalized therapeutic approach are discussed. |
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| AbstractList | The use of biomarkers in diagnosis, therapy and prognosis has gained increasing interest over the last decades. In particular, the analysis of biomarkers in cancer patients within the pre- and post-therapeutic period is required to identify several types of cells, which carry a risk for a disease progression and subsequent post-therapeutic relapse. Cancer stem cells (CSCs) are a subpopulation of tumor cells that can drive tumor initiation and can cause relapses. At the time point of tumor initiation, CSCs originate from either differentiated cells or adult tissue resident stem cells. Due to their importance, several biomarkers that characterize CSCs have been identified and correlated to diagnosis, therapy and prognosis. However, CSCs have been shown to display a high plasticity, which changes their phenotypic and functional appearance. Such changes are induced by chemo- and radiotherapeutics as well as senescent tumor cells, which cause alterations in the tumor microenvironment. Induction of senescence causes tumor shrinkage by modulating an anti-tumorigenic environment in which tumor cells undergo growth arrest and immune cells are attracted. Besides these positive effects after therapy, senescence can also have negative effects displayed post-therapeutically. These unfavorable effects can directly promote cancer stemness by increasing CSC plasticity phenotypes, by activating stemness pathways in non-CSCs, as well as by promoting senescence escape and subsequent activation of stemness pathways. At the end, all these effects can lead to tumor relapse and metastasis. This review provides an overview of the most frequently used CSC markers and their implementation as biomarkers by focussing on deadliest solid (lung, stomach, liver, breast and colorectal cancers) and hematological (acute myeloid leukemia, chronic myeloid leukemia) cancers. Furthermore, it gives examples on how the CSC markers might be influenced by therapeutics, such as chemo- and radiotherapy, and the tumor microenvironment. It points out, that it is crucial to identify and monitor residual CSCs, senescent tumor cells, and the pro-tumorigenic senescence-associated secretory phenotype in a therapy follow-up using specific biomarkers. As a future perspective, a targeted immune-mediated strategy using chimeric antigen receptor based approaches for the removal of remaining chemotherapy-resistant cells as well as CSCs in a personalized therapeutic approach are discussed. The use of biomarkers in diagnosis, therapy and prognosis has gained increasing interest over the last decades. In particular, the analysis of biomarkers in cancer patients within the pre- and post-therapeutic period is required to identify several types of cells, which carry a risk for a disease progression and subsequent post-therapeutic relapse. Cancer stem cells (CSCs) are a subpopulation of tumor cells that can drive tumor initiation and can cause relapses. At the time point of tumor initiation, CSCs originate from either differentiated cells or adult tissue resident stem cells. Due to their importance, several biomarkers that characterize CSCs have been identified and correlated to diagnosis, therapy and prognosis. However, CSCs have been shown to display a high plasticity, which changes their phenotypic and functional appearance. Such changes are induced by chemo- and radiotherapeutics as well as senescent tumor cells, which cause alterations in the tumor microenvironment. Induction of senescence causes tumor shrinkage by modulating an anti-tumorigenic environment in which tumor cells undergo growth arrest and immune cells are attracted. Besides these positive effects after therapy, senescence can also have negative effects displayed post-therapeutically. These unfavorable effects can directly promote cancer stemness by increasing CSC plasticity phenotypes, by activating stemness pathways in non-CSCs, as well as by promoting senescence escape and subsequent activation of stemness pathways. At the end, all these effects can lead to tumor relapse and metastasis. This review provides an overview of the most frequently used CSC markers and their implementation as biomarkers by focussing on deadliest solid (lung, stomach, liver, breast and colorectal cancers) and hematological (acute myeloid leukemia, chronic myeloid leukemia) cancers. Furthermore, it gives examples on how the CSC markers might be influenced by therapeutics, such as chemo- and radiotherapy, and the tumor microenvironment. It points out, that it is crucial to identify and monitor residual CSCs, senescent tumor cells, and the pro-tumorigenic senescence-associated secretory phenotype in a therapy follow-up using specific biomarkers. As a future perspective, a targeted immune-mediated strategy using chimeric antigen receptor based approaches for the removal of remaining chemotherapy-resistant cells as well as CSCs in a personalized therapeutic approach are discussed.The use of biomarkers in diagnosis, therapy and prognosis has gained increasing interest over the last decades. In particular, the analysis of biomarkers in cancer patients within the pre- and post-therapeutic period is required to identify several types of cells, which carry a risk for a disease progression and subsequent post-therapeutic relapse. Cancer stem cells (CSCs) are a subpopulation of tumor cells that can drive tumor initiation and can cause relapses. At the time point of tumor initiation, CSCs originate from either differentiated cells or adult tissue resident stem cells. Due to their importance, several biomarkers that characterize CSCs have been identified and correlated to diagnosis, therapy and prognosis. However, CSCs have been shown to display a high plasticity, which changes their phenotypic and functional appearance. Such changes are induced by chemo- and radiotherapeutics as well as senescent tumor cells, which cause alterations in the tumor microenvironment. Induction of senescence causes tumor shrinkage by modulating an anti-tumorigenic environment in which tumor cells undergo growth arrest and immune cells are attracted. Besides these positive effects after therapy, senescence can also have negative effects displayed post-therapeutically. These unfavorable effects can directly promote cancer stemness by increasing CSC plasticity phenotypes, by activating stemness pathways in non-CSCs, as well as by promoting senescence escape and subsequent activation of stemness pathways. At the end, all these effects can lead to tumor relapse and metastasis. This review provides an overview of the most frequently used CSC markers and their implementation as biomarkers by focussing on deadliest solid (lung, stomach, liver, breast and colorectal cancers) and hematological (acute myeloid leukemia, chronic myeloid leukemia) cancers. Furthermore, it gives examples on how the CSC markers might be influenced by therapeutics, such as chemo- and radiotherapy, and the tumor microenvironment. It points out, that it is crucial to identify and monitor residual CSCs, senescent tumor cells, and the pro-tumorigenic senescence-associated secretory phenotype in a therapy follow-up using specific biomarkers. As a future perspective, a targeted immune-mediated strategy using chimeric antigen receptor based approaches for the removal of remaining chemotherapy-resistant cells as well as CSCs in a personalized therapeutic approach are discussed. |
| Author | Kossatz-Boehlert, Uta Walcher, Lia Dluczek, Sarah Fricke, Stephan Strauß, Alexander Kistenmacher, Ann-Kathrin Suo, Huizhen Yevsa, Tetyana Kitte, Reni Blaudszun, André-René |
| AuthorAffiliation | 2 Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School , Hannover , Germany 1 Department of Immunology, Fraunhofer Institute for Cell Therapy and Immunology , Leipzig , Germany |
| AuthorAffiliation_xml | – name: 2 Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School , Hannover , Germany – name: 1 Department of Immunology, Fraunhofer Institute for Cell Therapy and Immunology , Leipzig , Germany |
| Author_xml | – sequence: 1 givenname: Lia surname: Walcher fullname: Walcher, Lia – sequence: 2 givenname: Ann-Kathrin surname: Kistenmacher fullname: Kistenmacher, Ann-Kathrin – sequence: 3 givenname: Huizhen surname: Suo fullname: Suo, Huizhen – sequence: 4 givenname: Reni surname: Kitte fullname: Kitte, Reni – sequence: 5 givenname: Sarah surname: Dluczek fullname: Dluczek, Sarah – sequence: 6 givenname: Alexander surname: Strauß fullname: Strauß, Alexander – sequence: 7 givenname: André-René surname: Blaudszun fullname: Blaudszun, André-René – sequence: 8 givenname: Tetyana surname: Yevsa fullname: Yevsa, Tetyana – sequence: 9 givenname: Stephan surname: Fricke fullname: Fricke, Stephan – sequence: 10 givenname: Uta surname: Kossatz-Boehlert fullname: Kossatz-Boehlert, Uta |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32849491$$D View this record in MEDLINE/PubMed |
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| Keywords | senescence targeted therapy cancer stem cells biomarkers CAR cells precision therapy |
| Language | English |
| License | Copyright © 2020 Walcher, Kistenmacher, Suo, Kitte, Dluczek, Strauß, Blaudszun, Yevsa, Fricke and Kossatz-Boehlert. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Reviewed by: Alessandro Poggi, San Martino Hospital (IRCCS), Italy; Xinhui Wang, Harvard Medical School, United States These authors have contributed equally to this work These authors have contributed equally to this work and share first authorship Edited by: Frank Preijers, Radboud University Nijmegen Medical Centre, Netherlands This article was submitted to Cancer Immunity and Immunotherapy, a section of the journal Frontiers in Immunology |
| OpenAccessLink | https://doaj.org/article/d9e7af0f5f55475aa3f7080f45e2a71f |
| PMID | 32849491 |
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| PublicationDate | 2020-08-07 |
| PublicationDateYYYYMMDD | 2020-08-07 |
| PublicationDate_xml | – month: 08 year: 2020 text: 2020-08-07 day: 07 |
| PublicationDecade | 2020 |
| PublicationPlace | Switzerland |
| PublicationPlace_xml | – name: Switzerland |
| PublicationTitle | Frontiers in immunology |
| PublicationTitleAlternate | Front Immunol |
| PublicationYear | 2020 |
| Publisher | Frontiers Media S.A |
| Publisher_xml | – name: Frontiers Media S.A |
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| Title | Cancer Stem Cells—Origins and Biomarkers: Perspectives for Targeted Personalized Therapies |
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