Cancer stem cells with increased metastatic potential as a therapeutic target for esophageal cancer
Abstract Esophageal cancers (EC) are highly aggressive tumors, commonly presented in a locally advanced stage with a poor prognosis and survival. Up to 50% of the patients are eligible for treated with curative intent and receive the standard treatment with neoadjuvant chemoradiotherapy (nCRT) and s...
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Veröffentlicht in: | Seminars in cancer biology 2017-06, Vol.44, p.60-66 |
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description | Abstract Esophageal cancers (EC) are highly aggressive tumors, commonly presented in a locally advanced stage with a poor prognosis and survival. Up to 50% of the patients are eligible for treated with curative intent and receive the standard treatment with neoadjuvant chemoradiotherapy (nCRT) and surgery. Currently, pathologic complete response to nCRT is 20-30%, with a partial or no response in about 50% and 20%, respectively. EC recurrences occur frequently even after successful anti-cancer treatment, suggesting high aggressiveness with increased metastatic potential. A tumor sub-population of so-called cancer stem cells (CSCs), is known to display a high metastatic potential and resistance to conventional anti-cancer therapy, hereby being responsible for the unbeneficial clinical features. In this review, a concise overview will be given of the current literature on esophageal CSCs and related metastases. Esophageal CSC markers will be discussed followed by the pathways that initiate and sustain these cells. In addition, the cellular processes, epithelial-mesenchymal transition (EMT), hypoxia and autophagy, known to contribute to cancer stemness and metastasis will be explained. Finally, potential option for treatment also related to cancer genome atlas (TCGA) data on EC will be discussed. |
doi_str_mv | 10.1016/j.semcancer.2017.03.010 |
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Up to 50% of the patients are eligible for treated with curative intent and receive the standard treatment with neoadjuvant chemoradiotherapy (nCRT) and surgery. Currently, pathologic complete response to nCRT is 20-30%, with a partial or no response in about 50% and 20%, respectively. EC recurrences occur frequently even after successful anti-cancer treatment, suggesting high aggressiveness with increased metastatic potential. A tumor sub-population of so-called cancer stem cells (CSCs), is known to display a high metastatic potential and resistance to conventional anti-cancer therapy, hereby being responsible for the unbeneficial clinical features. In this review, a concise overview will be given of the current literature on esophageal CSCs and related metastases. Esophageal CSC markers will be discussed followed by the pathways that initiate and sustain these cells. In addition, the cellular processes, epithelial-mesenchymal transition (EMT), hypoxia and autophagy, known to contribute to cancer stemness and metastasis will be explained. Finally, potential option for treatment also related to cancer genome atlas (TCGA) data on EC will be discussed.</description><identifier>ISSN: 1044-579X</identifier><identifier>EISSN: 1096-3650</identifier><identifier>DOI: 10.1016/j.semcancer.2017.03.010</identifier><identifier>PMID: 28366541</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Autophagy - drug effects ; Cancer stem cells ; Cell Hypoxia - drug effects ; Epithelial-Mesenchymal Transition - drug effects ; Esophageal Neoplasms - drug therapy ; Esophageal Neoplasms - genetics ; Esophageal Neoplasms - pathology ; Hematology, Oncology and Palliative Medicine ; Humans ; Metastases and esophageal cancer ; Neoadjuvant Therapy - methods ; Neoplasm Metastasis ; Neoplastic Stem Cells - drug effects</subject><ispartof>Seminars in cancer biology, 2017-06, Vol.44, p.60-66</ispartof><rights>2017 The Authors</rights><rights>Copyright © 2017 The Authors. Published by Elsevier Ltd.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-58c25342cfde2acb862aa16ed371815930aac3bc57534bd5c3626a6bd096a5bf3</citedby><cites>FETCH-LOGICAL-c475t-58c25342cfde2acb862aa16ed371815930aac3bc57534bd5c3626a6bd096a5bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1044579X17300822$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28366541$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, D</creatorcontrib><creatorcontrib>Plukker, J.Th.M</creatorcontrib><creatorcontrib>Coppes, R.P</creatorcontrib><title>Cancer stem cells with increased metastatic potential as a therapeutic target for esophageal cancer</title><title>Seminars in cancer biology</title><addtitle>Semin Cancer Biol</addtitle><description>Abstract Esophageal cancers (EC) are highly aggressive tumors, commonly presented in a locally advanced stage with a poor prognosis and survival. Up to 50% of the patients are eligible for treated with curative intent and receive the standard treatment with neoadjuvant chemoradiotherapy (nCRT) and surgery. Currently, pathologic complete response to nCRT is 20-30%, with a partial or no response in about 50% and 20%, respectively. EC recurrences occur frequently even after successful anti-cancer treatment, suggesting high aggressiveness with increased metastatic potential. A tumor sub-population of so-called cancer stem cells (CSCs), is known to display a high metastatic potential and resistance to conventional anti-cancer therapy, hereby being responsible for the unbeneficial clinical features. In this review, a concise overview will be given of the current literature on esophageal CSCs and related metastases. Esophageal CSC markers will be discussed followed by the pathways that initiate and sustain these cells. In addition, the cellular processes, epithelial-mesenchymal transition (EMT), hypoxia and autophagy, known to contribute to cancer stemness and metastasis will be explained. Finally, potential option for treatment also related to cancer genome atlas (TCGA) data on EC will be discussed.</description><subject>Autophagy - drug effects</subject><subject>Cancer stem cells</subject><subject>Cell Hypoxia - drug effects</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Esophageal Neoplasms - drug therapy</subject><subject>Esophageal Neoplasms - genetics</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Humans</subject><subject>Metastases and esophageal cancer</subject><subject>Neoadjuvant Therapy - methods</subject><subject>Neoplasm Metastasis</subject><subject>Neoplastic Stem Cells - drug effects</subject><issn>1044-579X</issn><issn>1096-3650</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUtv1TAQhSMEoqXwF8BLNgl-xE6yQaquCkWq1EWp1J01mUx6fckL2ynqv8fhli5YsbIln3PG55ss-yB4Ibgwnw5FoBFhQvKF5KIquCq44C-yU8Ebkyuj-cvtXpa5rpq7k-xNCAfOeVOK8nV2ImtljC7FaYa7PyEsRBoZ0jAE9svFPXMTeoJAHRspQogQHbJljjRFBwODwIDFPXlYaN2eIvh7iqyfPaMwL3u4pyQ7_vBt9qqHIdC7p_Msu_1y8X13mV9df_22O7_Ksax0zHWNUqtSYt-RBGxrIwGEoU5Voha6URwAVYu6Sqq206iMNGDaLjUG3fbqLPt4zF38_HOlEO3owtYJJprXYEVdq1o1iUKSVkcp-jkET71dvBvBP1rB7UbYHuwzYbsRtlzZRDg53z8NWduRumffX6RJcH4UUKr64JI9oKOU0zlPGG03u_8Y8vmfDBzc5BCGH_RI4TCvfkokrbBBWm5vtkVvexaV4ryWUv0G7LqnbQ</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Wang, D</creator><creator>Plukker, J.Th.M</creator><creator>Coppes, R.P</creator><general>Elsevier Ltd</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170601</creationdate><title>Cancer stem cells with increased metastatic potential as a therapeutic target for esophageal cancer</title><author>Wang, D ; Plukker, J.Th.M ; Coppes, R.P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-58c25342cfde2acb862aa16ed371815930aac3bc57534bd5c3626a6bd096a5bf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Autophagy - drug effects</topic><topic>Cancer stem cells</topic><topic>Cell Hypoxia - drug effects</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Esophageal Neoplasms - drug therapy</topic><topic>Esophageal Neoplasms - genetics</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Humans</topic><topic>Metastases and esophageal cancer</topic><topic>Neoadjuvant Therapy - methods</topic><topic>Neoplasm Metastasis</topic><topic>Neoplastic Stem Cells - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, D</creatorcontrib><creatorcontrib>Plukker, J.Th.M</creatorcontrib><creatorcontrib>Coppes, R.P</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Seminars in cancer biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, D</au><au>Plukker, J.Th.M</au><au>Coppes, R.P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer stem cells with increased metastatic potential as a therapeutic target for esophageal cancer</atitle><jtitle>Seminars in cancer biology</jtitle><addtitle>Semin Cancer Biol</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>44</volume><spage>60</spage><epage>66</epage><pages>60-66</pages><issn>1044-579X</issn><eissn>1096-3650</eissn><abstract>Abstract Esophageal cancers (EC) are highly aggressive tumors, commonly presented in a locally advanced stage with a poor prognosis and survival. Up to 50% of the patients are eligible for treated with curative intent and receive the standard treatment with neoadjuvant chemoradiotherapy (nCRT) and surgery. Currently, pathologic complete response to nCRT is 20-30%, with a partial or no response in about 50% and 20%, respectively. EC recurrences occur frequently even after successful anti-cancer treatment, suggesting high aggressiveness with increased metastatic potential. A tumor sub-population of so-called cancer stem cells (CSCs), is known to display a high metastatic potential and resistance to conventional anti-cancer therapy, hereby being responsible for the unbeneficial clinical features. In this review, a concise overview will be given of the current literature on esophageal CSCs and related metastases. Esophageal CSC markers will be discussed followed by the pathways that initiate and sustain these cells. In addition, the cellular processes, epithelial-mesenchymal transition (EMT), hypoxia and autophagy, known to contribute to cancer stemness and metastasis will be explained. Finally, potential option for treatment also related to cancer genome atlas (TCGA) data on EC will be discussed.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>28366541</pmid><doi>10.1016/j.semcancer.2017.03.010</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Autophagy - drug effects Cancer stem cells Cell Hypoxia - drug effects Epithelial-Mesenchymal Transition - drug effects Esophageal Neoplasms - drug therapy Esophageal Neoplasms - genetics Esophageal Neoplasms - pathology Hematology, Oncology and Palliative Medicine Humans Metastases and esophageal cancer Neoadjuvant Therapy - methods Neoplasm Metastasis Neoplastic Stem Cells - drug effects |
title | Cancer stem cells with increased metastatic potential as a therapeutic target for esophageal cancer |
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