Cancer stem cells in human gastrointestinal cancer
Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Gastrointestinal cancers are the most common malignancies and still the most frequent cause...
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description | Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Gastrointestinal cancers are the most common malignancies and still the most frequent cause of cancer‐related mortality worldwide. Because gastrointestinal CSCs are also thought to be resistant to conventional therapies, an effective and novel cancer treatment is imperative. The first reported CSCs in a gastrointestinal tumor were found in colorectal cancer in 2007. Subsequently, CSCs were reported in other gastrointestinal cancers, such as esophagus, stomach, liver, and pancreas. Specific phenotypes could be used to distinguish CSCs from non‐CSCs. For example, gastrointestinal CSCs express unique surface markers, exist in a side‐population fraction, show high aldehyde dehydrogenase‐1 activity, form tumorspheres when cultured in non‐adherent conditions, and demonstrate high tumorigenic potential in immunocompromised mice. The signal transduction pathways in gastrointestinal CSCs are similar to those involved in normal embryonic development. Moreover, CSCs are modified by the aberrant expression of several microRNAs. Thus, it is very difficult to target gastrointestinal CSCs. This review focuses on the current research on gastrointestinal CSCs and future strategies to abolish the gastrointestinal CSC phenotype.
Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Therefore, since CSCs are thought to be highly resistant to conventional therapies, an effective and novel cancer treatment would need to eliminate CSCs. This review focuses on current research on gastrointestinal CSCs and future strategies to abolish the CSC phenotype. |
doi_str_mv | 10.1111/cas.13069 |
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Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Therefore, since CSCs are thought to be highly resistant to conventional therapies, an effective and novel cancer treatment would need to eliminate CSCs. This review focuses on current research on gastrointestinal CSCs and future strategies to abolish the CSC phenotype.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.13069</identifier><identifier>PMID: 27575869</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Aldehyde dehydrogenase ; Biomarkers, Tumor - metabolism ; Breast cancer ; Cancer ; Cancer stem cell ; Cancer therapies ; Cell adhesion & migration ; Chemotherapy ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - pathology ; Dehydrogenases ; drug resistance ; Embryogenesis ; Esophageal Neoplasms - pathology ; Esophagus ; Gastric cancer ; gastrointestinal cancer ; Gastrointestinal Neoplasms - drug therapy ; Gastrointestinal Neoplasms - metabolism ; Gastrointestinal Neoplasms - pathology ; Growth factors ; Humans ; Hypoxia ; Invasiveness ; Kinases ; Liver cancer ; Liver Neoplasms - pathology ; Metastases ; Metastasis ; MicroRNAs ; miRNA ; neoplasm metastasis ; Neoplastic Stem Cells - drug effects ; Neoplastic Stem Cells - metabolism ; Neoplastic Stem Cells - pathology ; Ovarian cancer ; Pancreas ; Pancreatic Neoplasms - pathology ; phenotype of cancer stem cell ; Phenotypes ; Prostate ; Proteins ; Review ; Signal transduction ; Signal Transduction - drug effects ; Stem cell transplantation ; Stem cells ; Stomach Neoplasms - pathology ; Surface markers ; Tumors</subject><ispartof>Cancer science, 2016-11, Vol.107 (11), p.1556-1562</ispartof><rights>2016 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2016. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5669-424f2837c8d8be8ff9e23a41066de18b96e0c2a83335e7d6359b29867a52e9983</citedby><cites>FETCH-LOGICAL-c5669-424f2837c8d8be8ff9e23a41066de18b96e0c2a83335e7d6359b29867a52e9983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5132287/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5132287/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27575869$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Taniguchi, Hiroaki</creatorcontrib><creatorcontrib>Moriya, Chiharu</creatorcontrib><creatorcontrib>Igarashi, Hisayoshi</creatorcontrib><creatorcontrib>Saitoh, Anri</creatorcontrib><creatorcontrib>Yamamoto, Hiroyuki</creatorcontrib><creatorcontrib>Adachi, Yasushi</creatorcontrib><creatorcontrib>Imai, Kohzoh</creatorcontrib><title>Cancer stem cells in human gastrointestinal cancer</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Gastrointestinal cancers are the most common malignancies and still the most frequent cause of cancer‐related mortality worldwide. Because gastrointestinal CSCs are also thought to be resistant to conventional therapies, an effective and novel cancer treatment is imperative. The first reported CSCs in a gastrointestinal tumor were found in colorectal cancer in 2007. Subsequently, CSCs were reported in other gastrointestinal cancers, such as esophagus, stomach, liver, and pancreas. Specific phenotypes could be used to distinguish CSCs from non‐CSCs. For example, gastrointestinal CSCs express unique surface markers, exist in a side‐population fraction, show high aldehyde dehydrogenase‐1 activity, form tumorspheres when cultured in non‐adherent conditions, and demonstrate high tumorigenic potential in immunocompromised mice. The signal transduction pathways in gastrointestinal CSCs are similar to those involved in normal embryonic development. Moreover, CSCs are modified by the aberrant expression of several microRNAs. Thus, it is very difficult to target gastrointestinal CSCs. This review focuses on the current research on gastrointestinal CSCs and future strategies to abolish the gastrointestinal CSC phenotype.
Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Therefore, since CSCs are thought to be highly resistant to conventional therapies, an effective and novel cancer treatment would need to eliminate CSCs. This review focuses on current research on gastrointestinal CSCs and future strategies to abolish the CSC phenotype.</description><subject>Aldehyde dehydrogenase</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer stem cell</subject><subject>Cancer therapies</subject><subject>Cell adhesion & migration</subject><subject>Chemotherapy</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Dehydrogenases</subject><subject>drug resistance</subject><subject>Embryogenesis</subject><subject>Esophageal Neoplasms - pathology</subject><subject>Esophagus</subject><subject>Gastric cancer</subject><subject>gastrointestinal cancer</subject><subject>Gastrointestinal Neoplasms - drug therapy</subject><subject>Gastrointestinal Neoplasms - metabolism</subject><subject>Gastrointestinal Neoplasms - pathology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Invasiveness</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>Liver Neoplasms - pathology</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>miRNA</subject><subject>neoplasm metastasis</subject><subject>Neoplastic Stem Cells - drug effects</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Ovarian cancer</subject><subject>Pancreas</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>phenotype of cancer stem cell</subject><subject>Phenotypes</subject><subject>Prostate</subject><subject>Proteins</subject><subject>Review</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Stem cell transplantation</subject><subject>Stem cells</subject><subject>Stomach Neoplasms - pathology</subject><subject>Surface markers</subject><subject>Tumors</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkUlLxDAYhoMo7gf_gBS86KHjlz25CMPgBoIH9RzSNNVKlzFplfn3dhYHFQRzSSAPT743L0JHGEZ4WOfOxhGmIPQG2sWU6VQCiM3FWaYaKNlBezG-AlDBNNtGO0RyyZXQu4hMbON8SGLn68T5qopJ2SQvfW2b5NnGLrRl0_nYlY2tErdgD9BWYavoD1f7Pnq6unyc3KR399e3k_Fd6rgQOmWEFURR6VSuMq-KQntCLcMgRO6xyrTw4IhVlFLuZS4o1xnRSkjLidda0X10sfRO-6z2ufNNF2xlpqGsbZiZ1pbm501Tvpjn9t1wTAlRchCcrgShfeuHEKYu4zyjbXzbR4MVB6kkEPUPlDEBAjAM6Mkv9LXtw_A90RCigXAJbP722ZJyoY0x-GI9NwYzL80MpZlFaQN7_D3omvxqaQDOl8BHWfnZ3yYzGT8slZ_wPp7o</recordid><startdate>201611</startdate><enddate>201611</enddate><creator>Taniguchi, Hiroaki</creator><creator>Moriya, Chiharu</creator><creator>Igarashi, Hisayoshi</creator><creator>Saitoh, Anri</creator><creator>Yamamoto, Hiroyuki</creator><creator>Adachi, Yasushi</creator><creator>Imai, Kohzoh</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</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>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>7TO</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>201611</creationdate><title>Cancer stem cells in human gastrointestinal cancer</title><author>Taniguchi, Hiroaki ; Moriya, Chiharu ; Igarashi, Hisayoshi ; Saitoh, Anri ; Yamamoto, Hiroyuki ; Adachi, Yasushi ; Imai, Kohzoh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5669-424f2837c8d8be8ff9e23a41066de18b96e0c2a83335e7d6359b29867a52e9983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Aldehyde dehydrogenase</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer stem cell</topic><topic>Cancer therapies</topic><topic>Cell adhesion & migration</topic><topic>Chemotherapy</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Dehydrogenases</topic><topic>drug resistance</topic><topic>Embryogenesis</topic><topic>Esophageal Neoplasms - pathology</topic><topic>Esophagus</topic><topic>Gastric cancer</topic><topic>gastrointestinal cancer</topic><topic>Gastrointestinal Neoplasms - drug therapy</topic><topic>Gastrointestinal Neoplasms - metabolism</topic><topic>Gastrointestinal Neoplasms - pathology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Invasiveness</topic><topic>Kinases</topic><topic>Liver cancer</topic><topic>Liver Neoplasms - pathology</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>miRNA</topic><topic>neoplasm metastasis</topic><topic>Neoplastic Stem Cells - drug effects</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Ovarian cancer</topic><topic>Pancreas</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>phenotype of cancer stem cell</topic><topic>Phenotypes</topic><topic>Prostate</topic><topic>Proteins</topic><topic>Review</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Stem cell transplantation</topic><topic>Stem cells</topic><topic>Stomach Neoplasms - pathology</topic><topic>Surface markers</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Taniguchi, Hiroaki</creatorcontrib><creatorcontrib>Moriya, Chiharu</creatorcontrib><creatorcontrib>Igarashi, Hisayoshi</creatorcontrib><creatorcontrib>Saitoh, Anri</creatorcontrib><creatorcontrib>Yamamoto, Hiroyuki</creatorcontrib><creatorcontrib>Adachi, Yasushi</creatorcontrib><creatorcontrib>Imai, Kohzoh</creatorcontrib><collection>Wiley-Blackwell Open Access Titles</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Taniguchi, Hiroaki</au><au>Moriya, Chiharu</au><au>Igarashi, Hisayoshi</au><au>Saitoh, Anri</au><au>Yamamoto, Hiroyuki</au><au>Adachi, Yasushi</au><au>Imai, Kohzoh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cancer stem cells in human gastrointestinal cancer</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2016-11</date><risdate>2016</risdate><volume>107</volume><issue>11</issue><spage>1556</spage><epage>1562</epage><pages>1556-1562</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Gastrointestinal cancers are the most common malignancies and still the most frequent cause of cancer‐related mortality worldwide. Because gastrointestinal CSCs are also thought to be resistant to conventional therapies, an effective and novel cancer treatment is imperative. The first reported CSCs in a gastrointestinal tumor were found in colorectal cancer in 2007. Subsequently, CSCs were reported in other gastrointestinal cancers, such as esophagus, stomach, liver, and pancreas. Specific phenotypes could be used to distinguish CSCs from non‐CSCs. For example, gastrointestinal CSCs express unique surface markers, exist in a side‐population fraction, show high aldehyde dehydrogenase‐1 activity, form tumorspheres when cultured in non‐adherent conditions, and demonstrate high tumorigenic potential in immunocompromised mice. The signal transduction pathways in gastrointestinal CSCs are similar to those involved in normal embryonic development. Moreover, CSCs are modified by the aberrant expression of several microRNAs. Thus, it is very difficult to target gastrointestinal CSCs. This review focuses on the current research on gastrointestinal CSCs and future strategies to abolish the gastrointestinal CSC phenotype.
Cancer stem cells (CSCs) are thought to be responsible for tumor initiation, drug and radiation resistance, invasive growth, metastasis, and tumor relapse, which are the main causes of cancer‐related deaths. Therefore, since CSCs are thought to be highly resistant to conventional therapies, an effective and novel cancer treatment would need to eliminate CSCs. This review focuses on current research on gastrointestinal CSCs and future strategies to abolish the CSC phenotype.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>27575869</pmid><doi>10.1111/cas.13069</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Aldehyde dehydrogenase Biomarkers, Tumor - metabolism Breast cancer Cancer Cancer stem cell Cancer therapies Cell adhesion & migration Chemotherapy Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - pathology Dehydrogenases drug resistance Embryogenesis Esophageal Neoplasms - pathology Esophagus Gastric cancer gastrointestinal cancer Gastrointestinal Neoplasms - drug therapy Gastrointestinal Neoplasms - metabolism Gastrointestinal Neoplasms - pathology Growth factors Humans Hypoxia Invasiveness Kinases Liver cancer Liver Neoplasms - pathology Metastases Metastasis MicroRNAs miRNA neoplasm metastasis Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Ovarian cancer Pancreas Pancreatic Neoplasms - pathology phenotype of cancer stem cell Phenotypes Prostate Proteins Review Signal transduction Signal Transduction - drug effects Stem cell transplantation Stem cells Stomach Neoplasms - pathology Surface markers Tumors |
title | Cancer stem cells in human gastrointestinal cancer |
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