Cells with stem‐like properties are associated with the development of HPV18‐positive cervical cancer
The cellular origins of cervical cancer and the histological differentiation of human papillomavirus (HPV)‐infected cells remain unexplained. To gain new insights into the carcinogenesis and histological differentiation of HPV‐associated cervical cancer, we focused on cervical cancer with mixed hist...
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Veröffentlicht in: | Cancer science 2023-03, Vol.114 (3), p.885-895 |
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creator | Kusakabe, Misako Taguchi, Ayumi Tanikawa, Michihiro Wagatsuma, Ryota Yamazaki, Miki Tsuchimochi, Saki Toyohara, Yusuke Kawata, Akira Baba, Satoshi Ueno, Toshihide Sone, Kenbun Mori‐Uchino, Mayuyo Ikemura, Masako Matsunaga, Hiroko Nagamatsu, Takeshi Wada‐Hiraike, Osamu Kawazu, Masahito Ushiku, Tetsuo Takeyama, Haruko Oda, Katsutoshi Kawana, Kei Mano, Hiroyuki Osuga, Yutaka |
description | The cellular origins of cervical cancer and the histological differentiation of human papillomavirus (HPV)‐infected cells remain unexplained. To gain new insights into the carcinogenesis and histological differentiation of HPV‐associated cervical cancer, we focused on cervical cancer with mixed histological types. We conducted genomic and transcriptomic analyses of cervical cancers with mixed histological types. The commonality of the cellular origins of these cancers was inferred using phylogenetic analysis and by assessing the HPV integration sites. Carcinogenesis was estimated by analyzing human gene expression profiles in different histological types. Among 42 cervical cancers with known HPV types, mixed histological types were detected in four cases, and three of them were HPV18‐positive. Phylogenetic analysis of these three cases revealed that the different histological types had a common cell of origin. Moreover, the HPV‐derived transcriptome and HPV integration sites were common among different histological types, suggesting that HPV integration could occur before differentiation into each histological type. Human gene expression profiles indicated that HPV18‐positive cancer retained immunologically cold components with stem cell properties. Mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer.
To gain new insights into the carcinogenesis and histological differentiation of human papillomavirus (HPV)‐associated cervical cancer, we conducted genomic and transcriptomic analyses of cervical cancer with mixed histological types. The results suggest that mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer. In addition, cells with stem‐like properties are immunologically cold. |
doi_str_mv | 10.1111/cas.15664 |
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To gain new insights into the carcinogenesis and histological differentiation of human papillomavirus (HPV)‐associated cervical cancer, we conducted genomic and transcriptomic analyses of cervical cancer with mixed histological types. The results suggest that mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer. In addition, cells with stem‐like properties are immunologically cold.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.15664</identifier><identifier>PMID: 36404139</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Antigens ; Carcinogenesis ; cell of origin ; Cervical cancer ; Cloning ; DNA, Viral - genetics ; Female ; Gene expression ; Genes ; Genomes ; Human papillomavirus ; Human papillomavirus 18 - genetics ; Humans ; Integration ; Mutation ; Original ; Papillomaviridae - genetics ; Papillomavirus Infections ; Phylogenetics ; Phylogeny ; Principal components analysis ; Progenitor cells ; Software ; stem cell ; Transcription factors ; Transcriptomes ; Transcriptomics ; tumor immunogenicity ; Uterine Cervical Neoplasms - pathology</subject><ispartof>Cancer science, 2023-03, Vol.114 (3), p.885-895</ispartof><rights>2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2023. This work is published under http://creativecommons.org/licenses/by-nc/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-c4674-fef6dcb6682551de34e3a72fc33871a14ba2e2ad041de313fa94be78752005293</citedby><cites>FETCH-LOGICAL-c4674-fef6dcb6682551de34e3a72fc33871a14ba2e2ad041de313fa94be78752005293</cites><orcidid>0000-0002-7218-6401 ; 0000-0002-5491-3871 ; 0000-0001-5400-7521 ; 0000-0002-2468-9573 ; 0000-0003-4645-0181</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9986059/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9986059/$$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/36404139$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kusakabe, Misako</creatorcontrib><creatorcontrib>Taguchi, Ayumi</creatorcontrib><creatorcontrib>Tanikawa, Michihiro</creatorcontrib><creatorcontrib>Wagatsuma, Ryota</creatorcontrib><creatorcontrib>Yamazaki, Miki</creatorcontrib><creatorcontrib>Tsuchimochi, Saki</creatorcontrib><creatorcontrib>Toyohara, Yusuke</creatorcontrib><creatorcontrib>Kawata, Akira</creatorcontrib><creatorcontrib>Baba, Satoshi</creatorcontrib><creatorcontrib>Ueno, Toshihide</creatorcontrib><creatorcontrib>Sone, Kenbun</creatorcontrib><creatorcontrib>Mori‐Uchino, Mayuyo</creatorcontrib><creatorcontrib>Ikemura, Masako</creatorcontrib><creatorcontrib>Matsunaga, Hiroko</creatorcontrib><creatorcontrib>Nagamatsu, Takeshi</creatorcontrib><creatorcontrib>Wada‐Hiraike, Osamu</creatorcontrib><creatorcontrib>Kawazu, Masahito</creatorcontrib><creatorcontrib>Ushiku, Tetsuo</creatorcontrib><creatorcontrib>Takeyama, Haruko</creatorcontrib><creatorcontrib>Oda, Katsutoshi</creatorcontrib><creatorcontrib>Kawana, Kei</creatorcontrib><creatorcontrib>Mano, Hiroyuki</creatorcontrib><creatorcontrib>Osuga, Yutaka</creatorcontrib><title>Cells with stem‐like properties are associated with the development of HPV18‐positive cervical cancer</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>The cellular origins of cervical cancer and the histological differentiation of human papillomavirus (HPV)‐infected cells remain unexplained. To gain new insights into the carcinogenesis and histological differentiation of HPV‐associated cervical cancer, we focused on cervical cancer with mixed histological types. We conducted genomic and transcriptomic analyses of cervical cancers with mixed histological types. The commonality of the cellular origins of these cancers was inferred using phylogenetic analysis and by assessing the HPV integration sites. Carcinogenesis was estimated by analyzing human gene expression profiles in different histological types. Among 42 cervical cancers with known HPV types, mixed histological types were detected in four cases, and three of them were HPV18‐positive. Phylogenetic analysis of these three cases revealed that the different histological types had a common cell of origin. Moreover, the HPV‐derived transcriptome and HPV integration sites were common among different histological types, suggesting that HPV integration could occur before differentiation into each histological type. Human gene expression profiles indicated that HPV18‐positive cancer retained immunologically cold components with stem cell properties. Mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer.
To gain new insights into the carcinogenesis and histological differentiation of human papillomavirus (HPV)‐associated cervical cancer, we conducted genomic and transcriptomic analyses of cervical cancer with mixed histological types. The results suggest that mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer. In addition, cells with stem‐like properties are immunologically cold.</description><subject>Antigens</subject><subject>Carcinogenesis</subject><subject>cell of origin</subject><subject>Cervical cancer</subject><subject>Cloning</subject><subject>DNA, Viral - genetics</subject><subject>Female</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genomes</subject><subject>Human papillomavirus</subject><subject>Human papillomavirus 18 - genetics</subject><subject>Humans</subject><subject>Integration</subject><subject>Mutation</subject><subject>Original</subject><subject>Papillomaviridae - genetics</subject><subject>Papillomavirus Infections</subject><subject>Phylogenetics</subject><subject>Phylogeny</subject><subject>Principal components analysis</subject><subject>Progenitor cells</subject><subject>Software</subject><subject>stem cell</subject><subject>Transcription factors</subject><subject>Transcriptomes</subject><subject>Transcriptomics</subject><subject>tumor immunogenicity</subject><subject>Uterine Cervical Neoplasms - 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genetics</topic><topic>Female</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genomes</topic><topic>Human papillomavirus</topic><topic>Human papillomavirus 18 - genetics</topic><topic>Humans</topic><topic>Integration</topic><topic>Mutation</topic><topic>Original</topic><topic>Papillomaviridae - genetics</topic><topic>Papillomavirus Infections</topic><topic>Phylogenetics</topic><topic>Phylogeny</topic><topic>Principal components analysis</topic><topic>Progenitor cells</topic><topic>Software</topic><topic>stem cell</topic><topic>Transcription factors</topic><topic>Transcriptomes</topic><topic>Transcriptomics</topic><topic>tumor immunogenicity</topic><topic>Uterine Cervical Neoplasms - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kusakabe, Misako</creatorcontrib><creatorcontrib>Taguchi, Ayumi</creatorcontrib><creatorcontrib>Tanikawa, Michihiro</creatorcontrib><creatorcontrib>Wagatsuma, Ryota</creatorcontrib><creatorcontrib>Yamazaki, Miki</creatorcontrib><creatorcontrib>Tsuchimochi, Saki</creatorcontrib><creatorcontrib>Toyohara, Yusuke</creatorcontrib><creatorcontrib>Kawata, Akira</creatorcontrib><creatorcontrib>Baba, Satoshi</creatorcontrib><creatorcontrib>Ueno, Toshihide</creatorcontrib><creatorcontrib>Sone, Kenbun</creatorcontrib><creatorcontrib>Mori‐Uchino, Mayuyo</creatorcontrib><creatorcontrib>Ikemura, Masako</creatorcontrib><creatorcontrib>Matsunaga, Hiroko</creatorcontrib><creatorcontrib>Nagamatsu, Takeshi</creatorcontrib><creatorcontrib>Wada‐Hiraike, Osamu</creatorcontrib><creatorcontrib>Kawazu, Masahito</creatorcontrib><creatorcontrib>Ushiku, Tetsuo</creatorcontrib><creatorcontrib>Takeyama, Haruko</creatorcontrib><creatorcontrib>Oda, Katsutoshi</creatorcontrib><creatorcontrib>Kawana, Kei</creatorcontrib><creatorcontrib>Mano, Hiroyuki</creatorcontrib><creatorcontrib>Osuga, Yutaka</creatorcontrib><collection>Wiley Online Library 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>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>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kusakabe, Misako</au><au>Taguchi, Ayumi</au><au>Tanikawa, Michihiro</au><au>Wagatsuma, Ryota</au><au>Yamazaki, Miki</au><au>Tsuchimochi, Saki</au><au>Toyohara, Yusuke</au><au>Kawata, Akira</au><au>Baba, Satoshi</au><au>Ueno, Toshihide</au><au>Sone, Kenbun</au><au>Mori‐Uchino, Mayuyo</au><au>Ikemura, Masako</au><au>Matsunaga, Hiroko</au><au>Nagamatsu, Takeshi</au><au>Wada‐Hiraike, Osamu</au><au>Kawazu, Masahito</au><au>Ushiku, Tetsuo</au><au>Takeyama, Haruko</au><au>Oda, Katsutoshi</au><au>Kawana, Kei</au><au>Mano, Hiroyuki</au><au>Osuga, Yutaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cells with stem‐like properties are associated with the development of HPV18‐positive cervical cancer</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2023-03</date><risdate>2023</risdate><volume>114</volume><issue>3</issue><spage>885</spage><epage>895</epage><pages>885-895</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>The cellular origins of cervical cancer and the histological differentiation of human papillomavirus (HPV)‐infected cells remain unexplained. To gain new insights into the carcinogenesis and histological differentiation of HPV‐associated cervical cancer, we focused on cervical cancer with mixed histological types. We conducted genomic and transcriptomic analyses of cervical cancers with mixed histological types. The commonality of the cellular origins of these cancers was inferred using phylogenetic analysis and by assessing the HPV integration sites. Carcinogenesis was estimated by analyzing human gene expression profiles in different histological types. Among 42 cervical cancers with known HPV types, mixed histological types were detected in four cases, and three of them were HPV18‐positive. Phylogenetic analysis of these three cases revealed that the different histological types had a common cell of origin. Moreover, the HPV‐derived transcriptome and HPV integration sites were common among different histological types, suggesting that HPV integration could occur before differentiation into each histological type. Human gene expression profiles indicated that HPV18‐positive cancer retained immunologically cold components with stem cell properties. Mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer.
To gain new insights into the carcinogenesis and histological differentiation of human papillomavirus (HPV)‐associated cervical cancer, we conducted genomic and transcriptomic analyses of cervical cancer with mixed histological types. The results suggest that mixed cervical cancer has a common cellular origin among different histological types, and progenitor cells with stem‐like properties may be associated with the development of HPV18‐positive cervical cancer. In addition, cells with stem‐like properties are immunologically cold.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>36404139</pmid><doi>10.1111/cas.15664</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-7218-6401</orcidid><orcidid>https://orcid.org/0000-0002-5491-3871</orcidid><orcidid>https://orcid.org/0000-0001-5400-7521</orcidid><orcidid>https://orcid.org/0000-0002-2468-9573</orcidid><orcidid>https://orcid.org/0000-0003-4645-0181</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Antigens Carcinogenesis cell of origin Cervical cancer Cloning DNA, Viral - genetics Female Gene expression Genes Genomes Human papillomavirus Human papillomavirus 18 - genetics Humans Integration Mutation Original Papillomaviridae - genetics Papillomavirus Infections Phylogenetics Phylogeny Principal components analysis Progenitor cells Software stem cell Transcription factors Transcriptomes Transcriptomics tumor immunogenicity Uterine Cervical Neoplasms - pathology |
title | Cells with stem‐like properties are associated with the development of HPV18‐positive cervical cancer |
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