Loading…

Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment

Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity...

Full description

Saved in:
Bibliographic Details
Published in:PLoS biology 2016-09, Vol.14 (9), p.e1002537
Main Authors: Tamori, Yoichiro, Suzuki, Emiko, Deng, Wu-Min
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293
cites cdi_FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293
container_end_page
container_issue 9
container_start_page e1002537
container_title PLoS biology
container_volume 14
creator Tamori, Yoichiro
Suzuki, Emiko
Deng, Wu-Min
description Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this "tumor hotspot" where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the "tumor coldspot" nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism.
doi_str_mv 10.1371/journal.pbio.1002537
format article
fullrecord <record><control><sourceid>gale_plos_</sourceid><recordid>TN_cdi_plos_journals_1829444259</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A476858358</galeid><doaj_id>oai_doaj_org_article_8da3067896494571acf6db140dbd5715</doaj_id><sourcerecordid>A476858358</sourcerecordid><originalsourceid>FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293</originalsourceid><addsrcrecordid>eNqVksFu1DAQhiMEomXhDRBE4gISu9iOHTsXpKoqdKXCSmXhajnJOPUqsbd2UsHb47Bp1aAeQHEUZ_LN75nJnyQvMVrhjOMPOzd4q9rVvjRuhREiLOOPkmPMKFtyIdjje_uj5FkIu8iQgoinyRHhTFBO6HFyebY3_RW0RrXpduicD-nGm8ZY1UNq7CGWnrs-7OP9PlXp1oQwwHJte29sMFX6xVTegb0x3tkObP88eaJVG-DF9Fwk3z-dbU_Plxebz-vTk4tlxQvaLzUnSCEmsowUuiI6r3NMGFW6hBxqpbDGnBekZBwJQngNCHKkiNZABAJSZIvk9UF337ogp3EEiQUpKKWEjcT6QNRO7eTem075X9IpI_8EnG-k8r2pWpCiVhnKuShyWlDGsapiQSWmqC7r-Mqi1sfptKHsoK5io161M9H5F2uuZONuJENIcDoW83YS8O56gNDLzoQK2lZZcMNYd8azDPGCR_TNX-jD3U1Uo2IDxmoXz61GUXlCeS7iaONaJKsHqHjV0JnKWdAmxmcJ72YJkenhZ9-oIQS5_nb5H-zXf2c3P-YsPbDRWSF40HdzxkiO7r8diBzdLyf3x7RX9__RXdKt3bPfdof--w</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1829444259</pqid></control><display><type>article</type><title>Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment</title><source>Publicly Available Content Database</source><source>PubMed Central</source><creator>Tamori, Yoichiro ; Suzuki, Emiko ; Deng, Wu-Min</creator><contributor>Edgar, Bruce A</contributor><creatorcontrib>Tamori, Yoichiro ; Suzuki, Emiko ; Deng, Wu-Min ; Edgar, Bruce A</creatorcontrib><description>Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this "tumor hotspot" where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the "tumor coldspot" nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism.</description><identifier>ISSN: 1545-7885</identifier><identifier>ISSN: 1544-9173</identifier><identifier>EISSN: 1545-7885</identifier><identifier>DOI: 10.1371/journal.pbio.1002537</identifier><identifier>PMID: 27584724</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Biology and Life Sciences ; Cancer cells ; Carcinogenesis ; Cell interaction ; Cloning ; Drosophila ; Drosophila melanogaster ; Drosophila Proteins - genetics ; Drosophila Proteins - metabolism ; Epithelial cells ; Epithelial Cells - physiology ; Funding ; Gene Knockdown Techniques ; Genes ; Genetics ; Health aspects ; Imaginal Discs - pathology ; Insects ; Janus Kinases - metabolism ; Kinases ; Life sciences ; Medicine and Health Sciences ; Microtubules - metabolism ; Neoplasms, Glandular and Epithelial - pathology ; Organ Specificity ; Physical Sciences ; Protein Transport ; Research and Analysis Methods ; RNA Interference ; Rodents ; Signal Transduction ; STAT Transcription Factors - metabolism ; Studies ; Transcription Factors - metabolism ; Tumor Microenvironment ; Tumor necrosis factor-TNF ; Tumorigenesis ; Tumors</subject><ispartof>PLoS biology, 2016-09, Vol.14 (9), p.e1002537</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Tamori Y, Suzuki E, Deng W-M (2016) Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment. PLoS Biol 14(9): e1002537. doi:10.1371/journal.pbio.1002537</rights><rights>2016 Tamori et al 2016 Tamori et al</rights><rights>2016 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Tamori Y, Suzuki E, Deng W-M (2016) Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment. PLoS Biol 14(9): e1002537. doi:10.1371/journal.pbio.1002537</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293</citedby><cites>FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1829444259/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1829444259?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27584724$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Edgar, Bruce A</contributor><creatorcontrib>Tamori, Yoichiro</creatorcontrib><creatorcontrib>Suzuki, Emiko</creatorcontrib><creatorcontrib>Deng, Wu-Min</creatorcontrib><title>Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment</title><title>PLoS biology</title><addtitle>PLoS Biol</addtitle><description>Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this "tumor hotspot" where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the "tumor coldspot" nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism.</description><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Cancer cells</subject><subject>Carcinogenesis</subject><subject>Cell interaction</subject><subject>Cloning</subject><subject>Drosophila</subject><subject>Drosophila melanogaster</subject><subject>Drosophila Proteins - genetics</subject><subject>Drosophila Proteins - metabolism</subject><subject>Epithelial cells</subject><subject>Epithelial Cells - physiology</subject><subject>Funding</subject><subject>Gene Knockdown Techniques</subject><subject>Genes</subject><subject>Genetics</subject><subject>Health aspects</subject><subject>Imaginal Discs - pathology</subject><subject>Insects</subject><subject>Janus Kinases - metabolism</subject><subject>Kinases</subject><subject>Life sciences</subject><subject>Medicine and Health Sciences</subject><subject>Microtubules - metabolism</subject><subject>Neoplasms, Glandular and Epithelial - pathology</subject><subject>Organ Specificity</subject><subject>Physical Sciences</subject><subject>Protein Transport</subject><subject>Research and Analysis Methods</subject><subject>RNA Interference</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>STAT Transcription Factors - metabolism</subject><subject>Studies</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor Microenvironment</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1545-7885</issn><issn>1544-9173</issn><issn>1545-7885</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNqVksFu1DAQhiMEomXhDRBE4gISu9iOHTsXpKoqdKXCSmXhajnJOPUqsbd2UsHb47Bp1aAeQHEUZ_LN75nJnyQvMVrhjOMPOzd4q9rVvjRuhREiLOOPkmPMKFtyIdjje_uj5FkIu8iQgoinyRHhTFBO6HFyebY3_RW0RrXpduicD-nGm8ZY1UNq7CGWnrs-7OP9PlXp1oQwwHJte29sMFX6xVTegb0x3tkObP88eaJVG-DF9Fwk3z-dbU_Plxebz-vTk4tlxQvaLzUnSCEmsowUuiI6r3NMGFW6hBxqpbDGnBekZBwJQngNCHKkiNZABAJSZIvk9UF337ogp3EEiQUpKKWEjcT6QNRO7eTem075X9IpI_8EnG-k8r2pWpCiVhnKuShyWlDGsapiQSWmqC7r-Mqi1sfptKHsoK5io161M9H5F2uuZONuJENIcDoW83YS8O56gNDLzoQK2lZZcMNYd8azDPGCR_TNX-jD3U1Uo2IDxmoXz61GUXlCeS7iaONaJKsHqHjV0JnKWdAmxmcJ72YJkenhZ9-oIQS5_nb5H-zXf2c3P-YsPbDRWSF40HdzxkiO7r8diBzdLyf3x7RX9__RXdKt3bPfdof--w</recordid><startdate>201609</startdate><enddate>201609</enddate><creator>Tamori, Yoichiro</creator><creator>Suzuki, Emiko</creator><creator>Deng, Wu-Min</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><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>IOV</scope><scope>ISN</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PATMY</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope><scope>CZG</scope></search><sort><creationdate>201609</creationdate><title>Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment</title><author>Tamori, Yoichiro ; Suzuki, Emiko ; Deng, Wu-Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Cancer cells</topic><topic>Carcinogenesis</topic><topic>Cell interaction</topic><topic>Cloning</topic><topic>Drosophila</topic><topic>Drosophila melanogaster</topic><topic>Drosophila Proteins - genetics</topic><topic>Drosophila Proteins - metabolism</topic><topic>Epithelial cells</topic><topic>Epithelial Cells - physiology</topic><topic>Funding</topic><topic>Gene Knockdown Techniques</topic><topic>Genes</topic><topic>Genetics</topic><topic>Health aspects</topic><topic>Imaginal Discs - pathology</topic><topic>Insects</topic><topic>Janus Kinases - metabolism</topic><topic>Kinases</topic><topic>Life sciences</topic><topic>Medicine and Health Sciences</topic><topic>Microtubules - metabolism</topic><topic>Neoplasms, Glandular and Epithelial - pathology</topic><topic>Organ Specificity</topic><topic>Physical Sciences</topic><topic>Protein Transport</topic><topic>Research and Analysis Methods</topic><topic>RNA Interference</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>STAT Transcription Factors - metabolism</topic><topic>Studies</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor Microenvironment</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tamori, Yoichiro</creatorcontrib><creatorcontrib>Suzuki, Emiko</creatorcontrib><creatorcontrib>Deng, Wu-Min</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Opposing Viewpoints Resource Center</collection><collection>Gale In Context: Canada</collection><collection>Science in Context</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Agricultural &amp; Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental 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>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><collection>PLoS Biology</collection><jtitle>PLoS biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tamori, Yoichiro</au><au>Suzuki, Emiko</au><au>Deng, Wu-Min</au><au>Edgar, Bruce A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment</atitle><jtitle>PLoS biology</jtitle><addtitle>PLoS Biol</addtitle><date>2016-09</date><risdate>2016</risdate><volume>14</volume><issue>9</issue><spage>e1002537</spage><pages>e1002537-</pages><issn>1545-7885</issn><issn>1544-9173</issn><eissn>1545-7885</eissn><abstract>Malignant tumors are caused by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tissue integrity. Although a number of causative genetic backgrounds for tumor development have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger tumorigenesis remain elusive. Here, we show through analysis of conserved neoplastic tumor-suppressor genes (nTSGs) in Drosophila wing imaginal disc epithelia that tumor initiation depends on tissue-intrinsic local cytoarchitectures, causing tumors to consistently originate in a specific region of the tissue. In this "tumor hotspot" where cells constitute a network of robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the epithelium and begin tumorigenic overgrowth by exploiting endogenous Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling activity. Conversely, in other regions, the "tumor coldspot" nTSG-deficient cells are extruded toward the basal side and undergo apoptosis. When the direction of delamination is reversed through suppression of RhoGEF2, an activator of the Rho family small GTPases, and JAK/STAT is activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced. These data indicate that two independent processes, apical delamination and JAK/STAT activation, are concurrently required for the initiation of nTSG-deficient-induced tumorigenesis. Given the conservation of the epithelial cytoarchitecture, tumorigenesis may be generally initiated from tumor hotspots by a similar mechanism.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27584724</pmid><doi>10.1371/journal.pbio.1002537</doi><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1545-7885
ispartof PLoS biology, 2016-09, Vol.14 (9), p.e1002537
issn 1545-7885
1544-9173
1545-7885
language eng
recordid cdi_plos_journals_1829444259
source Publicly Available Content Database; PubMed Central
subjects Animals
Biology and Life Sciences
Cancer cells
Carcinogenesis
Cell interaction
Cloning
Drosophila
Drosophila melanogaster
Drosophila Proteins - genetics
Drosophila Proteins - metabolism
Epithelial cells
Epithelial Cells - physiology
Funding
Gene Knockdown Techniques
Genes
Genetics
Health aspects
Imaginal Discs - pathology
Insects
Janus Kinases - metabolism
Kinases
Life sciences
Medicine and Health Sciences
Microtubules - metabolism
Neoplasms, Glandular and Epithelial - pathology
Organ Specificity
Physical Sciences
Protein Transport
Research and Analysis Methods
RNA Interference
Rodents
Signal Transduction
STAT Transcription Factors - metabolism
Studies
Transcription Factors - metabolism
Tumor Microenvironment
Tumor necrosis factor-TNF
Tumorigenesis
Tumors
title Epithelial Tumors Originate in Tumor Hotspots, a Tissue-Intrinsic Microenvironment
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T09%3A34%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Epithelial%20Tumors%20Originate%20in%20Tumor%20Hotspots,%20a%20Tissue-Intrinsic%20Microenvironment&rft.jtitle=PLoS%20biology&rft.au=Tamori,%20Yoichiro&rft.date=2016-09&rft.volume=14&rft.issue=9&rft.spage=e1002537&rft.pages=e1002537-&rft.issn=1545-7885&rft.eissn=1545-7885&rft_id=info:doi/10.1371/journal.pbio.1002537&rft_dat=%3Cgale_plos_%3EA476858358%3C/gale_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c794t-f720a0583329fc2f6d61254afbe6edaa1f17792b5708227de0e60a2ffe280e293%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1829444259&rft_id=info:pmid/27584724&rft_galeid=A476858358&rfr_iscdi=true