Complement Pathway is Frequently Altered in Endometriosis and Endometriosis-Associated Ovarian Cancer
Identifieur interne : 003761 ( Main/Exploration ); précédent : 003760; suivant : 003762Complement Pathway is Frequently Altered in Endometriosis and Endometriosis-Associated Ovarian Cancer
Auteurs : Swati Suryawanshi ; Xin Huang ; Esther Elishaev ; Raluca A. Budiu ; Lixin Zhang ; Sunghwan Kim [États-Unis] ; Nicole Donnellan ; Gina Mantia-Smaldone [États-Unis] ; Tianzhou Ma [États-Unis] ; George Tseng [États-Unis] ; Ted Lee ; Suketu Mansuria ; Robert Edwards ; Anda M. VladSource :
- Clinical cancer research : an official journal of the American Association for Cancer Research [ 1078-0432 ] ; 2014.
Descripteurs français
- KwdFr :
- Activation du complément (génétique), Activation du complément (immunologie), Adulte, Adulte d'âge moyen, Analyse de profil d'expression de gènes, Analyse de regroupements, Animaux, Cellules épithéliales (métabolisme), Complément C7 (génétique), Complément C7 (immunologie), Endométriose (), Endométriose (anatomopathologie), Endométriose (génétique), Endométriose (immunologie), Facteurs de risque, Femelle, Humains, Modèles animaux de maladie humaine, Prolifération cellulaire, Protéines du système du complément (génétique), Protéines du système du complément (immunologie), Régulation de l'expression des gènes, Souris, Sujet âgé, Surveillance immunologique, Techniques de knock-down de gènes, Transformation cellulaire néoplasique (immunologie), Tumeurs de l'ovaire (anatomopathologie), Tumeurs de l'ovaire (étiologie).
- MESH :
- anatomopathologie : Endométriose, Tumeurs de l'ovaire.
- génétique : Activation du complément, Complément C7, Endométriose, Protéines du système du complément.
- immunologie : Activation du complément, Complément C7, Endométriose, Protéines du système du complément, Transformation cellulaire néoplasique.
- métabolisme : Cellules épithéliales.
- étiologie : Tumeurs de l'ovaire.
- Adulte, Adulte d'âge moyen, Analyse de profil d'expression de gènes, Analyse de regroupements, Animaux, Endométriose, Facteurs de risque, Femelle, Humains, Modèles animaux de maladie humaine, Prolifération cellulaire, Régulation de l'expression des gènes, Souris, Sujet âgé, Surveillance immunologique, Techniques de knock-down de gènes.
English descriptors
- KwdEn :
- Adult, Aged, Animals, Cell Proliferation, Cell Transformation, Neoplastic (immunology), Cluster Analysis, Complement Activation (genetics), Complement Activation (immunology), Complement C7 (genetics), Complement C7 (immunology), Complement System Proteins (genetics), Complement System Proteins (immunology), Disease Models, Animal, Endometriosis (complications), Endometriosis (genetics), Endometriosis (immunology), Endometriosis (pathology), Epithelial Cells (metabolism), Female, Gene Expression Profiling, Gene Expression Regulation, Gene Knockdown Techniques, Humans, Immunologic Surveillance, Mice, Middle Aged, Ovarian Neoplasms (etiology), Ovarian Neoplasms (pathology), Risk Factors.
- MESH :
- chemical , genetics : Complement C7, Complement System Proteins.
- complications : Endometriosis.
- etiology : Ovarian Neoplasms.
- genetics : Complement Activation, Endometriosis.
- immunology : Cell Transformation, Neoplastic, Complement Activation, Complement C7, Complement System Proteins, Endometriosis.
- metabolism : Epithelial Cells.
- pathology : Endometriosis, Ovarian Neoplasms.
- Adult, Aged, Animals, Cell Proliferation, Cluster Analysis, Disease Models, Animal, Female, Gene Expression Profiling, Gene Expression Regulation, Gene Knockdown Techniques, Humans, Immunologic Surveillance, Mice, Middle Aged, Risk Factors.
Abstract
Mechanisms of immune dysregulation associated with advanced tumors are relatively well understood. Much less is known about the role of immune effectors against cancer precursor lesions. Endometrioid and clear cell ovarian tumors partly derive from endometriosis, a commonly diagnosed chronic inflammatory disease. We performed here a comprehensive immune gene expression analysis of pelvic inflammation in endometriosis and endometriosis-associated ovarian cancer (EAOC).
RNA was extracted from 120 paraffin tissue blocks comprising of normal endometrium (n=32), benign endometriosis (n=30), atypical endometriosis (n=15) and EAOC (n=43). Serous tumors (n=15) were included as non-endometriosis associated controls. The immune microenvironment was profiled using Nanostring and the nCounter® GX Human Immunology Kit, comprising probes for a total of 511 immune genes.
One third of the endometriosis patients revealed a tumor-like inflammation profile, suggesting that cancer–like immune signatures may develop earlier, in patients classified as clinically benign. Gene expression analyses revealed the complement pathway as most prominently involved in both endometriosis and EAOC. Complement proteins are abundantly present in epithelial cells in both benign and malignant lesions. Mechanistic studies in ovarian surface epithelial (OSE) cells from mice with conditional (Cre-loxP) mutations show intrinsic production of complement in epithelia and demonstrate an early link between Kras- and Pten-driven pathways and complement upregulation. Downregulation of complement in these cells interferes with cell proliferation.
These findings reveal new characteristics of inflammation in precursor lesions and point to previously unknown roles of complement in endometriosis and EAOC.
Url:
DOI: 10.1158/1078-0432.CCR-14-1338
PubMed: 25294912
PubMed Central: 4252715
Affiliations:
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Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Complement Pathway is Frequently Altered in Endometriosis and Endometriosis-Associated Ovarian Cancer</title>
<author><name sortKey="Suryawanshi, Swati" sort="Suryawanshi, Swati" uniqKey="Suryawanshi S" first="Swati" last="Suryawanshi">Swati Suryawanshi</name>
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<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
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<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
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<author><name sortKey="Elishaev, Esther" sort="Elishaev, Esther" uniqKey="Elishaev E" first="Esther" last="Elishaev">Esther Elishaev</name>
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<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
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<author><name sortKey="Zhang, Lixin" sort="Zhang, Lixin" uniqKey="Zhang L" first="Lixin" last="Zhang">Lixin Zhang</name>
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<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
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<author><name sortKey="Kim, Sunghwan" sort="Kim, Sunghwan" uniqKey="Kim S" first="Sunghwan" last="Kim">Sunghwan Kim</name>
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<author><name sortKey="Donnellan, Nicole" sort="Donnellan, Nicole" uniqKey="Donnellan N" first="Nicole" last="Donnellan">Nicole Donnellan</name>
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<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
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<author><name sortKey="Mantia Smaldone, Gina" sort="Mantia Smaldone, Gina" uniqKey="Mantia Smaldone G" first="Gina" last="Mantia-Smaldone">Gina Mantia-Smaldone</name>
<affiliation wicri:level="2"><nlm:aff id="A5">Section of Gynecologic Oncology, Department of Surgical Oncology, Fox Chase Cancer Center, Philadelphia, PA</nlm:aff>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Pennsylvanie</region>
</placeName>
<wicri:cityArea>Section of Gynecologic Oncology, Department of Surgical Oncology, Fox Chase Cancer Center, Philadelphia</wicri:cityArea>
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<author><name sortKey="Ma, Tianzhou" sort="Ma, Tianzhou" uniqKey="Ma T" first="Tianzhou" last="Ma">Tianzhou Ma</name>
<affiliation wicri:level="4"><nlm:aff id="A4">Department of Statistics University of Pittsburgh, Graduate School of Public Health, Pittsburgh PA</nlm:aff>
<orgName type="university">Université de Pittsburgh</orgName>
<country>États-Unis</country>
<placeName><settlement type="city">Pittsburgh</settlement>
<region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
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<author><name sortKey="Tseng, George" sort="Tseng, George" uniqKey="Tseng G" first="George" last="Tseng">George Tseng</name>
<affiliation wicri:level="4"><nlm:aff id="A4">Department of Statistics University of Pittsburgh, Graduate School of Public Health, Pittsburgh PA</nlm:aff>
<orgName type="university">Université de Pittsburgh</orgName>
<country>États-Unis</country>
<placeName><settlement type="city">Pittsburgh</settlement>
<region type="state">Pennsylvanie</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lee, Ted" sort="Lee, Ted" uniqKey="Lee T" first="Ted" last="Lee">Ted Lee</name>
<affiliation><nlm:aff id="A3">Magee Women’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh PA</nlm:aff>
<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Mansuria, Suketu" sort="Mansuria, Suketu" uniqKey="Mansuria S" first="Suketu" last="Mansuria">Suketu Mansuria</name>
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<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Edwards, Robert" sort="Edwards, Robert" uniqKey="Edwards R" first="Robert" last="Edwards">Robert Edwards</name>
<affiliation><nlm:aff id="A1">Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine and Magee Womens Research Institute, Pittsburgh PA</nlm:aff>
<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
<affiliation><nlm:aff id="A3">Magee Women’s Hospital of Pittsburgh, University of Pittsburgh Medical Center, Pittsburgh PA</nlm:aff>
<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
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<author><name sortKey="Vlad, Anda M" sort="Vlad, Anda M" uniqKey="Vlad A" first="Anda M." last="Vlad">Anda M. Vlad</name>
<affiliation><nlm:aff id="A1">Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine and Magee Womens Research Institute, Pittsburgh PA</nlm:aff>
<wicri:noCountry code="subfield">Pittsburgh PA</wicri:noCountry>
</affiliation>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Animals</term>
<term>Cell Proliferation</term>
<term>Cell Transformation, Neoplastic (immunology)</term>
<term>Cluster Analysis</term>
<term>Complement Activation (genetics)</term>
<term>Complement Activation (immunology)</term>
<term>Complement C7 (genetics)</term>
<term>Complement C7 (immunology)</term>
<term>Complement System Proteins (genetics)</term>
<term>Complement System Proteins (immunology)</term>
<term>Disease Models, Animal</term>
<term>Endometriosis (complications)</term>
<term>Endometriosis (genetics)</term>
<term>Endometriosis (immunology)</term>
<term>Endometriosis (pathology)</term>
<term>Epithelial Cells (metabolism)</term>
<term>Female</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Gene Knockdown Techniques</term>
<term>Humans</term>
<term>Immunologic Surveillance</term>
<term>Mice</term>
<term>Middle Aged</term>
<term>Ovarian Neoplasms (etiology)</term>
<term>Ovarian Neoplasms (pathology)</term>
<term>Risk Factors</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation du complément (génétique)</term>
<term>Activation du complément (immunologie)</term>
<term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Analyse de profil d'expression de gènes</term>
<term>Analyse de regroupements</term>
<term>Animaux</term>
<term>Cellules épithéliales (métabolisme)</term>
<term>Complément C7 (génétique)</term>
<term>Complément C7 (immunologie)</term>
<term>Endométriose ()</term>
<term>Endométriose (anatomopathologie)</term>
<term>Endométriose (génétique)</term>
<term>Endométriose (immunologie)</term>
<term>Facteurs de risque</term>
<term>Femelle</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Prolifération cellulaire</term>
<term>Protéines du système du complément (génétique)</term>
<term>Protéines du système du complément (immunologie)</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris</term>
<term>Sujet âgé</term>
<term>Surveillance immunologique</term>
<term>Techniques de knock-down de gènes</term>
<term>Transformation cellulaire néoplasique (immunologie)</term>
<term>Tumeurs de l'ovaire (anatomopathologie)</term>
<term>Tumeurs de l'ovaire (étiologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Complement C7</term>
<term>Complement System Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Endométriose</term>
<term>Tumeurs de l'ovaire</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Endometriosis</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Ovarian Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Complement Activation</term>
<term>Endometriosis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Activation du complément</term>
<term>Complément C7</term>
<term>Endométriose</term>
<term>Protéines du système du complément</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Activation du complément</term>
<term>Complément C7</term>
<term>Endométriose</term>
<term>Protéines du système du complément</term>
<term>Transformation cellulaire néoplasique</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Cell Transformation, Neoplastic</term>
<term>Complement Activation</term>
<term>Complement C7</term>
<term>Complement System Proteins</term>
<term>Endometriosis</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Epithelial Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules épithéliales</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endometriosis</term>
<term>Ovarian Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Tumeurs de l'ovaire</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Animals</term>
<term>Cell Proliferation</term>
<term>Cluster Analysis</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Gene Expression Profiling</term>
<term>Gene Expression Regulation</term>
<term>Gene Knockdown Techniques</term>
<term>Humans</term>
<term>Immunologic Surveillance</term>
<term>Mice</term>
<term>Middle Aged</term>
<term>Risk Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte</term>
<term>Adulte d'âge moyen</term>
<term>Analyse de profil d'expression de gènes</term>
<term>Analyse de regroupements</term>
<term>Animaux</term>
<term>Endométriose</term>
<term>Facteurs de risque</term>
<term>Femelle</term>
<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Prolifération cellulaire</term>
<term>Régulation de l'expression des gènes</term>
<term>Souris</term>
<term>Sujet âgé</term>
<term>Surveillance immunologique</term>
<term>Techniques de knock-down de gènes</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><sec id="S1"><title>Purpose</title>
<p id="P1">Mechanisms of immune dysregulation associated with advanced tumors are relatively well understood. Much less is known about the role of immune effectors against cancer precursor lesions. Endometrioid and clear cell ovarian tumors partly derive from endometriosis, a commonly diagnosed chronic inflammatory disease. We performed here a comprehensive immune gene expression analysis of pelvic inflammation in endometriosis and endometriosis-associated ovarian cancer (EAOC).</p>
</sec>
<sec id="S2"><title>Experimental design</title>
<p id="P2">RNA was extracted from 120 paraffin tissue blocks comprising of normal endometrium (n=32), benign endometriosis (n=30), atypical endometriosis (n=15) and EAOC (n=43). Serous tumors (n=15) were included as non-endometriosis associated controls. The immune microenvironment was profiled using Nanostring and the nCounter® GX Human Immunology Kit, comprising probes for a total of 511 immune genes.</p>
</sec>
<sec id="S3"><title>Results</title>
<p id="P3">One third of the endometriosis patients revealed a tumor-like inflammation profile, suggesting that cancer–like immune signatures may develop earlier, in patients classified as clinically benign. Gene expression analyses revealed the complement pathway as most prominently involved in both endometriosis and EAOC. Complement proteins are abundantly present in epithelial cells in both benign and malignant lesions. Mechanistic studies in ovarian surface epithelial (OSE) cells from mice with conditional (Cre-loxP) mutations show intrinsic production of complement in epithelia and demonstrate an early link between Kras- and Pten-driven pathways and complement upregulation. Downregulation of complement in these cells interferes with cell proliferation.</p>
</sec>
<sec id="S4"><title>Conclusions</title>
<p id="P4">These findings reveal new characteristics of inflammation in precursor lesions and point to previously unknown roles of complement in endometriosis and EAOC.</p>
</sec>
</div>
</front>
</TEI>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Pennsylvanie</li>
</region>
<settlement><li>Pittsburgh</li>
</settlement>
<orgName><li>Université de Pittsburgh</li>
</orgName>
</list>
<tree><noCountry><name sortKey="Budiu, Raluca A" sort="Budiu, Raluca A" uniqKey="Budiu R" first="Raluca A." last="Budiu">Raluca A. Budiu</name>
<name sortKey="Donnellan, Nicole" sort="Donnellan, Nicole" uniqKey="Donnellan N" first="Nicole" last="Donnellan">Nicole Donnellan</name>
<name sortKey="Edwards, Robert" sort="Edwards, Robert" uniqKey="Edwards R" first="Robert" last="Edwards">Robert Edwards</name>
<name sortKey="Elishaev, Esther" sort="Elishaev, Esther" uniqKey="Elishaev E" first="Esther" last="Elishaev">Esther Elishaev</name>
<name sortKey="Huang, Xin" sort="Huang, Xin" uniqKey="Huang X" first="Xin" last="Huang">Xin Huang</name>
<name sortKey="Lee, Ted" sort="Lee, Ted" uniqKey="Lee T" first="Ted" last="Lee">Ted Lee</name>
<name sortKey="Mansuria, Suketu" sort="Mansuria, Suketu" uniqKey="Mansuria S" first="Suketu" last="Mansuria">Suketu Mansuria</name>
<name sortKey="Suryawanshi, Swati" sort="Suryawanshi, Swati" uniqKey="Suryawanshi S" first="Swati" last="Suryawanshi">Swati Suryawanshi</name>
<name sortKey="Vlad, Anda M" sort="Vlad, Anda M" uniqKey="Vlad A" first="Anda M." last="Vlad">Anda M. Vlad</name>
<name sortKey="Zhang, Lixin" sort="Zhang, Lixin" uniqKey="Zhang L" first="Lixin" last="Zhang">Lixin Zhang</name>
</noCountry>
<country name="États-Unis"><region name="Pennsylvanie"><name sortKey="Kim, Sunghwan" sort="Kim, Sunghwan" uniqKey="Kim S" first="Sunghwan" last="Kim">Sunghwan Kim</name>
</region>
<name sortKey="Ma, Tianzhou" sort="Ma, Tianzhou" uniqKey="Ma T" first="Tianzhou" last="Ma">Tianzhou Ma</name>
<name sortKey="Mantia Smaldone, Gina" sort="Mantia Smaldone, Gina" uniqKey="Mantia Smaldone G" first="Gina" last="Mantia-Smaldone">Gina Mantia-Smaldone</name>
<name sortKey="Tseng, George" sort="Tseng, George" uniqKey="Tseng G" first="George" last="Tseng">George Tseng</name>
</country>
</tree>
</affiliations>
</record>
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