High incidence of mammary intraepithelial neoplasia development in Men1‐disrupted murine mammary glands
Identifieur interne : 004A48 ( Main/Exploration ); précédent : 004A47; suivant : 004A49High incidence of mammary intraepithelial neoplasia development in Men1‐disrupted murine mammary glands
Auteurs : Christelle Seigne [France] ; Magdalena Auret [Australie] ; Isabelle Treilleux [France] ; Rémy Bonnavion [France] ; Fouzia Assade [France] ; Christine Carreira [France] ; Sophie Goddard-Léon [France] ; Emilie Lavergne [France] ; Sylvie Chabaud [France] ; Amandine Garcia [France] ; Sylvie Mazoyer [France] ; Jieli Lu [France] ; Thomas Bachelot [France] ; Lucien Frappart [France] ; Chang Xian Zhang [France]Source :
- The Journal of Pathology [ 0022-3417 ] ; 2013-03.
Descripteurs français
- Wicri :
- topic : Droit d'auteur, Recherche médicale.
English descriptors
- KwdEn :
- Adenosquamous, Adenosquamous carcinoma, Adenosquamous carcinomas, Allele, Annapolis pathology panel, Breast cancer, Breast cancer patients, Breast cancers, Carcinoma, Cell biol, Centre, Cohort, Control mice, Copyright, Corresponding percentage, Epithelial, Epithelial cells, Female mice, Gland, Gland development, Great britain, Heterozygous men1, Histological, Histological category, Human breast cancers, Inactivation, John wiley sons, Large proportion, Leakage, Lesion, Luminal, Luminal cells, Lyon, Mammary, Mammary carcinomas, Mammary cells, Mammary epithelial cells, Mammary epithelium, Mammary gland, Mammary glands, Mammary glands lesions, Mammary lesions, Mammary tumourigenesis, Mcf7 cells, Medical research, Membrane expression, Men1, Men1 control mice, Men1 disruption, Men1 gene, Men1 inactivation, Menin, Menin detection, Menin expression, Menin inactivation, Mouse, Mutant, Mutant mice, Mutation, Nuclear staining, Oestrogen receptor, Overall survival, Oxed, Pathol, Pathological society, Pituitary leakage, Pituitary tumour development, Proc natl acad, Prolactin, Prolactinoma development, Prolactinomas, Queensland institute, Rard, Representative images, Seigne, Staining intensity, Supplementary materials, Third pregnancy, Total number, Transgene, Transgenic mice, Tumour, Wapcre, Wapcremen1 mice.
- Teeft :
- Adenosquamous, Adenosquamous carcinoma, Adenosquamous carcinomas, Allele, Annapolis pathology panel, Breast cancer, Breast cancer patients, Breast cancers, Carcinoma, Cell biol, Centre, Cohort, Control mice, Copyright, Corresponding percentage, Epithelial, Epithelial cells, Female mice, Gland, Gland development, Great britain, Heterozygous men1, Histological, Histological category, Human breast cancers, Inactivation, John wiley sons, Large proportion, Leakage, Lesion, Luminal, Luminal cells, Lyon, Mammary, Mammary carcinomas, Mammary cells, Mammary epithelial cells, Mammary epithelium, Mammary gland, Mammary glands, Mammary glands lesions, Mammary lesions, Mammary tumourigenesis, Mcf7 cells, Medical research, Membrane expression, Men1, Men1 control mice, Men1 disruption, Men1 gene, Men1 inactivation, Menin, Menin detection, Menin expression, Menin inactivation, Mouse, Mutant, Mutant mice, Mutation, Nuclear staining, Oestrogen receptor, Overall survival, Oxed, Pathol, Pathological society, Pituitary leakage, Pituitary tumour development, Proc natl acad, Prolactin, Prolactinoma development, Prolactinomas, Queensland institute, Rard, Representative images, Seigne, Staining intensity, Supplementary materials, Third pregnancy, Total number, Transgene, Transgenic mice, Tumour, Wapcre, Wapcremen1 mice.
Abstract
Mutations of the MEN1 tumour suppressor gene predispose patients to the development of multiple endocrine neoplasia type 1 (MEN1) syndrome, which is characterized by multiple endocrine tumours, including prolactinomas. The recent findings of the interaction between menin, encoded by the MEN1 gene, and the oestrogen receptor, as well as the observation of rare cases of mammary carcinomas in our heterozygous Men1 mutant mice, led us to investigate a putative tumour suppressor function of the Men1 gene in mouse mammary cells by disrupting the gene in luminal epithelial cells. A significantly higher incidence of mammary intraepithelial neoplasia (MIN) was observed in mutant WapCre‐Men1F/F mice (51.5%) than in WapCre‐Men1+/+ (0%) or Men1F/F (7.1%) control mice. The majority of MIN observed in the mutant mice displayed complete menin inactivation. Because of the leakage of WapCre transgene expression, prolactinomas were observed in 83.3% of mutant mice, leading to premature death. As there was no correlation between MIN development and elevated serum prolactin levels, and phospho‐STAT5 expression was decreased in mammary lesions, the increased incidence of MIN lesions was most likely due to Men1 disruption rather than to prolactinoma development. Interestingly, in MIN lesions, we found a decrease in membrane‐associated E‐cadherin and beta‐catenin expression, the latter of which is a menin partner. Finally, reduced menin expression was found in a large proportion of two independent cohorts of patients with breast carcinomas. Taken together, the current work indicates a role of Men1 inactivation in the development of mammary pre‐cancerous lesions in mice and a potential role in human mammary cancer.
Url:
DOI: 10.1002/path.4146
Affiliations:
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Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>CNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Université de Lyon 1, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation></author><author><name sortKey="Mazoyer, Sylvie" sort="Mazoyer, Sylvie" uniqKey="Mazoyer S" first="Sylvie" last="Mazoyer">Sylvie Mazoyer</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Université Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Inserm U1052, Centre de Recherche en Cancérologie de Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>CNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement 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Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation></author><author><name sortKey="Frappart, Lucien" sort="Frappart, Lucien" uniqKey="Frappart L" first="Lucien" last="Frappart">Lucien Frappart</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Département de Pathologie, Hôpital Edouard Herriot, HCL, F‐69437, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation></author><author><name sortKey="Zhang, Chang Xian" sort="Zhang, Chang Xian" uniqKey="Zhang C" first="Chang Xian" last="Zhang">Chang Xian Zhang</name><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Université Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Inserm U1052, Centre de Recherche en Cancérologie de Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>CNRS UMR5286, Centre de Recherche en Cancérologie de Lyon, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="3"><country xml:lang="fr">France</country><wicri:regionArea>Université de Lyon 1, F‐69000, Lyon</wicri:regionArea><placeName><settlement type="city">Lyon</settlement><region type="region" nuts="2">Auvergne-Rhône-Alpes</region><region type="old region" nuts="2">Rhône-Alpes</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">France</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">The Journal of Pathology</title><title level="j" type="alt">THE JOURNAL OF PATHOLOGY</title><idno type="ISSN">0022-3417</idno><idno type="eISSN">1096-9896</idno><imprint><biblScope unit="vol">229</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="546">546</biblScope><biblScope unit="page" to="558">558</biblScope><biblScope unit="page-count">13</biblScope><publisher>John Wiley & Sons, Ltd</publisher><pubPlace>Chichester, UK</pubPlace><date type="published" when="2013-03">2013-03</date></imprint><idno type="ISSN">0022-3417</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0022-3417</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosquamous</term><term>Adenosquamous carcinoma</term><term>Adenosquamous carcinomas</term><term>Allele</term><term>Annapolis pathology panel</term><term>Breast cancer</term><term>Breast cancer patients</term><term>Breast cancers</term><term>Carcinoma</term><term>Cell biol</term><term>Centre</term><term>Cohort</term><term>Control mice</term><term>Copyright</term><term>Corresponding percentage</term><term>Epithelial</term><term>Epithelial cells</term><term>Female mice</term><term>Gland</term><term>Gland development</term><term>Great britain</term><term>Heterozygous men1</term><term>Histological</term><term>Histological category</term><term>Human breast cancers</term><term>Inactivation</term><term>John wiley sons</term><term>Large proportion</term><term>Leakage</term><term>Lesion</term><term>Luminal</term><term>Luminal cells</term><term>Lyon</term><term>Mammary</term><term>Mammary carcinomas</term><term>Mammary cells</term><term>Mammary epithelial cells</term><term>Mammary epithelium</term><term>Mammary gland</term><term>Mammary glands</term><term>Mammary glands lesions</term><term>Mammary lesions</term><term>Mammary tumourigenesis</term><term>Mcf7 cells</term><term>Medical research</term><term>Membrane expression</term><term>Men1</term><term>Men1 control mice</term><term>Men1 disruption</term><term>Men1 gene</term><term>Men1 inactivation</term><term>Menin</term><term>Menin detection</term><term>Menin expression</term><term>Menin inactivation</term><term>Mouse</term><term>Mutant</term><term>Mutant mice</term><term>Mutation</term><term>Nuclear staining</term><term>Oestrogen receptor</term><term>Overall survival</term><term>Oxed</term><term>Pathol</term><term>Pathological society</term><term>Pituitary leakage</term><term>Pituitary tumour development</term><term>Proc natl acad</term><term>Prolactin</term><term>Prolactinoma development</term><term>Prolactinomas</term><term>Queensland institute</term><term>Rard</term><term>Representative images</term><term>Seigne</term><term>Staining intensity</term><term>Supplementary materials</term><term>Third pregnancy</term><term>Total number</term><term>Transgene</term><term>Transgenic mice</term><term>Tumour</term><term>Wapcre</term><term>Wapcremen1 mice</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Adenosquamous</term><term>Adenosquamous carcinoma</term><term>Adenosquamous carcinomas</term><term>Allele</term><term>Annapolis pathology panel</term><term>Breast cancer</term><term>Breast cancer patients</term><term>Breast cancers</term><term>Carcinoma</term><term>Cell biol</term><term>Centre</term><term>Cohort</term><term>Control mice</term><term>Copyright</term><term>Corresponding percentage</term><term>Epithelial</term><term>Epithelial cells</term><term>Female mice</term><term>Gland</term><term>Gland development</term><term>Great britain</term><term>Heterozygous men1</term><term>Histological</term><term>Histological category</term><term>Human breast cancers</term><term>Inactivation</term><term>John wiley sons</term><term>Large proportion</term><term>Leakage</term><term>Lesion</term><term>Luminal</term><term>Luminal cells</term><term>Lyon</term><term>Mammary</term><term>Mammary carcinomas</term><term>Mammary cells</term><term>Mammary epithelial cells</term><term>Mammary epithelium</term><term>Mammary gland</term><term>Mammary glands</term><term>Mammary glands lesions</term><term>Mammary lesions</term><term>Mammary tumourigenesis</term><term>Mcf7 cells</term><term>Medical research</term><term>Membrane expression</term><term>Men1</term><term>Men1 control mice</term><term>Men1 disruption</term><term>Men1 gene</term><term>Men1 inactivation</term><term>Menin</term><term>Menin detection</term><term>Menin expression</term><term>Menin inactivation</term><term>Mouse</term><term>Mutant</term><term>Mutant mice</term><term>Mutation</term><term>Nuclear staining</term><term>Oestrogen receptor</term><term>Overall survival</term><term>Oxed</term><term>Pathol</term><term>Pathological society</term><term>Pituitary leakage</term><term>Pituitary tumour development</term><term>Proc natl acad</term><term>Prolactin</term><term>Prolactinoma development</term><term>Prolactinomas</term><term>Queensland institute</term><term>Rard</term><term>Representative images</term><term>Seigne</term><term>Staining intensity</term><term>Supplementary materials</term><term>Third pregnancy</term><term>Total number</term><term>Transgene</term><term>Transgenic mice</term><term>Tumour</term><term>Wapcre</term><term>Wapcremen1 mice</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Droit d'auteur</term><term>Recherche médicale</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract">Mutations of the MEN1 tumour suppressor gene predispose patients to the development of multiple endocrine neoplasia type 1 (MEN1) syndrome, which is characterized by multiple endocrine tumours, including prolactinomas. The recent findings of the interaction between menin, encoded by the MEN1 gene, and the oestrogen receptor, as well as the observation of rare cases of mammary carcinomas in our heterozygous Men1 mutant mice, led us to investigate a putative tumour suppressor function of the Men1 gene in mouse mammary cells by disrupting the gene in luminal epithelial cells. A significantly higher incidence of mammary intraepithelial neoplasia (MIN) was observed in mutant WapCre‐Men1F/F mice (51.5%) than in WapCre‐Men1+/+ (0%) or Men1F/F (7.1%) control mice. The majority of MIN observed in the mutant mice displayed complete menin inactivation. Because of the leakage of WapCre transgene expression, prolactinomas were observed in 83.3% of mutant mice, leading to premature death. As there was no correlation between MIN development and elevated serum prolactin levels, and phospho‐STAT5 expression was decreased in mammary lesions, the increased incidence of MIN lesions was most likely due to Men1 disruption rather than to prolactinoma development. Interestingly, in MIN lesions, we found a decrease in membrane‐associated E‐cadherin and beta‐catenin expression, the latter of which is a menin partner. Finally, reduced menin expression was found in a large proportion of two independent cohorts of patients with breast carcinomas. Taken together, the current work indicates a role of Men1 inactivation in the development of mammary pre‐cancerous lesions in mice and a potential role in human mammary cancer.</div></front></TEI><affiliations><list><country><li>Australie</li><li>France</li></country><region><li>Auvergne-Rhône-Alpes</li><li>Rhône-Alpes</li></region><settlement><li>Lyon</li></settlement></list><tree><country name="France"><region name="Auvergne-Rhône-Alpes"><name sortKey="Seigne, Christelle" sort="Seigne, Christelle" uniqKey="Seigne C" first="Christelle" last="Seigne">Christelle Seigne</name></region><name sortKey="Assade, Fouzia" sort="Assade, Fouzia" uniqKey="Assade F" first="Fouzia" last="Assade">Fouzia Assade</name><name sortKey="Assade, Fouzia" sort="Assade, Fouzia" uniqKey="Assade F" first="Fouzia" last="Assade">Fouzia Assade</name><name sortKey="Assade, Fouzia" sort="Assade, Fouzia" uniqKey="Assade F" first="Fouzia" last="Assade">Fouzia Assade</name><name sortKey="Assade, Fouzia" sort="Assade, Fouzia" uniqKey="Assade F" first="Fouzia" last="Assade">Fouzia Assade</name><name sortKey="Bachelot, Thomas" sort="Bachelot, Thomas" uniqKey="Bachelot T" first="Thomas" last="Bachelot">Thomas Bachelot</name><name sortKey="Bonnavion, Remy" sort="Bonnavion, Remy" uniqKey="Bonnavion R" first="Rémy" last="Bonnavion">Rémy Bonnavion</name><name sortKey="Bonnavion, Remy" sort="Bonnavion, Remy" uniqKey="Bonnavion R" first="Rémy" last="Bonnavion">Rémy Bonnavion</name><name sortKey="Bonnavion, Remy" sort="Bonnavion, Remy" uniqKey="Bonnavion R" first="Rémy" last="Bonnavion">Rémy Bonnavion</name><name sortKey="Bonnavion, Remy" sort="Bonnavion, Remy" uniqKey="Bonnavion R" first="Rémy" last="Bonnavion">Rémy Bonnavion</name><name sortKey="Carreira, Christine" sort="Carreira, Christine" uniqKey="Carreira C" first="Christine" last="Carreira">Christine Carreira</name><name sortKey="Carreira, Christine" sort="Carreira, Christine" uniqKey="Carreira C" first="Christine" last="Carreira">Christine Carreira</name><name sortKey="Carreira, Christine" sort="Carreira, Christine" uniqKey="Carreira C" first="Christine" last="Carreira">Christine Carreira</name><name sortKey="Carreira, Christine" sort="Carreira, Christine" uniqKey="Carreira C" first="Christine" last="Carreira">Christine Carreira</name><name sortKey="Chabaud, Sylvie" sort="Chabaud, Sylvie" uniqKey="Chabaud S" first="Sylvie" last="Chabaud">Sylvie Chabaud</name><name sortKey="Frappart, Lucien" sort="Frappart, Lucien" uniqKey="Frappart L" first="Lucien" last="Frappart">Lucien Frappart</name><name sortKey="Garcia, Amandine" sort="Garcia, Amandine" uniqKey="Garcia A" first="Amandine" last="Garcia">Amandine Garcia</name><name sortKey="Garcia, Amandine" sort="Garcia, Amandine" uniqKey="Garcia A" first="Amandine" last="Garcia">Amandine Garcia</name><name sortKey="Garcia, Amandine" sort="Garcia, Amandine" uniqKey="Garcia A" first="Amandine" last="Garcia">Amandine Garcia</name><name sortKey="Garcia, Amandine" sort="Garcia, Amandine" uniqKey="Garcia A" first="Amandine" last="Garcia">Amandine Garcia</name><name sortKey="Goddard Eon, Sophie" sort="Goddard Eon, Sophie" uniqKey="Goddard Eon S" first="Sophie" last="Goddard-Léon">Sophie Goddard-Léon</name><name sortKey="Lavergne, Emilie" sort="Lavergne, Emilie" uniqKey="Lavergne E" first="Emilie" last="Lavergne">Emilie Lavergne</name><name sortKey="Lu, Jieli" sort="Lu, Jieli" uniqKey="Lu J" first="Jieli" last="Lu">Jieli Lu</name><name sortKey="Lu, Jieli" sort="Lu, Jieli" uniqKey="Lu J" first="Jieli" last="Lu">Jieli Lu</name><name sortKey="Lu, Jieli" sort="Lu, Jieli" uniqKey="Lu J" first="Jieli" last="Lu">Jieli Lu</name><name sortKey="Mazoyer, Sylvie" sort="Mazoyer, Sylvie" uniqKey="Mazoyer S" first="Sylvie" last="Mazoyer">Sylvie Mazoyer</name><name sortKey="Mazoyer, Sylvie" sort="Mazoyer, Sylvie" uniqKey="Mazoyer S" first="Sylvie" last="Mazoyer">Sylvie Mazoyer</name><name sortKey="Mazoyer, Sylvie" sort="Mazoyer, Sylvie" uniqKey="Mazoyer S" first="Sylvie" last="Mazoyer">Sylvie Mazoyer</name><name sortKey="Mazoyer, Sylvie" sort="Mazoyer, Sylvie" uniqKey="Mazoyer S" first="Sylvie" last="Mazoyer">Sylvie Mazoyer</name><name sortKey="Seigne, Christelle" sort="Seigne, Christelle" uniqKey="Seigne C" first="Christelle" last="Seigne">Christelle Seigne</name><name sortKey="Seigne, Christelle" sort="Seigne, Christelle" uniqKey="Seigne C" first="Christelle" last="Seigne">Christelle Seigne</name><name sortKey="Seigne, Christelle" sort="Seigne, Christelle" uniqKey="Seigne C" first="Christelle" last="Seigne">Christelle Seigne</name><name sortKey="Treilleux, Isabelle" sort="Treilleux, Isabelle" uniqKey="Treilleux I" first="Isabelle" last="Treilleux">Isabelle Treilleux</name><name sortKey="Zhang, Chang Xian" sort="Zhang, Chang Xian" uniqKey="Zhang C" first="Chang Xian" last="Zhang">Chang Xian Zhang</name><name sortKey="Zhang, Chang Xian" sort="Zhang, Chang Xian" uniqKey="Zhang C" first="Chang Xian" last="Zhang">Chang Xian Zhang</name><name sortKey="Zhang, Chang Xian" sort="Zhang, Chang Xian" uniqKey="Zhang C" first="Chang Xian" last="Zhang">Chang Xian Zhang</name><name sortKey="Zhang, Chang Xian" sort="Zhang, Chang Xian" uniqKey="Zhang C" first="Chang Xian" last="Zhang">Chang Xian Zhang</name><name sortKey="Zhang, Chang Xian" sort="Zhang, Chang Xian" uniqKey="Zhang C" first="Chang Xian" last="Zhang">Chang Xian Zhang</name></country><country name="Australie"><noRegion><name sortKey="Auret, Magdalena" sort="Auret, Magdalena" uniqKey="Auret M" first="Magdalena" last="Auret">Magdalena Auret</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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