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miR-23b as a potential tumor suppressor and its regulation by DNA methylation in cervical cancer
The aberrant expression of miR-23b is involved in the development and progression of cancer. The aim of this study was to evaluate the potential role of methylation in the silencing of miR-23b in cervical cancer cell lines and to determine its expression in stages of malignant progression and in cer...
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Published in: | Infectious agents and cancer 2015-11, Vol.10 (1), p.42-42, Article 42 |
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creator | Campos-Viguri, Gabriela Elizabeth Jiménez-Wences, Hilda Peralta-Zaragoza, Oscar Torres-Altamirano, Gricenda Soto-Flores, Diana Guillermina Hernández-Sotelo, Daniel Alarcón-Romero, Luz Del Carmen Jiménez-López, Marco Antonio Illades-Aguiar, Berenice Fernández-Tilapa, Gloria |
description | The aberrant expression of miR-23b is involved in the development and progression of cancer. The aim of this study was to evaluate the potential role of methylation in the silencing of miR-23b in cervical cancer cell lines and to determine its expression in stages of malignant progression and in cervical cancer tissues HPV16-positive.
The methylation of the miR-23b promoter was determined in HeLa, SiHa, CaSki and C33A cells using a Human Cancer miRNA EpiTectMethyl II Signature PCR Array®. The cells were treated with 5-Aza-2'-deoxycytidine, and the expression of miR-23b, uPa, c-Met and Zeb1 was determined by qRT-PCR. miR-92a and GAPDH were used as controls. The expression of miR-23b was determined in cervical scrapes and biopsies of women without squamous intraepithelial lesions, with precursor lesions and with cervical cancer, all were HPV16-positive. The Fisher exact and Mann-Whitney tests were used to compare the differences of the expression of miR-23b, uPa, c-Met and Zeb1 among cell groups, and the difference among patients, respectively. The association between the expression of miR-23b and cervical cancer was determined by logistic regression with a confidence level of 95 %. A value of p |
doi_str_mv | 10.1186/s13027-015-0037-6 |
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The methylation of the miR-23b promoter was determined in HeLa, SiHa, CaSki and C33A cells using a Human Cancer miRNA EpiTectMethyl II Signature PCR Array®. The cells were treated with 5-Aza-2'-deoxycytidine, and the expression of miR-23b, uPa, c-Met and Zeb1 was determined by qRT-PCR. miR-92a and GAPDH were used as controls. The expression of miR-23b was determined in cervical scrapes and biopsies of women without squamous intraepithelial lesions, with precursor lesions and with cervical cancer, all were HPV16-positive. The Fisher exact and Mann-Whitney tests were used to compare the differences of the expression of miR-23b, uPa, c-Met and Zeb1 among cell groups, and the difference among patients, respectively. The association between the expression of miR-23b and cervical cancer was determined by logistic regression with a confidence level of 95 %. A value of p < 0.05 was considered statistically significant.
In C33A, HeLa and CaSki cells, methylation was associated with decreased expression of miR-23b. After treatment with 5-Aza-CdR, the expression of miR-23b increased in all cell lines and the expression of c-Met decreased in HeLa cells, while uPa and Zeb1 decreased in C33A and CaSki cells. In SiHa cells the expression of uPa, c-Met and Zeb1 increased. The expression of miR-23b decreased in relation to the increase in the severity of the lesion and was significantly lower in cervical cancer. In women with premalignant lesions HPV16-positive, decreased levels of miR-23b increased the risk of cervical cancer (OR = 36, 95 % CI = 6.7-192.6, p < 0.05).
The results suggest that the expression of miR-23b is regulated by the methylation of its promoter and is possible that this microRNA influence the expression of uPa, c-Met and Zeb1 in cervical cancer cells lines. In women with premalignant lesions and cervical cancer infected with HPV16, the expression level of miR-23b agree with a tumor suppressor gene.</description><identifier>ISSN: 1750-9378</identifier><identifier>EISSN: 1750-9378</identifier><identifier>DOI: 10.1186/s13027-015-0037-6</identifier><identifier>PMID: 26622315</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Cancer ; Cervical cancer ; Development and progression ; DNA ; Genetic aspects ; Methylation ; Oncology, Experimental ; Tumors</subject><ispartof>Infectious agents and cancer, 2015-11, Vol.10 (1), p.42-42, Article 42</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>Campos-Viguri et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-57cfb52221261c7a4d08ea2e4a9c8484816d99791cdb669c82124efa72b52263</citedby><cites>FETCH-LOGICAL-c494t-57cfb52221261c7a4d08ea2e4a9c8484816d99791cdb669c82124efa72b52263</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/PMC4663735/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1779705660?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26622315$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Campos-Viguri, Gabriela Elizabeth</creatorcontrib><creatorcontrib>Jiménez-Wences, Hilda</creatorcontrib><creatorcontrib>Peralta-Zaragoza, Oscar</creatorcontrib><creatorcontrib>Torres-Altamirano, Gricenda</creatorcontrib><creatorcontrib>Soto-Flores, Diana Guillermina</creatorcontrib><creatorcontrib>Hernández-Sotelo, Daniel</creatorcontrib><creatorcontrib>Alarcón-Romero, Luz Del Carmen</creatorcontrib><creatorcontrib>Jiménez-López, Marco Antonio</creatorcontrib><creatorcontrib>Illades-Aguiar, Berenice</creatorcontrib><creatorcontrib>Fernández-Tilapa, Gloria</creatorcontrib><title>miR-23b as a potential tumor suppressor and its regulation by DNA methylation in cervical cancer</title><title>Infectious agents and cancer</title><addtitle>Infect Agent Cancer</addtitle><description>The aberrant expression of miR-23b is involved in the development and progression of cancer. The aim of this study was to evaluate the potential role of methylation in the silencing of miR-23b in cervical cancer cell lines and to determine its expression in stages of malignant progression and in cervical cancer tissues HPV16-positive.
The methylation of the miR-23b promoter was determined in HeLa, SiHa, CaSki and C33A cells using a Human Cancer miRNA EpiTectMethyl II Signature PCR Array®. The cells were treated with 5-Aza-2'-deoxycytidine, and the expression of miR-23b, uPa, c-Met and Zeb1 was determined by qRT-PCR. miR-92a and GAPDH were used as controls. The expression of miR-23b was determined in cervical scrapes and biopsies of women without squamous intraepithelial lesions, with precursor lesions and with cervical cancer, all were HPV16-positive. The Fisher exact and Mann-Whitney tests were used to compare the differences of the expression of miR-23b, uPa, c-Met and Zeb1 among cell groups, and the difference among patients, respectively. The association between the expression of miR-23b and cervical cancer was determined by logistic regression with a confidence level of 95 %. A value of p < 0.05 was considered statistically significant.
In C33A, HeLa and CaSki cells, methylation was associated with decreased expression of miR-23b. After treatment with 5-Aza-CdR, the expression of miR-23b increased in all cell lines and the expression of c-Met decreased in HeLa cells, while uPa and Zeb1 decreased in C33A and CaSki cells. In SiHa cells the expression of uPa, c-Met and Zeb1 increased. The expression of miR-23b decreased in relation to the increase in the severity of the lesion and was significantly lower in cervical cancer. In women with premalignant lesions HPV16-positive, decreased levels of miR-23b increased the risk of cervical cancer (OR = 36, 95 % CI = 6.7-192.6, p < 0.05).
The results suggest that the expression of miR-23b is regulated by the methylation of its promoter and is possible that this microRNA influence the expression of uPa, c-Met and Zeb1 in cervical cancer cells lines. In women with premalignant lesions and cervical cancer infected with HPV16, the expression level of miR-23b agree with a tumor suppressor gene.</description><subject>Cancer</subject><subject>Cervical cancer</subject><subject>Development and progression</subject><subject>DNA</subject><subject>Genetic aspects</subject><subject>Methylation</subject><subject>Oncology, Experimental</subject><subject>Tumors</subject><issn>1750-9378</issn><issn>1750-9378</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNptkktr3DAUhUVpaNKkPyCbIOimGyd6WY9NYUjaphASCNmrsixPFGzJlezA_PvKzORVgha6XH3niHs5ABxjdIqx5GcZU0REhXBdIURFxT-AAyxqVCkq5MdX9T74nPMDQkwSKT-BfcI5IRTXB-DP4G8rQhtoMjRwjJMLkzc9nOYhJpjncUwu51Ka0EI_ZZjceu7N5GOAzQZeXK_g4Kb7za7lA7QuPXpbLKwJpT4Ce53ps_uyuw_B3c8fd-eX1dXNr9_nq6vKMsWmqha2a2pCCCYcW2FYi6QzxDGjrGTlYN4qJRS2bcN56RWQuc4Isqg4PQTft7bj3AyutWWMZHo9Jj-YtNHReP32Jfh7vY6PmnFOBa2LwbedQYp_Z5cnPfhsXd-b4OKcNRZMcUQoUQX9-h_6EOcUynSFEkqgmnP0Qq1N77QPXSz_2sVUrxhXSDIhSaFO36HKad3gbQyu86X_RoC3Aptizsl1zzNipJdU6G0qdEmFXlKhl-WcvF7Os-IpBvQfZNyw6A</recordid><startdate>20151130</startdate><enddate>20151130</enddate><creator>Campos-Viguri, Gabriela Elizabeth</creator><creator>Jiménez-Wences, Hilda</creator><creator>Peralta-Zaragoza, Oscar</creator><creator>Torres-Altamirano, Gricenda</creator><creator>Soto-Flores, Diana Guillermina</creator><creator>Hernández-Sotelo, Daniel</creator><creator>Alarcón-Romero, Luz Del Carmen</creator><creator>Jiménez-López, Marco Antonio</creator><creator>Illades-Aguiar, Berenice</creator><creator>Fernández-Tilapa, Gloria</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151130</creationdate><title>miR-23b as a potential tumor suppressor and its regulation by DNA methylation in cervical cancer</title><author>Campos-Viguri, Gabriela Elizabeth ; Jiménez-Wences, Hilda ; Peralta-Zaragoza, Oscar ; Torres-Altamirano, Gricenda ; Soto-Flores, Diana Guillermina ; Hernández-Sotelo, Daniel ; Alarcón-Romero, Luz Del Carmen ; Jiménez-López, Marco Antonio ; Illades-Aguiar, Berenice ; Fernández-Tilapa, Gloria</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-57cfb52221261c7a4d08ea2e4a9c8484816d99791cdb669c82124efa72b52263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Cancer</topic><topic>Cervical cancer</topic><topic>Development and progression</topic><topic>DNA</topic><topic>Genetic aspects</topic><topic>Methylation</topic><topic>Oncology, Experimental</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Campos-Viguri, Gabriela Elizabeth</creatorcontrib><creatorcontrib>Jiménez-Wences, Hilda</creatorcontrib><creatorcontrib>Peralta-Zaragoza, Oscar</creatorcontrib><creatorcontrib>Torres-Altamirano, Gricenda</creatorcontrib><creatorcontrib>Soto-Flores, Diana Guillermina</creatorcontrib><creatorcontrib>Hernández-Sotelo, Daniel</creatorcontrib><creatorcontrib>Alarcón-Romero, Luz Del Carmen</creatorcontrib><creatorcontrib>Jiménez-López, Marco Antonio</creatorcontrib><creatorcontrib>Illades-Aguiar, Berenice</creatorcontrib><creatorcontrib>Fernández-Tilapa, Gloria</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</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 UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest 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>PubMed Central (Full Participant titles)</collection><jtitle>Infectious agents and cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Campos-Viguri, Gabriela Elizabeth</au><au>Jiménez-Wences, Hilda</au><au>Peralta-Zaragoza, Oscar</au><au>Torres-Altamirano, Gricenda</au><au>Soto-Flores, Diana Guillermina</au><au>Hernández-Sotelo, Daniel</au><au>Alarcón-Romero, Luz Del Carmen</au><au>Jiménez-López, Marco Antonio</au><au>Illades-Aguiar, Berenice</au><au>Fernández-Tilapa, Gloria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-23b as a potential tumor suppressor and its regulation by DNA methylation in cervical cancer</atitle><jtitle>Infectious agents and cancer</jtitle><addtitle>Infect Agent Cancer</addtitle><date>2015-11-30</date><risdate>2015</risdate><volume>10</volume><issue>1</issue><spage>42</spage><epage>42</epage><pages>42-42</pages><artnum>42</artnum><issn>1750-9378</issn><eissn>1750-9378</eissn><abstract>The aberrant expression of miR-23b is involved in the development and progression of cancer. The aim of this study was to evaluate the potential role of methylation in the silencing of miR-23b in cervical cancer cell lines and to determine its expression in stages of malignant progression and in cervical cancer tissues HPV16-positive.
The methylation of the miR-23b promoter was determined in HeLa, SiHa, CaSki and C33A cells using a Human Cancer miRNA EpiTectMethyl II Signature PCR Array®. The cells were treated with 5-Aza-2'-deoxycytidine, and the expression of miR-23b, uPa, c-Met and Zeb1 was determined by qRT-PCR. miR-92a and GAPDH were used as controls. The expression of miR-23b was determined in cervical scrapes and biopsies of women without squamous intraepithelial lesions, with precursor lesions and with cervical cancer, all were HPV16-positive. The Fisher exact and Mann-Whitney tests were used to compare the differences of the expression of miR-23b, uPa, c-Met and Zeb1 among cell groups, and the difference among patients, respectively. The association between the expression of miR-23b and cervical cancer was determined by logistic regression with a confidence level of 95 %. A value of p < 0.05 was considered statistically significant.
In C33A, HeLa and CaSki cells, methylation was associated with decreased expression of miR-23b. After treatment with 5-Aza-CdR, the expression of miR-23b increased in all cell lines and the expression of c-Met decreased in HeLa cells, while uPa and Zeb1 decreased in C33A and CaSki cells. In SiHa cells the expression of uPa, c-Met and Zeb1 increased. The expression of miR-23b decreased in relation to the increase in the severity of the lesion and was significantly lower in cervical cancer. In women with premalignant lesions HPV16-positive, decreased levels of miR-23b increased the risk of cervical cancer (OR = 36, 95 % CI = 6.7-192.6, p < 0.05).
The results suggest that the expression of miR-23b is regulated by the methylation of its promoter and is possible that this microRNA influence the expression of uPa, c-Met and Zeb1 in cervical cancer cells lines. In women with premalignant lesions and cervical cancer infected with HPV16, the expression level of miR-23b agree with a tumor suppressor gene.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26622315</pmid><doi>10.1186/s13027-015-0037-6</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Cancer Cervical cancer Development and progression DNA Genetic aspects Methylation Oncology, Experimental Tumors |
title | miR-23b as a potential tumor suppressor and its regulation by DNA methylation in cervical cancer |
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