Histological Characterization of Aldosterone-producing Adrenocortical Adenomas with Different Somatic Mutations
Abstract Context Aldosterone-producing adrenocortical adenomas (APAs) are mainly composed of clear (lipid rich) and compact (eosinophilic) tumor cells. The detailed association between these histological features and somatic mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) in APAs is unknown. Objectiv...
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| Veröffentlicht in: | The journal of clinical endocrinology and metabolism 2020-03, Vol.105 (3), p.e282-e289 |
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| creator | Ono, Yoshikiyo Yamazaki, Yuto Omata, Kei Else, Tobias Tomlins, Scott A Rhayem, Yara Williams, Tracy Ann Reincke, Martin Carling, Tobias Monticone, Silvia Mulatero, Paolo Beuschlein, Felix Ito, Sadayoshi Satoh, Fumitoshi Rainey, William E Sasano, Hironobu |
| description | Abstract
Context
Aldosterone-producing adrenocortical adenomas (APAs) are mainly composed of clear (lipid rich) and compact (eosinophilic) tumor cells. The detailed association between these histological features and somatic mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) in APAs is unknown.
Objective
To examine the association between histological features and individual genotypes in APAs.
Methods
Examination of 39 APAs subjected to targeted next-generation sequencing (11 KCNJ5, 10 ATP1A1, 10 ATP2B3, and 8 CACNA1D) and quantitative morphological and immunohistochemical (CYP11B2 and CYP17A1) analyses using digital imaging software.
Results
KCNJ5- and ATP2B3-mutated APAs had clear cell dominant features (KCNJ5: clear 59.8% [54.4–64.6%] vs compact 40.2% (35.4–45.6%), P = .0022; ATP2B3: clear 54.3% [48.2–62.4 %] vs compact 45.7% (37.6–51.8 %), P = .0696). ATP1A1- and CACNA1D-mutated APAs presented with marked intratumoral heterogeneity. A significantly positive correlation of immunoreactivity was detected between CYP11B2 and CYP17A1 in tumor cells of KCNJ5-mutated APAs (P = .0112; ρ = 0.7237), in contrast, significantly inverse correlation was detected in ATP1A1-mutated APAs (P = .0025; ρ = −0.8667).
Conclusion
KCNJ5-mutated APAs, coexpressing CYP11B2 and CYP17A1, were more deviated in terms of zonation-specific differentiation of adrenocortical cells than ATP1A1- and ATP2B3-mutated APAs. |
| doi_str_mv | 10.1210/clinem/dgz235 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7048684</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1210/clinem/dgz235</oup_id><sourcerecordid>2320640811</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4905-ef7ee39637d47463a627faab162ecb238eb4e9ecee420ec3685c4b7f204fb7233</originalsourceid><addsrcrecordid>eNqFkc1v1DAQxS0EosvCkSuKxIVLWn8lTi5Iq-WjlVpxACRuluOMNy5OvNgOK_rXY5qlAqSKk-WZn9_M80PoOcGnhBJ8pp2dYDzrdzeUVQ_QirS8KgVpxUO0wpiSshX0ywl6EuM1xoTzij1GJ4yIpmUNXiF_bmPyzu-sVq7YDioonSDYG5Wsnwpvio3rfcwlP0G5D76ftZ12xaYPMHntQ7p9uOnzbVSxONg0FG-sMZD7qfiYi5koruZ0KxifokdGuQjPjucafX739tP2vLz88P5iu7ksNW9xVYIRAKytmei54DVTNRVGqY7UFHRHWQMdhxY0AKcYNKubSvNOGIq56QRlbI1eL7r7uRuh13mZoJzcBzuq8EN6ZeXfnckOcue_S4F5Uzc8C7w6CgT_bYaY5GijBufUBH6OkjKKa44bQjL68h_02s9hyvYk5YxgKkT-9jUqF0oHH2MAc7cMwfJXlHKJUi5RZv7Fnw7u6N_ZZYAswMG7nE_86uYDBDmAcmm4V_Toys_7_8z_CShfvvk</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2431027745</pqid></control><display><type>article</type><title>Histological Characterization of Aldosterone-producing Adrenocortical Adenomas with Different Somatic Mutations</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><source>ProQuest Central</source><creator>Ono, Yoshikiyo ; Yamazaki, Yuto ; Omata, Kei ; Else, Tobias ; Tomlins, Scott A ; Rhayem, Yara ; Williams, Tracy Ann ; Reincke, Martin ; Carling, Tobias ; Monticone, Silvia ; Mulatero, Paolo ; Beuschlein, Felix ; Ito, Sadayoshi ; Satoh, Fumitoshi ; Rainey, William E ; Sasano, Hironobu</creator><creatorcontrib>Ono, Yoshikiyo ; Yamazaki, Yuto ; Omata, Kei ; Else, Tobias ; Tomlins, Scott A ; Rhayem, Yara ; Williams, Tracy Ann ; Reincke, Martin ; Carling, Tobias ; Monticone, Silvia ; Mulatero, Paolo ; Beuschlein, Felix ; Ito, Sadayoshi ; Satoh, Fumitoshi ; Rainey, William E ; Sasano, Hironobu</creatorcontrib><description>Abstract
Context
Aldosterone-producing adrenocortical adenomas (APAs) are mainly composed of clear (lipid rich) and compact (eosinophilic) tumor cells. The detailed association between these histological features and somatic mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) in APAs is unknown.
Objective
To examine the association between histological features and individual genotypes in APAs.
Methods
Examination of 39 APAs subjected to targeted next-generation sequencing (11 KCNJ5, 10 ATP1A1, 10 ATP2B3, and 8 CACNA1D) and quantitative morphological and immunohistochemical (CYP11B2 and CYP17A1) analyses using digital imaging software.
Results
KCNJ5- and ATP2B3-mutated APAs had clear cell dominant features (KCNJ5: clear 59.8% [54.4–64.6%] vs compact 40.2% (35.4–45.6%), P = .0022; ATP2B3: clear 54.3% [48.2–62.4 %] vs compact 45.7% (37.6–51.8 %), P = .0696). ATP1A1- and CACNA1D-mutated APAs presented with marked intratumoral heterogeneity. A significantly positive correlation of immunoreactivity was detected between CYP11B2 and CYP17A1 in tumor cells of KCNJ5-mutated APAs (P = .0112; ρ = 0.7237), in contrast, significantly inverse correlation was detected in ATP1A1-mutated APAs (P = .0025; ρ = −0.8667).
Conclusion
KCNJ5-mutated APAs, coexpressing CYP11B2 and CYP17A1, were more deviated in terms of zonation-specific differentiation of adrenocortical cells than ATP1A1- and ATP2B3-mutated APAs.</description><identifier>ISSN: 0021-972X</identifier><identifier>EISSN: 1945-7197</identifier><identifier>DOI: 10.1210/clinem/dgz235</identifier><identifier>PMID: 31789380</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>Aldosterone ; Aldosterone synthase ; Cell differentiation ; Endocrine disorders ; Genotypes ; Immunoreactivity ; Leukocytes (eosinophilic) ; Mutation ; Neuroendocrine tumors ; Next-generation sequencing ; Online Only ; Tumor cells ; Tumors ; Zonation</subject><ispartof>The journal of clinical endocrinology and metabolism, 2020-03, Vol.105 (3), p.e282-e289</ispartof><rights>Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2019</rights><rights>Copyright © Oxford University Press 2015</rights><rights>Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><rights>Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4905-ef7ee39637d47463a627faab162ecb238eb4e9ecee420ec3685c4b7f204fb7233</citedby><cites>FETCH-LOGICAL-c4905-ef7ee39637d47463a627faab162ecb238eb4e9ecee420ec3685c4b7f204fb7233</cites><orcidid>0000-0002-6600-8641 ; 0000-0003-1873-7388 ; 0000-0002-9817-9875</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/2431027745?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>230,314,776,780,881,21367,27901,27902,33721,33722,43781</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31789380$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ono, Yoshikiyo</creatorcontrib><creatorcontrib>Yamazaki, Yuto</creatorcontrib><creatorcontrib>Omata, Kei</creatorcontrib><creatorcontrib>Else, Tobias</creatorcontrib><creatorcontrib>Tomlins, Scott A</creatorcontrib><creatorcontrib>Rhayem, Yara</creatorcontrib><creatorcontrib>Williams, Tracy Ann</creatorcontrib><creatorcontrib>Reincke, Martin</creatorcontrib><creatorcontrib>Carling, Tobias</creatorcontrib><creatorcontrib>Monticone, Silvia</creatorcontrib><creatorcontrib>Mulatero, Paolo</creatorcontrib><creatorcontrib>Beuschlein, Felix</creatorcontrib><creatorcontrib>Ito, Sadayoshi</creatorcontrib><creatorcontrib>Satoh, Fumitoshi</creatorcontrib><creatorcontrib>Rainey, William E</creatorcontrib><creatorcontrib>Sasano, Hironobu</creatorcontrib><title>Histological Characterization of Aldosterone-producing Adrenocortical Adenomas with Different Somatic Mutations</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description>Abstract
Context
Aldosterone-producing adrenocortical adenomas (APAs) are mainly composed of clear (lipid rich) and compact (eosinophilic) tumor cells. The detailed association between these histological features and somatic mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) in APAs is unknown.
Objective
To examine the association between histological features and individual genotypes in APAs.
Methods
Examination of 39 APAs subjected to targeted next-generation sequencing (11 KCNJ5, 10 ATP1A1, 10 ATP2B3, and 8 CACNA1D) and quantitative morphological and immunohistochemical (CYP11B2 and CYP17A1) analyses using digital imaging software.
Results
KCNJ5- and ATP2B3-mutated APAs had clear cell dominant features (KCNJ5: clear 59.8% [54.4–64.6%] vs compact 40.2% (35.4–45.6%), P = .0022; ATP2B3: clear 54.3% [48.2–62.4 %] vs compact 45.7% (37.6–51.8 %), P = .0696). ATP1A1- and CACNA1D-mutated APAs presented with marked intratumoral heterogeneity. A significantly positive correlation of immunoreactivity was detected between CYP11B2 and CYP17A1 in tumor cells of KCNJ5-mutated APAs (P = .0112; ρ = 0.7237), in contrast, significantly inverse correlation was detected in ATP1A1-mutated APAs (P = .0025; ρ = −0.8667).
Conclusion
KCNJ5-mutated APAs, coexpressing CYP11B2 and CYP17A1, were more deviated in terms of zonation-specific differentiation of adrenocortical cells than ATP1A1- and ATP2B3-mutated APAs.</description><subject>Aldosterone</subject><subject>Aldosterone synthase</subject><subject>Cell differentiation</subject><subject>Endocrine disorders</subject><subject>Genotypes</subject><subject>Immunoreactivity</subject><subject>Leukocytes (eosinophilic)</subject><subject>Mutation</subject><subject>Neuroendocrine tumors</subject><subject>Next-generation sequencing</subject><subject>Online Only</subject><subject>Tumor cells</subject><subject>Tumors</subject><subject>Zonation</subject><issn>0021-972X</issn><issn>1945-7197</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNqFkc1v1DAQxS0EosvCkSuKxIVLWn8lTi5Iq-WjlVpxACRuluOMNy5OvNgOK_rXY5qlAqSKk-WZn9_M80PoOcGnhBJ8pp2dYDzrdzeUVQ_QirS8KgVpxUO0wpiSshX0ywl6EuM1xoTzij1GJ4yIpmUNXiF_bmPyzu-sVq7YDioonSDYG5Wsnwpvio3rfcwlP0G5D76ftZ12xaYPMHntQ7p9uOnzbVSxONg0FG-sMZD7qfiYi5koruZ0KxifokdGuQjPjucafX739tP2vLz88P5iu7ksNW9xVYIRAKytmei54DVTNRVGqY7UFHRHWQMdhxY0AKcYNKubSvNOGIq56QRlbI1eL7r7uRuh13mZoJzcBzuq8EN6ZeXfnckOcue_S4F5Uzc8C7w6CgT_bYaY5GijBufUBH6OkjKKa44bQjL68h_02s9hyvYk5YxgKkT-9jUqF0oHH2MAc7cMwfJXlHKJUi5RZv7Fnw7u6N_ZZYAswMG7nE_86uYDBDmAcmm4V_Toys_7_8z_CShfvvk</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Ono, Yoshikiyo</creator><creator>Yamazaki, Yuto</creator><creator>Omata, Kei</creator><creator>Else, Tobias</creator><creator>Tomlins, Scott A</creator><creator>Rhayem, Yara</creator><creator>Williams, Tracy Ann</creator><creator>Reincke, Martin</creator><creator>Carling, Tobias</creator><creator>Monticone, Silvia</creator><creator>Mulatero, Paolo</creator><creator>Beuschlein, Felix</creator><creator>Ito, Sadayoshi</creator><creator>Satoh, Fumitoshi</creator><creator>Rainey, William E</creator><creator>Sasano, Hironobu</creator><general>Oxford University Press</general><general>Copyright Oxford University Press</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7T5</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-6600-8641</orcidid><orcidid>https://orcid.org/0000-0003-1873-7388</orcidid><orcidid>https://orcid.org/0000-0002-9817-9875</orcidid></search><sort><creationdate>20200301</creationdate><title>Histological Characterization of Aldosterone-producing Adrenocortical Adenomas with Different Somatic Mutations</title><author>Ono, Yoshikiyo ; Yamazaki, Yuto ; Omata, Kei ; Else, Tobias ; Tomlins, Scott A ; Rhayem, Yara ; Williams, Tracy Ann ; Reincke, Martin ; Carling, Tobias ; Monticone, Silvia ; Mulatero, Paolo ; Beuschlein, Felix ; Ito, Sadayoshi ; Satoh, Fumitoshi ; Rainey, William E ; Sasano, Hironobu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4905-ef7ee39637d47463a627faab162ecb238eb4e9ecee420ec3685c4b7f204fb7233</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Aldosterone</topic><topic>Aldosterone synthase</topic><topic>Cell differentiation</topic><topic>Endocrine disorders</topic><topic>Genotypes</topic><topic>Immunoreactivity</topic><topic>Leukocytes (eosinophilic)</topic><topic>Mutation</topic><topic>Neuroendocrine tumors</topic><topic>Next-generation sequencing</topic><topic>Online Only</topic><topic>Tumor cells</topic><topic>Tumors</topic><topic>Zonation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ono, Yoshikiyo</creatorcontrib><creatorcontrib>Yamazaki, Yuto</creatorcontrib><creatorcontrib>Omata, Kei</creatorcontrib><creatorcontrib>Else, Tobias</creatorcontrib><creatorcontrib>Tomlins, Scott A</creatorcontrib><creatorcontrib>Rhayem, Yara</creatorcontrib><creatorcontrib>Williams, Tracy Ann</creatorcontrib><creatorcontrib>Reincke, Martin</creatorcontrib><creatorcontrib>Carling, Tobias</creatorcontrib><creatorcontrib>Monticone, Silvia</creatorcontrib><creatorcontrib>Mulatero, Paolo</creatorcontrib><creatorcontrib>Beuschlein, Felix</creatorcontrib><creatorcontrib>Ito, Sadayoshi</creatorcontrib><creatorcontrib>Satoh, Fumitoshi</creatorcontrib><creatorcontrib>Rainey, William E</creatorcontrib><creatorcontrib>Sasano, Hironobu</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</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>Medical Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</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>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ono, Yoshikiyo</au><au>Yamazaki, Yuto</au><au>Omata, Kei</au><au>Else, Tobias</au><au>Tomlins, Scott A</au><au>Rhayem, Yara</au><au>Williams, Tracy Ann</au><au>Reincke, Martin</au><au>Carling, Tobias</au><au>Monticone, Silvia</au><au>Mulatero, Paolo</au><au>Beuschlein, Felix</au><au>Ito, Sadayoshi</au><au>Satoh, Fumitoshi</au><au>Rainey, William E</au><au>Sasano, Hironobu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Histological Characterization of Aldosterone-producing Adrenocortical Adenomas with Different Somatic Mutations</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>105</volume><issue>3</issue><spage>e282</spage><epage>e289</epage><pages>e282-e289</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><abstract>Abstract
Context
Aldosterone-producing adrenocortical adenomas (APAs) are mainly composed of clear (lipid rich) and compact (eosinophilic) tumor cells. The detailed association between these histological features and somatic mutations (KCNJ5, ATP1A1, ATP2B3, and CACNA1D) in APAs is unknown.
Objective
To examine the association between histological features and individual genotypes in APAs.
Methods
Examination of 39 APAs subjected to targeted next-generation sequencing (11 KCNJ5, 10 ATP1A1, 10 ATP2B3, and 8 CACNA1D) and quantitative morphological and immunohistochemical (CYP11B2 and CYP17A1) analyses using digital imaging software.
Results
KCNJ5- and ATP2B3-mutated APAs had clear cell dominant features (KCNJ5: clear 59.8% [54.4–64.6%] vs compact 40.2% (35.4–45.6%), P = .0022; ATP2B3: clear 54.3% [48.2–62.4 %] vs compact 45.7% (37.6–51.8 %), P = .0696). ATP1A1- and CACNA1D-mutated APAs presented with marked intratumoral heterogeneity. A significantly positive correlation of immunoreactivity was detected between CYP11B2 and CYP17A1 in tumor cells of KCNJ5-mutated APAs (P = .0112; ρ = 0.7237), in contrast, significantly inverse correlation was detected in ATP1A1-mutated APAs (P = .0025; ρ = −0.8667).
Conclusion
KCNJ5-mutated APAs, coexpressing CYP11B2 and CYP17A1, were more deviated in terms of zonation-specific differentiation of adrenocortical cells than ATP1A1- and ATP2B3-mutated APAs.</abstract><cop>US</cop><pub>Oxford University Press</pub><pmid>31789380</pmid><doi>10.1210/clinem/dgz235</doi><orcidid>https://orcid.org/0000-0002-6600-8641</orcidid><orcidid>https://orcid.org/0000-0003-1873-7388</orcidid><orcidid>https://orcid.org/0000-0002-9817-9875</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; ProQuest Central |
| subjects | Aldosterone Aldosterone synthase Cell differentiation Endocrine disorders Genotypes Immunoreactivity Leukocytes (eosinophilic) Mutation Neuroendocrine tumors Next-generation sequencing Online Only Tumor cells Tumors Zonation |
| title | Histological Characterization of Aldosterone-producing Adrenocortical Adenomas with Different Somatic Mutations |
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