Somatic Molecular Heterogeneity in Bilateral Macronodular Adrenocortical Disease (BMAD) Differs Among the Pathological Subgroups
Bilateral macronodular adrenocortical disease (BMAD) is an uncommon cause of Cushing’s syndrome leading to bilateral macronodules. Isolated BMAD has been classified into three molecular groups: patients with ARMC5 alteration, KDM1A alteration, and patients without known genetic cause. The aim of thi...
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| Veröffentlicht in: | Endocrine pathology 2024-09, Vol.35 (3), p.194-206 |
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| creator | Violon, Florian Bouys, Lucas Vaduva, Patricia Chansavang, Albain Vaquier, Louis Letourneur, Franck Izac, Brigitte Giannone, Gaëtan De Murat, Daniel Gaillard, Martin Berthon, Annabel Ragazzon, Bruno Pasmant, Eric Sibony, Mathilde Bertherat, Jérôme |
| description | Bilateral macronodular adrenocortical disease (BMAD) is an uncommon cause of Cushing’s syndrome leading to bilateral macronodules. Isolated BMAD has been classified into three molecular groups: patients with
ARMC5
alteration,
KDM1A
alteration, and patients without known genetic cause. The aim of this study was to identify by NGS, in a cohort of 26 patients with BMAD, the somatic alterations acquired in different nodules after macrodissection from patients with germline
ARMC5
or
KDM1A
alterations and to analyze potential somatic alterations in a panel of five other genes involved in adrenal pathology (
GNAS
,
PDE8B
,
PDE11A
,
PRKAR1A
, and
PRKACA
). Twenty-three patients (7
ARMC5
, 3
KDM1A
, and 13 BMAD with unknown genetic cause) were analyzable. Somatic
ARMC5
or
KDM1A
events were exclusively observed in patients with germline
ARMC5
and
KDM1A
alterations, respectively. Six out of 7
ARMC5
patients have a high heterogeneity in identified somatic events, whereas one
ARMC5
and all
KDM1A
patients show a loss of heterozygosity (LOH) in all nodules. Except for passenger alterations of
GNAS
, no genetic alteration susceptible to causing the disease was detected in the BMAD with unknown genetic cause. Our study reinforces our knowledge of the somatic genetic heterogeneity of
ARMC5
and the somatic homogeneity of
KDM1A
. It reveals the absence of purely somatic events in these two genes and provides a new tool for detecting
KDM1A
alterations by FISH 1p36/1q25. |
| doi_str_mv | 10.1007/s12022-024-09824-1 |
| format | Article |
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ARMC5
alteration,
KDM1A
alteration, and patients without known genetic cause. The aim of this study was to identify by NGS, in a cohort of 26 patients with BMAD, the somatic alterations acquired in different nodules after macrodissection from patients with germline
ARMC5
or
KDM1A
alterations and to analyze potential somatic alterations in a panel of five other genes involved in adrenal pathology (
GNAS
,
PDE8B
,
PDE11A
,
PRKAR1A
, and
PRKACA
). Twenty-three patients (7
ARMC5
, 3
KDM1A
, and 13 BMAD with unknown genetic cause) were analyzable. Somatic
ARMC5
or
KDM1A
events were exclusively observed in patients with germline
ARMC5
and
KDM1A
alterations, respectively. Six out of 7
ARMC5
patients have a high heterogeneity in identified somatic events, whereas one
ARMC5
and all
KDM1A
patients show a loss of heterozygosity (LOH) in all nodules. Except for passenger alterations of
GNAS
, no genetic alteration susceptible to causing the disease was detected in the BMAD with unknown genetic cause. Our study reinforces our knowledge of the somatic genetic heterogeneity of
ARMC5
and the somatic homogeneity of
KDM1A
. It reveals the absence of purely somatic events in these two genes and provides a new tool for detecting
KDM1A
alterations by FISH 1p36/1q25.</description><identifier>ISSN: 1046-3976</identifier><identifier>ISSN: 1559-0097</identifier><identifier>EISSN: 1559-0097</identifier><identifier>DOI: 10.1007/s12022-024-09824-1</identifier><identifier>PMID: 39180662</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Adrenal Cortex Diseases - complications ; Adrenal Cortex Diseases - genetics ; Adrenal Cortex Diseases - pathology ; Adult ; Aged ; Armadillo Domain Proteins - genetics ; Chromosome 1 ; Endocrinology ; Female ; Genes ; Genetic Heterogeneity ; Heterozygosity ; Histone Demethylases - genetics ; Hormones ; Humans ; Hyperplasia ; Kinases ; Loss of heterozygosity ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Nodules ; Oncology ; Pathology ; Patients ; Proteins ; Tumors</subject><ispartof>Endocrine pathology, 2024-09, Vol.35 (3), p.194-206</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c256t-6747d0ca4e775b6b166ee7e9ced0998e7f5f1d4f9b87b67f9fdbfd4a1e121af93</cites><orcidid>0000-0003-2067-2253 ; 0000-0001-9465-4774 ; 0000-0001-9476-4973 ; 0000-0003-1743-1598 ; 0000-0003-2551-3008 ; 0000-0002-5576-9525 ; 0000-0002-1881-8762 ; 0000-0003-1539-2118 ; 0000-0003-3195-1629 ; 0000-0002-9835-2156 ; 0000-0002-7990-3434 ; 0000-0002-5006-1317 ; 0009-0004-5083-3681 ; 0000-0002-1282-8732</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12022-024-09824-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12022-024-09824-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39180662$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Violon, Florian</creatorcontrib><creatorcontrib>Bouys, Lucas</creatorcontrib><creatorcontrib>Vaduva, Patricia</creatorcontrib><creatorcontrib>Chansavang, Albain</creatorcontrib><creatorcontrib>Vaquier, Louis</creatorcontrib><creatorcontrib>Letourneur, Franck</creatorcontrib><creatorcontrib>Izac, Brigitte</creatorcontrib><creatorcontrib>Giannone, Gaëtan</creatorcontrib><creatorcontrib>De Murat, Daniel</creatorcontrib><creatorcontrib>Gaillard, Martin</creatorcontrib><creatorcontrib>Berthon, Annabel</creatorcontrib><creatorcontrib>Ragazzon, Bruno</creatorcontrib><creatorcontrib>Pasmant, Eric</creatorcontrib><creatorcontrib>Sibony, Mathilde</creatorcontrib><creatorcontrib>Bertherat, Jérôme</creatorcontrib><title>Somatic Molecular Heterogeneity in Bilateral Macronodular Adrenocortical Disease (BMAD) Differs Among the Pathological Subgroups</title><title>Endocrine pathology</title><addtitle>Endocr Pathol</addtitle><addtitle>Endocr Pathol</addtitle><description>Bilateral macronodular adrenocortical disease (BMAD) is an uncommon cause of Cushing’s syndrome leading to bilateral macronodules. Isolated BMAD has been classified into three molecular groups: patients with
ARMC5
alteration,
KDM1A
alteration, and patients without known genetic cause. The aim of this study was to identify by NGS, in a cohort of 26 patients with BMAD, the somatic alterations acquired in different nodules after macrodissection from patients with germline
ARMC5
or
KDM1A
alterations and to analyze potential somatic alterations in a panel of five other genes involved in adrenal pathology (
GNAS
,
PDE8B
,
PDE11A
,
PRKAR1A
, and
PRKACA
). Twenty-three patients (7
ARMC5
, 3
KDM1A
, and 13 BMAD with unknown genetic cause) were analyzable. Somatic
ARMC5
or
KDM1A
events were exclusively observed in patients with germline
ARMC5
and
KDM1A
alterations, respectively. Six out of 7
ARMC5
patients have a high heterogeneity in identified somatic events, whereas one
ARMC5
and all
KDM1A
patients show a loss of heterozygosity (LOH) in all nodules. Except for passenger alterations of
GNAS
, no genetic alteration susceptible to causing the disease was detected in the BMAD with unknown genetic cause. Our study reinforces our knowledge of the somatic genetic heterogeneity of
ARMC5
and the somatic homogeneity of
KDM1A
. It reveals the absence of purely somatic events in these two genes and provides a new tool for detecting
KDM1A
alterations by FISH 1p36/1q25.</description><subject>Adrenal Cortex Diseases - complications</subject><subject>Adrenal Cortex Diseases - genetics</subject><subject>Adrenal Cortex Diseases - pathology</subject><subject>Adult</subject><subject>Aged</subject><subject>Armadillo Domain Proteins - genetics</subject><subject>Chromosome 1</subject><subject>Endocrinology</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic Heterogeneity</subject><subject>Heterozygosity</subject><subject>Histone Demethylases - genetics</subject><subject>Hormones</subject><subject>Humans</subject><subject>Hyperplasia</subject><subject>Kinases</subject><subject>Loss of heterozygosity</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Nodules</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Patients</subject><subject>Proteins</subject><subject>Tumors</subject><issn>1046-3976</issn><issn>1559-0097</issn><issn>1559-0097</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtP3DAUha2qVXmUP9AFstQNLNJe24kdL4fnIDFqpYG15STXISiJBztZsOOn485AK3XRjR_3fuf4yoeQrwy-MwD1IzIOnGfA8wx0mVb2geyzotAZgFYf0xlymQmt5B45iPERgAkA_pnsCc1KkJLvk5e1H-zU1XTle6zn3ga6xAmDb3HEbnqm3UjPut6mku3pytbBj77Zcosm4OhrH5I89S66iDYiPTlbLS5O09U5DJEuBj-2dHpA-stOD7737ZZez1Ub_LyJX8gnZ_uIR2_7Ibm_urw7X2a3P69vzhe3Wc0LOWVS5aqB2uaoVFHJikmJqFDX2IDWJSpXONbkTlelqqRy2jWVa3LLkHFmnRaH5GTnuwn-acY4maGLNfa9HdHP0QjQUspcqDKh3_5BH_0cxjSdEQx4URZMyETxHZW-JMaAzmxCN9jwbBiY3_mYXT4m5WO2-RiWRMdv1nM1YPNH8h5IAsQOiKk1thj-vv0f21fowpyG</recordid><startdate>20240901</startdate><enddate>20240901</enddate><creator>Violon, Florian</creator><creator>Bouys, Lucas</creator><creator>Vaduva, Patricia</creator><creator>Chansavang, Albain</creator><creator>Vaquier, Louis</creator><creator>Letourneur, Franck</creator><creator>Izac, Brigitte</creator><creator>Giannone, Gaëtan</creator><creator>De Murat, Daniel</creator><creator>Gaillard, Martin</creator><creator>Berthon, Annabel</creator><creator>Ragazzon, Bruno</creator><creator>Pasmant, Eric</creator><creator>Sibony, Mathilde</creator><creator>Bertherat, Jérôme</creator><general>Springer US</general><general>Springer Nature B.V</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>7QP</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2067-2253</orcidid><orcidid>https://orcid.org/0000-0001-9465-4774</orcidid><orcidid>https://orcid.org/0000-0001-9476-4973</orcidid><orcidid>https://orcid.org/0000-0003-1743-1598</orcidid><orcidid>https://orcid.org/0000-0003-2551-3008</orcidid><orcidid>https://orcid.org/0000-0002-5576-9525</orcidid><orcidid>https://orcid.org/0000-0002-1881-8762</orcidid><orcidid>https://orcid.org/0000-0003-1539-2118</orcidid><orcidid>https://orcid.org/0000-0003-3195-1629</orcidid><orcidid>https://orcid.org/0000-0002-9835-2156</orcidid><orcidid>https://orcid.org/0000-0002-7990-3434</orcidid><orcidid>https://orcid.org/0000-0002-5006-1317</orcidid><orcidid>https://orcid.org/0009-0004-5083-3681</orcidid><orcidid>https://orcid.org/0000-0002-1282-8732</orcidid></search><sort><creationdate>20240901</creationdate><title>Somatic Molecular Heterogeneity in Bilateral Macronodular Adrenocortical Disease (BMAD) Differs Among the Pathological Subgroups</title><author>Violon, Florian ; Bouys, Lucas ; Vaduva, Patricia ; Chansavang, Albain ; Vaquier, Louis ; Letourneur, Franck ; Izac, Brigitte ; Giannone, Gaëtan ; De Murat, Daniel ; Gaillard, Martin ; Berthon, Annabel ; Ragazzon, Bruno ; Pasmant, Eric ; Sibony, Mathilde ; Bertherat, Jérôme</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c256t-6747d0ca4e775b6b166ee7e9ced0998e7f5f1d4f9b87b67f9fdbfd4a1e121af93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Adrenal Cortex Diseases - complications</topic><topic>Adrenal Cortex Diseases - genetics</topic><topic>Adrenal Cortex Diseases - pathology</topic><topic>Adult</topic><topic>Aged</topic><topic>Armadillo Domain Proteins - genetics</topic><topic>Chromosome 1</topic><topic>Endocrinology</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic Heterogeneity</topic><topic>Heterozygosity</topic><topic>Histone Demethylases - genetics</topic><topic>Hormones</topic><topic>Humans</topic><topic>Hyperplasia</topic><topic>Kinases</topic><topic>Loss of heterozygosity</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Nodules</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Patients</topic><topic>Proteins</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Violon, Florian</creatorcontrib><creatorcontrib>Bouys, Lucas</creatorcontrib><creatorcontrib>Vaduva, Patricia</creatorcontrib><creatorcontrib>Chansavang, Albain</creatorcontrib><creatorcontrib>Vaquier, Louis</creatorcontrib><creatorcontrib>Letourneur, Franck</creatorcontrib><creatorcontrib>Izac, Brigitte</creatorcontrib><creatorcontrib>Giannone, Gaëtan</creatorcontrib><creatorcontrib>De Murat, Daniel</creatorcontrib><creatorcontrib>Gaillard, Martin</creatorcontrib><creatorcontrib>Berthon, Annabel</creatorcontrib><creatorcontrib>Ragazzon, Bruno</creatorcontrib><creatorcontrib>Pasmant, Eric</creatorcontrib><creatorcontrib>Sibony, Mathilde</creatorcontrib><creatorcontrib>Bertherat, Jérôme</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrine pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Violon, Florian</au><au>Bouys, Lucas</au><au>Vaduva, Patricia</au><au>Chansavang, Albain</au><au>Vaquier, Louis</au><au>Letourneur, Franck</au><au>Izac, Brigitte</au><au>Giannone, Gaëtan</au><au>De Murat, Daniel</au><au>Gaillard, Martin</au><au>Berthon, Annabel</au><au>Ragazzon, Bruno</au><au>Pasmant, Eric</au><au>Sibony, Mathilde</au><au>Bertherat, Jérôme</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Somatic Molecular Heterogeneity in Bilateral Macronodular Adrenocortical Disease (BMAD) Differs Among the Pathological Subgroups</atitle><jtitle>Endocrine pathology</jtitle><stitle>Endocr Pathol</stitle><addtitle>Endocr Pathol</addtitle><date>2024-09-01</date><risdate>2024</risdate><volume>35</volume><issue>3</issue><spage>194</spage><epage>206</epage><pages>194-206</pages><issn>1046-3976</issn><issn>1559-0097</issn><eissn>1559-0097</eissn><abstract>Bilateral macronodular adrenocortical disease (BMAD) is an uncommon cause of Cushing’s syndrome leading to bilateral macronodules. Isolated BMAD has been classified into three molecular groups: patients with
ARMC5
alteration,
KDM1A
alteration, and patients without known genetic cause. The aim of this study was to identify by NGS, in a cohort of 26 patients with BMAD, the somatic alterations acquired in different nodules after macrodissection from patients with germline
ARMC5
or
KDM1A
alterations and to analyze potential somatic alterations in a panel of five other genes involved in adrenal pathology (
GNAS
,
PDE8B
,
PDE11A
,
PRKAR1A
, and
PRKACA
). Twenty-three patients (7
ARMC5
, 3
KDM1A
, and 13 BMAD with unknown genetic cause) were analyzable. Somatic
ARMC5
or
KDM1A
events were exclusively observed in patients with germline
ARMC5
and
KDM1A
alterations, respectively. Six out of 7
ARMC5
patients have a high heterogeneity in identified somatic events, whereas one
ARMC5
and all
KDM1A
patients show a loss of heterozygosity (LOH) in all nodules. Except for passenger alterations of
GNAS
, no genetic alteration susceptible to causing the disease was detected in the BMAD with unknown genetic cause. Our study reinforces our knowledge of the somatic genetic heterogeneity of
ARMC5
and the somatic homogeneity of
KDM1A
. It reveals the absence of purely somatic events in these two genes and provides a new tool for detecting
KDM1A
alterations by FISH 1p36/1q25.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>39180662</pmid><doi>10.1007/s12022-024-09824-1</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0003-2067-2253</orcidid><orcidid>https://orcid.org/0000-0001-9465-4774</orcidid><orcidid>https://orcid.org/0000-0001-9476-4973</orcidid><orcidid>https://orcid.org/0000-0003-1743-1598</orcidid><orcidid>https://orcid.org/0000-0003-2551-3008</orcidid><orcidid>https://orcid.org/0000-0002-5576-9525</orcidid><orcidid>https://orcid.org/0000-0002-1881-8762</orcidid><orcidid>https://orcid.org/0000-0003-1539-2118</orcidid><orcidid>https://orcid.org/0000-0003-3195-1629</orcidid><orcidid>https://orcid.org/0000-0002-9835-2156</orcidid><orcidid>https://orcid.org/0000-0002-7990-3434</orcidid><orcidid>https://orcid.org/0000-0002-5006-1317</orcidid><orcidid>https://orcid.org/0009-0004-5083-3681</orcidid><orcidid>https://orcid.org/0000-0002-1282-8732</orcidid></addata></record> |
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| ispartof | Endocrine pathology, 2024-09, Vol.35 (3), p.194-206 |
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| subjects | Adrenal Cortex Diseases - complications Adrenal Cortex Diseases - genetics Adrenal Cortex Diseases - pathology Adult Aged Armadillo Domain Proteins - genetics Chromosome 1 Endocrinology Female Genes Genetic Heterogeneity Heterozygosity Histone Demethylases - genetics Hormones Humans Hyperplasia Kinases Loss of heterozygosity Male Medicine Medicine & Public Health Middle Aged Nodules Oncology Pathology Patients Proteins Tumors |
| title | Somatic Molecular Heterogeneity in Bilateral Macronodular Adrenocortical Disease (BMAD) Differs Among the Pathological Subgroups |
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