SNP Array Profiling of Childhood Adrenocortical Tumors Reveals Distinct Pathways of Tumorigenesis and Highlights Candidate Driver Genes

Context: Childhood adrenocortical tumors (ACT) are rare malignancies, except in southern Brazil, where a higher incidence rate is associated to a high frequency of the founder R337H TP53 mutation. To date, copy number alterations in these tumors have only been analyzed by low-resolution comparative...

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Veröffentlicht in:The journal of clinical endocrinology and metabolism 2012-07, Vol.97 (7), p.E1284-E1293
Hauptverfasser: Letouzé, Eric, Rosati, Roberto, Komechen, Heloisa, Doghman, Mabrouka, Marisa, Laetitia, Flück, Christa, de Krijger, Ronald R, van Noesel, Max M, Mas, Jean-Christophe, Pianovski, Mara A. D, Zambetti, Gerard P, Figueiredo, Bonald C, Lalli, Enzo
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container_end_page E1293
container_issue 7
container_start_page E1284
container_title The journal of clinical endocrinology and metabolism
container_volume 97
creator Letouzé, Eric
Rosati, Roberto
Komechen, Heloisa
Doghman, Mabrouka
Marisa, Laetitia
Flück, Christa
de Krijger, Ronald R
van Noesel, Max M
Mas, Jean-Christophe
Pianovski, Mara A. D
Zambetti, Gerard P
Figueiredo, Bonald C
Lalli, Enzo
description Context: Childhood adrenocortical tumors (ACT) are rare malignancies, except in southern Brazil, where a higher incidence rate is associated to a high frequency of the founder R337H TP53 mutation. To date, copy number alterations in these tumors have only been analyzed by low-resolution comparative genomic hybridization. Objective: We analyzed an international series of 25 childhood ACT using high-resolution single nucleotide polymorphism arrays to: 1) detect focal copy number alterations highlighting candidate driver genes; and 2) compare genetic alterations between Brazilian patients carrying the R337H TP53 mutation and non-Brazilian patients. Results: We identified 16 significantly recurrent chromosomal alterations (q-value < 0.05), the most frequent being −4q34, +9q33-q34, +19p, loss of heterozygosity (LOH) of chromosome 17 and 11p15. Focal amplifications and homozygous deletions comprising well-known oncogenes (MYC, MDM2, PDGFRA, KIT, MCL1, BCL2L1) and tumor suppressors (TP53, RB1, RPH3AL) were identified. In addition, eight focal deletions were detected at 4q34, defining a sharp peak region around the noncoding RNA LINC00290 gene. Although non-Brazilian tumors with a mutated TP53 were similar to Brazilian tumors, those with a wild-type TP53 displayed distinct genomic profiles, with significantly fewer rearrangements (P = 0.019). In particular, three alterations (LOH of chromosome 17, +9q33-q34, and −4q34) were significantly more frequent in TP53-mutated samples. Finally, two of four TP53 wild-type tumors displayed as sole rearrangement a copy-neutral LOH of the imprinted region at 11p15, supporting a major role for this region in ACT development. Conclusions: Our findings highlight potential driver genes and cellular pathways implicated in childhood ACT and demonstrate the existence of different oncogenic routes in this pathology.
doi_str_mv 10.1210/jc.2012-1184
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Objective: We analyzed an international series of 25 childhood ACT using high-resolution single nucleotide polymorphism arrays to: 1) detect focal copy number alterations highlighting candidate driver genes; and 2) compare genetic alterations between Brazilian patients carrying the R337H TP53 mutation and non-Brazilian patients. Results: We identified 16 significantly recurrent chromosomal alterations (q-value &lt; 0.05), the most frequent being −4q34, +9q33-q34, +19p, loss of heterozygosity (LOH) of chromosome 17 and 11p15. Focal amplifications and homozygous deletions comprising well-known oncogenes (MYC, MDM2, PDGFRA, KIT, MCL1, BCL2L1) and tumor suppressors (TP53, RB1, RPH3AL) were identified. In addition, eight focal deletions were detected at 4q34, defining a sharp peak region around the noncoding RNA LINC00290 gene. Although non-Brazilian tumors with a mutated TP53 were similar to Brazilian tumors, those with a wild-type TP53 displayed distinct genomic profiles, with significantly fewer rearrangements (P = 0.019). In particular, three alterations (LOH of chromosome 17, +9q33-q34, and −4q34) were significantly more frequent in TP53-mutated samples. Finally, two of four TP53 wild-type tumors displayed as sole rearrangement a copy-neutral LOH of the imprinted region at 11p15, supporting a major role for this region in ACT development. 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D</creatorcontrib><creatorcontrib>Zambetti, Gerard P</creatorcontrib><creatorcontrib>Figueiredo, Bonald C</creatorcontrib><creatorcontrib>Lalli, Enzo</creatorcontrib><title>SNP Array Profiling of Childhood Adrenocortical Tumors Reveals Distinct Pathways of Tumorigenesis and Highlights Candidate Driver Genes</title><title>The journal of clinical endocrinology and metabolism</title><addtitle>J Clin Endocrinol Metab</addtitle><description>Context: Childhood adrenocortical tumors (ACT) are rare malignancies, except in southern Brazil, where a higher incidence rate is associated to a high frequency of the founder R337H TP53 mutation. To date, copy number alterations in these tumors have only been analyzed by low-resolution comparative genomic hybridization. Objective: We analyzed an international series of 25 childhood ACT using high-resolution single nucleotide polymorphism arrays to: 1) detect focal copy number alterations highlighting candidate driver genes; and 2) compare genetic alterations between Brazilian patients carrying the R337H TP53 mutation and non-Brazilian patients. Results: We identified 16 significantly recurrent chromosomal alterations (q-value &lt; 0.05), the most frequent being −4q34, +9q33-q34, +19p, loss of heterozygosity (LOH) of chromosome 17 and 11p15. Focal amplifications and homozygous deletions comprising well-known oncogenes (MYC, MDM2, PDGFRA, KIT, MCL1, BCL2L1) and tumor suppressors (TP53, RB1, RPH3AL) were identified. In addition, eight focal deletions were detected at 4q34, defining a sharp peak region around the noncoding RNA LINC00290 gene. Although non-Brazilian tumors with a mutated TP53 were similar to Brazilian tumors, those with a wild-type TP53 displayed distinct genomic profiles, with significantly fewer rearrangements (P = 0.019). In particular, three alterations (LOH of chromosome 17, +9q33-q34, and −4q34) were significantly more frequent in TP53-mutated samples. Finally, two of four TP53 wild-type tumors displayed as sole rearrangement a copy-neutral LOH of the imprinted region at 11p15, supporting a major role for this region in ACT development. 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D</creatorcontrib><creatorcontrib>Zambetti, Gerard P</creatorcontrib><creatorcontrib>Figueiredo, Bonald C</creatorcontrib><creatorcontrib>Lalli, Enzo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>The journal of clinical endocrinology and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Letouzé, Eric</au><au>Rosati, Roberto</au><au>Komechen, Heloisa</au><au>Doghman, Mabrouka</au><au>Marisa, Laetitia</au><au>Flück, Christa</au><au>de Krijger, Ronald R</au><au>van Noesel, Max M</au><au>Mas, Jean-Christophe</au><au>Pianovski, Mara A. D</au><au>Zambetti, Gerard P</au><au>Figueiredo, Bonald C</au><au>Lalli, Enzo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SNP Array Profiling of Childhood Adrenocortical Tumors Reveals Distinct Pathways of Tumorigenesis and Highlights Candidate Driver Genes</atitle><jtitle>The journal of clinical endocrinology and metabolism</jtitle><addtitle>J Clin Endocrinol Metab</addtitle><date>2012-07</date><risdate>2012</risdate><volume>97</volume><issue>7</issue><spage>E1284</spage><epage>E1293</epage><pages>E1284-E1293</pages><issn>0021-972X</issn><eissn>1945-7197</eissn><abstract>Context: Childhood adrenocortical tumors (ACT) are rare malignancies, except in southern Brazil, where a higher incidence rate is associated to a high frequency of the founder R337H TP53 mutation. To date, copy number alterations in these tumors have only been analyzed by low-resolution comparative genomic hybridization. Objective: We analyzed an international series of 25 childhood ACT using high-resolution single nucleotide polymorphism arrays to: 1) detect focal copy number alterations highlighting candidate driver genes; and 2) compare genetic alterations between Brazilian patients carrying the R337H TP53 mutation and non-Brazilian patients. Results: We identified 16 significantly recurrent chromosomal alterations (q-value &lt; 0.05), the most frequent being −4q34, +9q33-q34, +19p, loss of heterozygosity (LOH) of chromosome 17 and 11p15. Focal amplifications and homozygous deletions comprising well-known oncogenes (MYC, MDM2, PDGFRA, KIT, MCL1, BCL2L1) and tumor suppressors (TP53, RB1, RPH3AL) were identified. In addition, eight focal deletions were detected at 4q34, defining a sharp peak region around the noncoding RNA LINC00290 gene. Although non-Brazilian tumors with a mutated TP53 were similar to Brazilian tumors, those with a wild-type TP53 displayed distinct genomic profiles, with significantly fewer rearrangements (P = 0.019). In particular, three alterations (LOH of chromosome 17, +9q33-q34, and −4q34) were significantly more frequent in TP53-mutated samples. Finally, two of four TP53 wild-type tumors displayed as sole rearrangement a copy-neutral LOH of the imprinted region at 11p15, supporting a major role for this region in ACT development. Conclusions: Our findings highlight potential driver genes and cellular pathways implicated in childhood ACT and demonstrate the existence of different oncogenic routes in this pathology.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>22539591</pmid><doi>10.1210/jc.2012-1184</doi><orcidid>https://orcid.org/0000-0002-0584-5681</orcidid><orcidid>https://orcid.org/0000-0001-5112-7755</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adolescent
Adrenal Cortex Neoplasms - complications
Adrenal Cortex Neoplasms - epidemiology
Adrenal Cortex Neoplasms - genetics
Adrenocortical Adenoma - complications
Adrenocortical Adenoma - epidemiology
Adrenocortical Adenoma - genetics
Adrenocortical Carcinoma - complications
Adrenocortical Carcinoma - epidemiology
Adrenocortical Carcinoma - genetics
Age of Onset
Cell Transformation, Neoplastic - genetics
Child
Child, Preschool
Cohort Studies
Female
Gene Expression Profiling
Genetic Association Studies
Human health and pathology
Humans
Infant
Infant, Newborn
Life Sciences
Male
Microarray Analysis
Polymorphism, Single Nucleotide - physiology
Signal Transduction - genetics
title SNP Array Profiling of Childhood Adrenocortical Tumors Reveals Distinct Pathways of Tumorigenesis and Highlights Candidate Driver Genes
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