Clinical and molecular aspects of adrenocortical tumourigenesis
Identifieur interne : 000686 ( Istex/Corpus ); précédent : 000685; suivant : 000687Clinical and molecular aspects of adrenocortical tumourigenesis
Auteurs : Stan Sidhu ; Christine Gicquel ; Christopher P. Bambach ; Peter Campbell ; Christopher Magarey ; Bruce G. Robinson ; Leigh W. DelbridgeSource :
- ANZ Journal of Surgery [ 1445-1433 ] ; 2003-09.
English descriptors
- KwdEn :
- Acth, Acth receptor, Adenoma, Adrenal, Adrenal adenoma, Adrenal adenomas, Adrenal gland, Adrenal glands, Adrenal mass, Adrenal masses, Adrenal tumors, Adrenalectomy, Adrenocortical, Adrenocortical adenomas, Adrenocortical cancer, Adrenocortical carcinoma, Adrenocortical tumors, Adrenocortical tumourigenesis, Adrenocortical tumours, Aldosterone, Aldosteronism, Allele, Benign, Best chance, Bilateral, Breast cancer, Carcinoma, Cdkn1c, Cell cycle, Cell proliferation, Chromosomal, Chromosomal region, Chromosome, Clin, Comparative genomic hybridization, Complete resection, Cortisol, Cyclin, Endocrine, Endocrinol, Exon, Familial cancer syndromes, Gene, Genomic, Germline, Gicquel, Growth factors, Heterozygosity, Human adrenocortical neoplasms, Human cancers, Hypercortisolism, Hyperplasia, Hypertension, Igf2, Igf2 gene, Kinase, Kinase inhibitor, Laparoscopic, Laparoscopic adrenalectomy, Lesion, Locus, Malignancy, Malignant, Malignant tumours, Maternal allele, Men1, Metab, Molecular markers, Mutation, Neoplasm, Oncogene, Oncogenic mutations, Overexpression, Paternal, Paternal allele, Pathway, Plasma renin activity, Primary aldosteronism, Progression, Receptor, Reincke, Resection, Shore hospital, Sidhu, Sporadic adrenocortical tumors, Subclinical syndrome, Suppressor, Surg, Syndrome, Tumour, Tumour suppressor gene, Tumour suppressor genes, Tumourigenesis.
- Teeft :
- Acth, Acth receptor, Adenoma, Adrenal, Adrenal adenoma, Adrenal adenomas, Adrenal gland, Adrenal glands, Adrenal mass, Adrenal masses, Adrenal tumors, Adrenalectomy, Adrenocortical, Adrenocortical adenomas, Adrenocortical cancer, Adrenocortical carcinoma, Adrenocortical tumors, Adrenocortical tumourigenesis, Adrenocortical tumours, Aldosterone, Aldosteronism, Allele, Benign, Best chance, Bilateral, Breast cancer, Carcinoma, Cdkn1c, Cell cycle, Cell proliferation, Chromosomal, Chromosomal region, Chromosome, Clin, Comparative genomic hybridization, Complete resection, Cortisol, Cyclin, Endocrine, Endocrinol, Exon, Familial cancer syndromes, Gene, Genomic, Germline, Gicquel, Growth factors, Heterozygosity, Human adrenocortical neoplasms, Human cancers, Hypercortisolism, Hyperplasia, Hypertension, Igf2, Igf2 gene, Kinase, Kinase inhibitor, Laparoscopic, Laparoscopic adrenalectomy, Lesion, Locus, Malignancy, Malignant, Malignant tumours, Maternal allele, Men1, Metab, Molecular markers, Mutation, Neoplasm, Oncogene, Oncogenic mutations, Overexpression, Paternal, Paternal allele, Pathway, Plasma renin activity, Primary aldosteronism, Progression, Receptor, Reincke, Resection, Shore hospital, Sidhu, Sporadic adrenocortical tumors, Subclinical syndrome, Suppressor, Surg, Syndrome, Tumour, Tumour suppressor gene, Tumour suppressor genes, Tumourigenesis.
Abstract
Adrenal masses are a common problem affecting 3−7% of the population. The majority turn out to be benign adrenocortical adenomas, which may be functional or non‐functional. Much more rarely, these masses represent a primary adrenal carcinoma. It is becoming increasingly recognized that of the benign functioning adenomas or hyperplasias, the majority will hypersecrete aldosterone and this will be more frequently detected when hypertensive populations are screened for this disease. In contrast, the incidence of primary adrenocortical carcinoma has remained steady and for this disease, surgery represents the mainstay of treatment. The advent of laparoscopic adrenal surgery has lowered the threshold size for recommending surgery for asymptomatic adrenal masses and as such, an increased proportion of adrenocortical cancers are being resected and detected at an earlier stage. Recent progress has been made in our understanding of the key genetic changes which underpin the biology of this disease. Progression from adrenal adenoma to carcinoma involves a monoclonal proliferation of cells which, among other defects, have undergone chromosomal duplication at the 11p15.5 locus leading to overexpression of the IGF2 gene and abrogation of expression of the CDKN1C and H19 genes. TP53 is involved in progression to carcinoma in a subset of patients and the frequency of ACTH receptor deletion needs to be more fully explored. Other key oncogenes and tumour suppressor genes remain to be identified although the chromosomal loci in which they lie can be identified at 17p, 1p, 2p16 and 11q13 for tumour suppressor genes and chromosomes 4, 5 and 12 for oncogenes.
Url:
DOI: 10.1046/j.1445-2197.2003.02746.x
Links to Exploration step
ISTEX:231F98E3854ED9F6125B9D2AA392BAFAA12D16B1Le document en format XML
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Robinson</name><affiliation><mods:affiliation>Department of Endocrinology, Royal North Shore Hospital,</mods:affiliation></affiliation><affiliation><mods:affiliation>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medicine and</mods:affiliation></affiliation></author><author><name sortKey="Delbridge, Leigh W" sort="Delbridge, Leigh W" uniqKey="Delbridge L" first="Leigh W." last="Delbridge">Leigh W. 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xml:lang="en"><term>Acth</term><term>Acth receptor</term><term>Adenoma</term><term>Adrenal</term><term>Adrenal adenoma</term><term>Adrenal adenomas</term><term>Adrenal gland</term><term>Adrenal glands</term><term>Adrenal mass</term><term>Adrenal masses</term><term>Adrenal tumors</term><term>Adrenalectomy</term><term>Adrenocortical</term><term>Adrenocortical adenomas</term><term>Adrenocortical cancer</term><term>Adrenocortical carcinoma</term><term>Adrenocortical tumors</term><term>Adrenocortical tumourigenesis</term><term>Adrenocortical tumours</term><term>Aldosterone</term><term>Aldosteronism</term><term>Allele</term><term>Benign</term><term>Best chance</term><term>Bilateral</term><term>Breast cancer</term><term>Carcinoma</term><term>Cdkn1c</term><term>Cell cycle</term><term>Cell proliferation</term><term>Chromosomal</term><term>Chromosomal region</term><term>Chromosome</term><term>Clin</term><term>Comparative genomic hybridization</term><term>Complete resection</term><term>Cortisol</term><term>Cyclin</term><term>Endocrine</term><term>Endocrinol</term><term>Exon</term><term>Familial cancer syndromes</term><term>Gene</term><term>Genomic</term><term>Germline</term><term>Gicquel</term><term>Growth factors</term><term>Heterozygosity</term><term>Human adrenocortical neoplasms</term><term>Human cancers</term><term>Hypercortisolism</term><term>Hyperplasia</term><term>Hypertension</term><term>Igf2</term><term>Igf2 gene</term><term>Kinase</term><term>Kinase inhibitor</term><term>Laparoscopic</term><term>Laparoscopic adrenalectomy</term><term>Lesion</term><term>Locus</term><term>Malignancy</term><term>Malignant</term><term>Malignant tumours</term><term>Maternal allele</term><term>Men1</term><term>Metab</term><term>Molecular markers</term><term>Mutation</term><term>Neoplasm</term><term>Oncogene</term><term>Oncogenic mutations</term><term>Overexpression</term><term>Paternal</term><term>Paternal allele</term><term>Pathway</term><term>Plasma renin activity</term><term>Primary aldosteronism</term><term>Progression</term><term>Receptor</term><term>Reincke</term><term>Resection</term><term>Shore hospital</term><term>Sidhu</term><term>Sporadic adrenocortical tumors</term><term>Subclinical syndrome</term><term>Suppressor</term><term>Surg</term><term>Syndrome</term><term>Tumour</term><term>Tumour suppressor gene</term><term>Tumour suppressor genes</term><term>Tumourigenesis</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Acth</term><term>Acth receptor</term><term>Adenoma</term><term>Adrenal</term><term>Adrenal adenoma</term><term>Adrenal adenomas</term><term>Adrenal gland</term><term>Adrenal glands</term><term>Adrenal mass</term><term>Adrenal masses</term><term>Adrenal tumors</term><term>Adrenalectomy</term><term>Adrenocortical</term><term>Adrenocortical adenomas</term><term>Adrenocortical cancer</term><term>Adrenocortical carcinoma</term><term>Adrenocortical tumors</term><term>Adrenocortical tumourigenesis</term><term>Adrenocortical tumours</term><term>Aldosterone</term><term>Aldosteronism</term><term>Allele</term><term>Benign</term><term>Best chance</term><term>Bilateral</term><term>Breast cancer</term><term>Carcinoma</term><term>Cdkn1c</term><term>Cell cycle</term><term>Cell proliferation</term><term>Chromosomal</term><term>Chromosomal region</term><term>Chromosome</term><term>Clin</term><term>Comparative genomic hybridization</term><term>Complete resection</term><term>Cortisol</term><term>Cyclin</term><term>Endocrine</term><term>Endocrinol</term><term>Exon</term><term>Familial cancer syndromes</term><term>Gene</term><term>Genomic</term><term>Germline</term><term>Gicquel</term><term>Growth factors</term><term>Heterozygosity</term><term>Human adrenocortical neoplasms</term><term>Human cancers</term><term>Hypercortisolism</term><term>Hyperplasia</term><term>Hypertension</term><term>Igf2</term><term>Igf2 gene</term><term>Kinase</term><term>Kinase inhibitor</term><term>Laparoscopic</term><term>Laparoscopic adrenalectomy</term><term>Lesion</term><term>Locus</term><term>Malignancy</term><term>Malignant</term><term>Malignant tumours</term><term>Maternal allele</term><term>Men1</term><term>Metab</term><term>Molecular markers</term><term>Mutation</term><term>Neoplasm</term><term>Oncogene</term><term>Oncogenic mutations</term><term>Overexpression</term><term>Paternal</term><term>Paternal allele</term><term>Pathway</term><term>Plasma renin activity</term><term>Primary aldosteronism</term><term>Progression</term><term>Receptor</term><term>Reincke</term><term>Resection</term><term>Shore hospital</term><term>Sidhu</term><term>Sporadic adrenocortical tumors</term><term>Subclinical syndrome</term><term>Suppressor</term><term>Surg</term><term>Syndrome</term><term>Tumour</term><term>Tumour suppressor gene</term><term>Tumour suppressor genes</term><term>Tumourigenesis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Adrenal masses are a common problem affecting 3−7% of the population. The majority turn out to be benign adrenocortical adenomas, which may be functional or non‐functional. Much more rarely, these masses represent a primary adrenal carcinoma. It is becoming increasingly recognized that of the benign functioning adenomas or hyperplasias, the majority will hypersecrete aldosterone and this will be more frequently detected when hypertensive populations are screened for this disease. In contrast, the incidence of primary adrenocortical carcinoma has remained steady and for this disease, surgery represents the mainstay of treatment. The advent of laparoscopic adrenal surgery has lowered the threshold size for recommending surgery for asymptomatic adrenal masses and as such, an increased proportion of adrenocortical cancers are being resected and detected at an earlier stage. Recent progress has been made in our understanding of the key genetic changes which underpin the biology of this disease. Progression from adrenal adenoma to carcinoma involves a monoclonal proliferation of cells which, among other defects, have undergone chromosomal duplication at the 11p15.5 locus leading to overexpression of the IGF2 gene and abrogation of expression of the CDKN1C and H19 genes. TP53 is involved in progression to carcinoma in a subset of patients and the frequency of ACTH receptor deletion needs to be more fully explored. Other key oncogenes and tumour suppressor genes remain to be identified although the chromosomal loci in which they lie can be identified at 17p, 1p, 2p16 and 11q13 for tumour suppressor genes and chromosomes 4, 5 and 12 for oncogenes.</div></front></TEI><istex><corpusName>wiley</corpusName><keywords><teeft><json:string>tumour</json:string><json:string>adrenocortical</json:string><json:string>mutation</json:string><json:string>adenoma</json:string><json:string>clin</json:string><json:string>endocrinol</json:string><json:string>malignant</json:string><json:string>suppressor</json:string><json:string>igf2</json:string><json:string>metab</json:string><json:string>adrenalectomy</json:string><json:string>oncogene</json:string><json:string>laparoscopic</json:string><json:string>allele</json:string><json:string>surg</json:string><json:string>carcinoma</json:string><json:string>adrenal</json:string><json:string>receptor</json:string><json:string>tumourigenesis</json:string><json:string>chromosome</json:string><json:string>hypertension</json:string><json:string>kinase</json:string><json:string>chromosomal</json:string><json:string>reincke</json:string><json:string>men1</json:string><json:string>tumour suppressor genes</json:string><json:string>hypercortisolism</json:string><json:string>neoplasm</json:string><json:string>gicquel</json:string><json:string>aldosterone</json:string><json:string>cdkn1c</json:string><json:string>cyclin</json:string><json:string>laparoscopic adrenalectomy</json:string><json:string>resection</json:string><json:string>adrenocortical cancer</json:string><json:string>cortisol</json:string><json:string>sidhu</json:string><json:string>aldosteronism</json:string><json:string>overexpression</json:string><json:string>adrenocortical carcinoma</json:string><json:string>pathway</json:string><json:string>benign</json:string><json:string>syndrome</json:string><json:string>germline</json:string><json:string>genomic</json:string><json:string>adrenocortical tumours</json:string><json:string>adrenocortical tumourigenesis</json:string><json:string>heterozygosity</json:string><json:string>primary aldosteronism</json:string><json:string>paternal</json:string><json:string>exon</json:string><json:string>endocrine</json:string><json:string>sporadic adrenocortical tumors</json:string><json:string>acth</json:string><json:string>hyperplasia</json:string><json:string>adrenal adenoma</json:string><json:string>adrenal tumors</json:string><json:string>molecular markers</json:string><json:string>maternal allele</json:string><json:string>adrenocortical tumors</json:string><json:string>adrenal masses</json:string><json:string>malignancy</json:string><json:string>gene</json:string><json:string>tumour suppressor gene</json:string><json:string>adrenocortical adenomas</json:string><json:string>human adrenocortical neoplasms</json:string><json:string>chromosomal region</json:string><json:string>breast cancer</json:string><json:string>adrenal mass</json:string><json:string>lesion</json:string><json:string>locus</json:string><json:string>progression</json:string><json:string>cell proliferation</json:string><json:string>human cancers</json:string><json:string>plasma renin activity</json:string><json:string>growth factors</json:string><json:string>adrenal glands</json:string><json:string>shore hospital</json:string><json:string>adrenal adenomas</json:string><json:string>oncogenic mutations</json:string><json:string>kinase inhibitor</json:string><json:string>cell cycle</json:string><json:string>comparative genomic hybridization</json:string><json:string>paternal allele</json:string><json:string>acth receptor</json:string><json:string>adrenal gland</json:string><json:string>best chance</json:string><json:string>familial cancer syndromes</json:string><json:string>complete resection</json:string><json:string>subclinical syndrome</json:string><json:string>malignant tumours</json:string><json:string>igf2 gene</json:string><json:string>bilateral</json:string></teeft></keywords><author><json:item><name>Stan Sidhu</name><affiliations><json:string>University of Sydney Endocrine Surgical Unit and</json:string><json:string>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</json:string><json:string>Department of Surgery, University of Sydney,</json:string></affiliations></json:item><json:item><name>Christine Gicquel</name><affiliations><json:string>Laboratoire d’Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, Paris, France</json:string></affiliations></json:item><json:item><name>Christopher P. Bambach</name><affiliations><json:string>University of Sydney Endocrine Surgical Unit and</json:string></affiliations></json:item><json:item><name>Peter Campbell</name><affiliations><json:string>Endocrine Surgical Unit, St George Hospital,</json:string><json:string>Endocrine Surgical Unit, Liverpool Hospital, Sydney, Australia,</json:string></affiliations></json:item><json:item><name>Christopher Magarey</name><affiliations><json:string>Endocrine Surgical Unit, St George Hospital,</json:string></affiliations></json:item><json:item><name>Bruce G. Robinson</name><affiliations><json:string>Department of Endocrinology, Royal North Shore Hospital,</json:string><json:string>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</json:string><json:string>Department of Medicine and</json:string></affiliations></json:item><json:item><name>Leigh W. Delbridge</name><affiliations><json:string>University of Sydney Endocrine Surgical Unit and</json:string><json:string>Department of Surgery, University of Sydney,</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>adrenal cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>adrenal cortical adenoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>adrenal cortical carcinoma</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>adrenal gland neoplasm</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>adrenal glands</value></json:item></subject><articleId><json:string>ANS2746</json:string></articleId><arkIstex>ark:/67375/WNG-T5DDFVW6-C</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>reviewArticle</json:string></originalGenre><abstract>Adrenal masses are a common problem affecting 3−7% of the population. The majority turn out to be benign adrenocortical adenomas, which may be functional or non‐functional. Much more rarely, these masses represent a primary adrenal carcinoma. It is becoming increasingly recognized that of the benign functioning adenomas or hyperplasias, the majority will hypersecrete aldosterone and this will be more frequently detected when hypertensive populations are screened for this disease. In contrast, the incidence of primary adrenocortical carcinoma has remained steady and for this disease, surgery represents the mainstay of treatment. The advent of laparoscopic adrenal surgery has lowered the threshold size for recommending surgery for asymptomatic adrenal masses and as such, an increased proportion of adrenocortical cancers are being resected and detected at an earlier stage. Recent progress has been made in our understanding of the key genetic changes which underpin the biology of this disease. Progression from adrenal adenoma to carcinoma involves a monoclonal proliferation of cells which, among other defects, have undergone chromosomal duplication at the 11p15.5 locus leading to overexpression of the IGF2 gene and abrogation of expression of the CDKN1C and H19 genes. TP53 is involved in progression to carcinoma in a subset of patients and the frequency of ACTH receptor deletion needs to be more fully explored. Other key oncogenes and tumour suppressor genes remain to be identified although the chromosomal loci in which they lie can be identified at 17p, 1p, 2p16 and 11q13 for tumour suppressor genes and chromosomes 4, 5 and 12 for oncogenes.</abstract><qualityIndicators><score>10</score><pdfWordCount>8969</pdfWordCount><pdfCharCount>57298</pdfCharCount><pdfVersion>1.2</pdfVersion><pdfPageCount>12</pdfPageCount><pdfPageSize>595 x 780 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>252</abstractWordCount><abstractCharCount>1666</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>Clinical and molecular aspects of adrenocortical tumourigenesis</title><pmid><json:string>12956790</json:string></pmid><genre><json:string>review-article</json:string></genre><host><title>ANZ Journal of Surgery</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1445-2197</json:string></doi><issn><json:string>1445-1433</json:string></issn><eissn><json:string>1445-2197</json:string></eissn><publisherId><json:string>ANS</json:string></publisherId><volume>73</volume><issue>9</issue><pages><first>727</first><last>738</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1969</json:string><json:string>2003</json:string></date><geogName></geogName><orgName><json:string>France Adrenal</json:string><json:string>Swedish and American Registries</json:string><json:string>Department of Surgery, Royal North Shore Hospital, St Leonards, New South Wales</json:string><json:string>Department of Endocrinology, Royal North Shore Hospital</json:string><json:string>Department of Surgery, University of Sydney</json:string><json:string>Surgeons Research Foundation</json:string><json:string>Department of Medicine</json:string><json:string>Liverpool Hospital, Sydney, Australia</json:string><json:string>Kolling Institute of Medical Research, Royal North Shore Hospital</json:string><json:string>National Italian Study Group on Adrenal Tumours</json:string></orgName><orgName_funder></orgName_funder><orgName_provider></orgName_provider><persName><json:string>C. P. Bambach</json:string><json:string>College</json:string><json:string>George Hospital</json:string><json:string>B. G. Robinson</json:string><json:string>L. W. Delbridge</json:string><json:string>C. Gicquel</json:string><json:string>P. Campbell</json:string><json:string>Polyclonality</json:string><json:string>S. 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Pty</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-09"></date></publicationStmt><notesStmt><note type="content-type" subtype="review-article" source="reviewArticle" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="review-article"><analytic><title level="a" type="main">Clinical and molecular aspects of adrenocortical tumourigenesis</title><title level="a" type="short">Adrenocortical tumourigenesis</title><author xml:id="author-0000"><persName><forename type="first">Stan</forename><surname>Sidhu</surname></persName><affiliation>University of Sydney Endocrine Surgical Unit and</affiliation><affiliation>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</affiliation><affiliation>Department of Surgery, University of Sydney,</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Christine</forename><surname>Gicquel</surname></persName><affiliation>Laboratoire d’Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, Paris, France<address><country key="FR"></country></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Christopher P.</forename><surname>Bambach</surname></persName><affiliation>University of Sydney Endocrine Surgical Unit and</affiliation></author><author xml:id="author-0003"><persName><forename type="first">Peter</forename><surname>Campbell</surname></persName><affiliation>Endocrine Surgical Unit, St George Hospital,</affiliation><affiliation>Endocrine Surgical Unit, Liverpool Hospital, Sydney, Australia,<address><country key="AU"></country></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first"> Christopher</forename><surname>Magarey</surname></persName><affiliation>Endocrine Surgical Unit, St George Hospital,</affiliation></author><author xml:id="author-0005"><persName><forename type="first">Bruce G.</forename><surname>Robinson</surname></persName><affiliation>Department of Endocrinology, Royal North Shore Hospital,</affiliation><affiliation>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</affiliation><affiliation>Department of Medicine and</affiliation></author><author xml:id="author-0006"><persName><forename type="first">Leigh W.</forename><surname>Delbridge</surname></persName><affiliation>University of Sydney Endocrine Surgical Unit and</affiliation><affiliation>Department of Surgery, University of Sydney,</affiliation></author><idno type="istex">231F98E3854ED9F6125B9D2AA392BAFAA12D16B1</idno><idno type="ark">ark:/67375/WNG-T5DDFVW6-C</idno><idno type="DOI">10.1046/j.1445-2197.2003.02746.x</idno><idno type="unit">ANS2746</idno><idno type="toTypesetVersion">file:ANS.ANS2746.pdf</idno></analytic><monogr><title level="j" type="main">ANZ Journal of Surgery</title><title level="j" type="alt">ANZ JOURNAL SURGERY</title><idno type="pISSN">1445-1433</idno><idno type="eISSN">1445-2197</idno><idno type="book-DOI">10.1111/(ISSN)1445-2197</idno><idno type="book-part-DOI">10.1111/ans.2003.73.issue-9</idno><idno type="product">ANS</idno><idno type="publisherDivision">ST</idno><imprint><biblScope unit="vol">73</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="727">727</biblScope><biblScope unit="page" to="738">738</biblScope><publisher>Blackwell Science Pty</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2003-09"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p>Adrenal masses are a common problem affecting 3−7% of the population. The majority turn out to be benign adrenocortical adenomas, which may be functional or non‐functional. Much more rarely, these masses represent a primary adrenal carcinoma. It is becoming increasingly recognized that of the benign functioning adenomas or hyperplasias, the majority will hypersecrete aldosterone and this will be more frequently detected when hypertensive populations are screened for this disease. In contrast, the incidence of primary adrenocortical carcinoma has remained steady and for this disease, surgery represents the mainstay of treatment. The advent of laparoscopic adrenal surgery has lowered the threshold size for recommending surgery for asymptomatic adrenal masses and as such, an increased proportion of adrenocortical cancers are being resected and detected at an earlier stage. Recent progress has been made in our understanding of the key genetic changes which underpin the biology of this disease. Progression from adrenal adenoma to carcinoma involves a monoclonal proliferation of cells which, among other defects, have undergone chromosomal duplication at the 11p15.5 locus leading to overexpression of the <hi rend="italic">IGF2</hi> gene and abrogation of expression of the <hi rend="italic">CDKN1C</hi> and <hi rend="italic">H19</hi> genes. <hi rend="italic">TP53</hi> is involved in progression to carcinoma in a subset of patients and the frequency of ACTH receptor deletion needs to be more fully explored. Other key oncogenes and tumour suppressor genes remain to be identified although the chromosomal loci in which they lie can be identified at 17p, 1p, 2p16 and 11q13 for tumour suppressor genes and chromosomes 4, 5 and 12 for oncogenes.</p></abstract><textClass><keywords xml:lang="en"><term xml:id="k1">adrenal cortex</term><term xml:id="k2">adrenal cortical adenoma</term><term xml:id="k3">adrenal cortical carcinoma</term><term xml:id="k4">adrenal gland neoplasm</term><term xml:id="k5">adrenal glands</term></keywords><keywords rend="tocHeading1"><term>Review Articles</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/231F98E3854ED9F6125B9D2AA392BAFAA12D16B1/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Pty</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1445-2197</doi><issn type="print">1445-1433</issn><issn type="electronic">1445-2197</issn><idGroup><id type="product" value="ANS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANZ JOURNAL SURGERY">ANZ Journal of Surgery</title></titleGroup></publicationMeta><publicationMeta level="part" position="09009"><doi origin="wiley">10.1111/ans.2003.73.issue-9</doi><numberingGroup><numbering type="journalVolume" number="73">73</numbering><numbering type="journalIssue" number="9">9</numbering></numberingGroup><coverDate startDate="2003-09">September 2003</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="0072700" status="forIssue"><doi origin="wiley">10.1046/j.1445-2197.2003.02746.x</doi><idGroup><id type="unit" value="ANS2746"></id></idGroup><titleGroup><title type="tocHeading1">Review Articles</title></titleGroup><eventGroup><event type="firstOnline" date="2003-09-08"></event><event type="publishedOnlineFinalForm" date="2003-09-08"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:Header result:Header" date="2010-02-28"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-04"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="727">727</numbering><numbering type="pageLast" number="738">738</numbering></numberingGroup><correspondenceTo>Dr S. Sidhu, Department of Surgery, Royal North Shore Hospital, St Leonards, New South Wales 2065, Australia.
Email: <email>sidhu@med.usyd.edu.au</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANS.ANS2746.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication 27 March 2003.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="105"></count><count type="wordTotal" number="6734"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Clinical and molecular aspects of adrenocortical tumourigenesis</title><title type="shortAuthors">Sidhu <i>et al.</i></title><title type="short">Adrenocortical tumourigenesis</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Stan</givenNames><familyName>Sidhu</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a4"><personName><givenNames>Christine</givenNames><familyName>Gicquel</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Christopher P.</givenNames><familyName>Bambach</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a5 #a6"><personName><givenNames>Peter</givenNames><familyName>Campbell</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a5"><personName><givenNames> Christopher</givenNames><familyName>Magarey</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a7 #a2 #a8"><personName><givenNames>Bruce G.</givenNames><familyName>Robinson</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1 #a3"><personName><givenNames>Leigh W.</givenNames><familyName>Delbridge</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>University of Sydney Endocrine Surgical Unit and</unparsedAffiliation></affiliation><affiliation xml:id="a7"><unparsedAffiliation>Department of Endocrinology, Royal North Shore Hospital,</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</unparsedAffiliation></affiliation><affiliation xml:id="a8"><unparsedAffiliation>Department of Medicine and</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Department of Surgery, University of Sydney,</unparsedAffiliation></affiliation><affiliation xml:id="a5"><unparsedAffiliation>Endocrine Surgical Unit, St George Hospital,</unparsedAffiliation></affiliation><affiliation xml:id="a6" countryCode="AU"><unparsedAffiliation>Endocrine Surgical Unit, Liverpool Hospital, Sydney, Australia,</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="FR"><unparsedAffiliation>Laboratoire d’Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, Paris, France</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">adrenal cortex</keyword><keyword xml:id="k2">adrenal cortical adenoma</keyword><keyword xml:id="k3">adrenal cortical carcinoma</keyword><keyword xml:id="k4">adrenal gland neoplasm</keyword><keyword xml:id="k5">adrenal glands</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Adrenal masses are a common problem affecting 3−7% of the population. The majority turn out to be benign adrenocortical adenomas, which may be functional or non‐functional. Much more rarely, these masses represent a primary adrenal carcinoma. It is becoming increasingly recognized that of the benign functioning adenomas or hyperplasias, the majority will hypersecrete aldosterone and this will be more frequently detected when hypertensive populations are screened for this disease. In contrast, the incidence of primary adrenocortical carcinoma has remained steady and for this disease, surgery represents the mainstay of treatment. The advent of laparoscopic adrenal surgery has lowered the threshold size for recommending surgery for asymptomatic adrenal masses and as such, an increased proportion of adrenocortical cancers are being resected and detected at an earlier stage. Recent progress has been made in our understanding of the key genetic changes which underpin the biology of this disease. Progression from adrenal adenoma to carcinoma involves a monoclonal proliferation of cells which, among other defects, have undergone chromosomal duplication at the 11p15.5 locus leading to overexpression of the <i>IGF2</i> gene and abrogation of expression of the <i>CDKN1C</i> and <i>H19</i> genes. <i>TP53</i> is involved in progression to carcinoma in a subset of patients and the frequency of ACTH receptor deletion needs to be more fully explored. Other key oncogenes and tumour suppressor genes remain to be identified although the chromosomal loci in which they lie can be identified at 17p, 1p, 2p16 and 11q13 for tumour suppressor genes and chromosomes 4, 5 and 12 for oncogenes.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="n-fnt-1" numbered="no"><p> <b>S. Sidhu</b> PhD, FRACS; <b>C. Gicquel</b> MD, PhD; <b>C. P. Bambach</b> MD, FRACS; <b>P. Campbell</b> FRACS; <b>C. Magarey</b> MS, FRACS; <b>B. G. Robinson</b> MD, FRACP; <b>L. W. Delbridge</b> MD, FRACS.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Clinical and molecular aspects of adrenocortical tumourigenesis</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Adrenocortical tumourigenesis</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Clinical and molecular aspects of adrenocortical tumourigenesis</title></titleInfo><name type="personal"><namePart type="given">Stan</namePart><namePart type="family">Sidhu</namePart><affiliation>University of Sydney Endocrine Surgical Unit and</affiliation><affiliation>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</affiliation><affiliation>Department of Surgery, University of Sydney,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Gicquel</namePart><affiliation>Laboratoire d’Explorations Fonctionnelles Endocriniennes, Hôpital Trousseau, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher P.</namePart><namePart type="family">Bambach</namePart><affiliation>University of Sydney Endocrine Surgical Unit and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Peter</namePart><namePart type="family">Campbell</namePart><affiliation>Endocrine Surgical Unit, St George Hospital,</affiliation><affiliation>Endocrine Surgical Unit, Liverpool Hospital, Sydney, Australia,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher</namePart><namePart type="family">Magarey</namePart><affiliation>Endocrine Surgical Unit, St George Hospital,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bruce G.</namePart><namePart type="family">Robinson</namePart><affiliation>Department of Endocrinology, Royal North Shore Hospital,</affiliation><affiliation>Cancer Genetics, Kolling Institute of Medical Research, Royal North Shore Hospital,</affiliation><affiliation>Department of Medicine and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Leigh W.</namePart><namePart type="family">Delbridge</namePart><affiliation>University of Sydney Endocrine Surgical Unit and</affiliation><affiliation>Department of Surgery, University of Sydney,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Blackwell Science Pty</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2003-09</dateIssued><edition>Accepted for publication 27 March 2003.</edition><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><extent unit="figures">2</extent><extent unit="tables">2</extent><extent unit="formulas">0</extent><extent unit="references">105</extent><extent unit="linksCrossRef">0</extent><extent unit="words">6734</extent></physicalDescription><abstract lang="en">Adrenal masses are a common problem affecting 3−7% of the population. The majority turn out to be benign adrenocortical adenomas, which may be functional or non‐functional. Much more rarely, these masses represent a primary adrenal carcinoma. It is becoming increasingly recognized that of the benign functioning adenomas or hyperplasias, the majority will hypersecrete aldosterone and this will be more frequently detected when hypertensive populations are screened for this disease. In contrast, the incidence of primary adrenocortical carcinoma has remained steady and for this disease, surgery represents the mainstay of treatment. The advent of laparoscopic adrenal surgery has lowered the threshold size for recommending surgery for asymptomatic adrenal masses and as such, an increased proportion of adrenocortical cancers are being resected and detected at an earlier stage. Recent progress has been made in our understanding of the key genetic changes which underpin the biology of this disease. Progression from adrenal adenoma to carcinoma involves a monoclonal proliferation of cells which, among other defects, have undergone chromosomal duplication at the 11p15.5 locus leading to overexpression of the IGF2 gene and abrogation of expression of the CDKN1C and H19 genes. TP53 is involved in progression to carcinoma in a subset of patients and the frequency of ACTH receptor deletion needs to be more fully explored. Other key oncogenes and tumour suppressor genes remain to be identified although the chromosomal loci in which they lie can be identified at 17p, 1p, 2p16 and 11q13 for tumour suppressor genes and chromosomes 4, 5 and 12 for oncogenes.</abstract><subject lang="en"><genre>keywords</genre><topic>adrenal cortex</topic><topic>adrenal cortical adenoma</topic><topic>adrenal cortical carcinoma</topic><topic>adrenal gland neoplasm</topic><topic>adrenal glands</topic></subject><relatedItem type="host"><titleInfo><title>ANZ Journal of Surgery</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">1445-1433</identifier><identifier type="eISSN">1445-2197</identifier><identifier type="DOI">10.1111/(ISSN)1445-2197</identifier><identifier type="PublisherID">ANS</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>73</number></detail><detail type="issue"><caption>no.</caption><number>9</number></detail><extent unit="pages"><start>727</start><end>738</end></extent></part></relatedItem><identifier type="istex">231F98E3854ED9F6125B9D2AA392BAFAA12D16B1</identifier><identifier type="ark">ark:/67375/WNG-T5DDFVW6-C</identifier><identifier type="DOI">10.1046/j.1445-2197.2003.02746.x</identifier><identifier type="ArticleID">ANS2746</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Blackwell Science Pty</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/document/231F98E3854ED9F6125B9D2AA392BAFAA12D16B1/metadata/json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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