Clinical and molecular aspects of adrenocortical tumourigenesis
Identifieur interne : 000686 ( Istex/Curation ); précédent : 000685; suivant : 000687Clinical and molecular aspects of adrenocortical tumourigenesis
Auteurs : Stan Sidhu [Australie] ; Christine Gicquel [France] ; Christopher P. Bambach ; Peter Campbell ; Christopher Magarey ; Bruce G. Robinson ; Leigh W. Delbridge [Australie]Source :
- 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.
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DOI: 10.1046/j.1445-2197.2003.02746.x
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Christopher P. Bambach<affiliation><mods:affiliation>University of Sydney Endocrine Surgical Unit and</mods:affiliation><wicri:noCountry code="no comma">University of Sydney Endocrine Surgical Unit and</wicri:noCountry></affiliation><affiliation><mods:affiliation>Endocrine Surgical Unit, Liverpool Hospital, Sydney, Australia,</mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation><affiliation><mods:affiliation>Endocrine Surgical Unit, St George Hospital,</mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation><affiliation><mods:affiliation>Department of Medicine and</mods:affiliation><wicri:noCountry code="no comma">Department of Medicine and</wicri:noCountry></affiliation>Le document en format XML
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Bambach</name><affiliation><mods:affiliation>University of Sydney Endocrine Surgical Unit and</mods:affiliation><wicri:noCountry code="no comma">University of Sydney Endocrine Surgical Unit and</wicri:noCountry></affiliation></author><author><name sortKey="Campbell, Peter" sort="Campbell, Peter" uniqKey="Campbell P" first="Peter" last="Campbell">Peter Campbell</name><affiliation><mods:affiliation>Endocrine Surgical Unit, St George Hospital,</mods:affiliation></affiliation><affiliation><mods:affiliation>Endocrine Surgical Unit, Liverpool Hospital, Sydney, Australia,</mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation></author><author><name sortKey="Magarey, Christopher" sort="Magarey, Christopher" uniqKey="Magarey C" first="Christopher" last="Magarey">Christopher Magarey</name><affiliation><mods:affiliation>Endocrine Surgical Unit, St George Hospital,</mods:affiliation><wicri:noCountry code="subField"></wicri:noCountry></affiliation></author><author><name sortKey="Robinson, Bruce G" sort="Robinson, Bruce G" uniqKey="Robinson B" first="Bruce G." last="Robinson">Bruce G. 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Delbridge</name><affiliation><mods:affiliation>University of Sydney Endocrine Surgical Unit and</mods:affiliation></affiliation><affiliation wicri:level="4"><mods:affiliation>Department of Surgery, University of Sydney,</mods:affiliation><orgName type="university">Université de Sydney</orgName><country>Australie</country><placeName><settlement type="city">Sydney</settlement><region type="état">Nouvelle-Galles du Sud</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">ANZ Journal of Surgery</title><title level="j" type="alt">ANZ JOURNAL SURGERY</title><idno type="ISSN">1445-1433</idno><idno type="eISSN">1445-2197</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">2003-09</date></imprint><idno type="ISSN">1445-1433</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1445-1433</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" 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></record>Pour manipuler ce document sous Unix (Dilib)
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