ArticleBritish journal of cancer1999
Highly consistent genetic alterations in childhood adrenocortical tumours detected by comparative genomic hybridization.
Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed.
- Development and function of the fetal adrenal.Reviews in endocrine & metabolic disorders · 2023Review
- Article
- A Novel Population of Inner Cortical Cells in the Adrenal Gland That Displays Sexually Dimorphic Expression of Thyroid Hormone Receptor-β1.Endocrinology · 2015Article
- Pediatric adrenocortical tumors: what they can tell us on adrenal development and comparison with adult adrenal tumors.Frontiers in endocrinology · 2015Review
- Genetics and epigenetics of adrenocortical tumors.Molecular and cellular endocrinology · 2014Review
- Inhibin alpha-subunit (INHA) expression in adrenocortical cancer is linked to genetic and epigenetic INHA promoter variation.PloS one · 2014Article
- Towards an understanding of the role of p53 in adrenocortical carcinogenesis.Molecular and cellular endocrinology · 2012Review
- Article
- Identification of recurrent regions of chromosome loss and gain in vestibular schwannomas using comparative genomic hybridisation.Journal of medical genetics · 2003Article
- Activin induces x-zone apoptosis that inhibits luteinizing hormone-dependent adrenocortical tumor formation in inhibin-deficient mice.Molecular and cellular biology · 2003Article
- Genetic background of adrenocortical tumor development.World journal of surgery · 2001Review
- Are there low-penetrance TP53 Alleles? evidence from childhood adrenocortical tumors.American journal of human genetics · 1999Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have examined 11 cases of childhood adrenocortical tumours for copy number changes using comparative genomic hybridization (CGH). The changes seen are highly consistent between cases, and are independent of tumour type (carcinoma versus adenoma) or the presence of a germline TP53 mutation. The regions of chromosomal gain and loss identified in this study indicate the location of genes that are potentially important in the development and progression of childhood adrenocortical tumours. Finally, the copy number changes identified in childhood tumours are distinctly different to those seen in adult cases (Kjellman et al (1996) Cancer Res 56: 4219-4223), and we propose that this indicates that childhood tumours are of embryonal origin.
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