ReviewThe molecular basis of adrenocortical cancer
Section snippets
Diagnosis
Most frequently, malignant tumors in the adrenal glands are formed from the metastasis of cancers that have initiated growth in other organs, largely the lungs and breast. Most nonmetastatic adrenal masses are asymptomatic, benign tumors called adrenocortical adenomas (ACAs). The adrenocortical tumors (ACTs) revealed during diagnostic procedures for unrelated disorders are called incidentaloma (1). Most ACAs are likely undiagnosed, and among all diagnosed ACAs, 52% are subsequently removed
Genetics of adrenocortical tumors
Various analyses were applied to characterize the genetic background of ACA and ACC and to distinguish between both types of tumors. Comparative genomic hybridization (CGH) analysis has shown that the accumulation of chromosomal aberrations correlates with the size of a tumor (31).
The loss or gain of chromosomes 17 and 9 was observed in 28–75% of ACA cases 31, 32, 33, 34, 35. The most frequent aberrations (39–47%) in ACC cases were the amplification of chromosomes 5 and 12 and the loss of
Treatment
The treatment strategies for ACCs include resection with or without adjuvant therapy or radiotherapy. Tumors diagnosed in stages I–III by imagining techniques are removed surgically. Surgery may also be considered for stage IV tumors, yet the therapy depends on the metastasis of the cancer. The overall 5-year survival rate after tumor resection has been estimated at 35% 65, 66. The elimination of an adrenocortical tumor in stage IV could diminish steroid hypersecretion and improve the
Future considerations
ACA and ACC tumors are highly heterogeneous. It remains a goal to design a reliable method to distinguish between benign ACA and malignant ACC based on differences among the transcriptomes. However, transcriptome analysis has revealed many abnormalities in gene expression. Additionally, the primary cause of adrenocortical cancer is still unclear. The prognostic value of the mRNA-based test is also limited. These types of cancers, such as ACC, require international coordinated cooperation to
Acknowledgments
We thank Ms. Beata Raczak and M.Sc. Bogumiła Ratajczak for their indispensable help during the preparation of this manuscript.
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2016, Current Problems in Diagnostic RadiologyCitation Excerpt :Incidental adrenal masses are seen in up to 5% of abdominal computed tomography (CT) studies.1 Most of these “incidentalomas” seen in the general population are benign nonfunctioning adrenocortical adenomas, with a minority being adrenocortical carcinomas, pheochromocytomas, or metastatic lesions.2,3 Some have argued that follow-up imaging may have a limited role in benign-appearing incidentalomas in patients without a known history of malignancy, although metaanalysis suggests that up to 19% of incidentally discovered adrenal masses may be metastases.1,4,5
Microwave-assisted derivatization: Application to steroid profiling by gas chromatography/mass spectrometry
2014, Journal of Chromatography B: Analytical Technologies in the Biomedical and Life SciencesCitation Excerpt :Thus, steroid profiling in humans is a tool of paramount importance for the establishment of the biochemical phenotype of many pathologies [1,2]. Despite all the progress in steroid biosynthesis research brought about through molecular biology techniques [3,4] and by the introduction of liquid chromatography tandem mass spectrometers (LC–MS/MS) in clinical laboratories [5–8], gas chromatography coupled to mass spectrometry (GC–MS) remains as the reference technique in clinical steroid investigations [9]. The first methods for the determination of the steroid profile by GC–MS were developed by Horning et al. back in 1969 [10].
Analysis of circulating microRNAs in adrenocortical tumors
2014, Laboratory InvestigationMiR-34a and miR-483-5p are candidate serum biomarkers for adrenocortical tumors
2013, Surgery (United States)Citation Excerpt :After finding different levels of miR-34a and miR-483-5p in serum samples from patients with malignant and benign adrenocortical neoplasms, we set out to better understand whether these miRNAs were secreted from tumor cells in vitro. Our in vitro data in the H295R cell line shows that miR-483-5p is highly expressed and is secreted into the supernatant, which is consistent with overexpression of miR-483-5p in ACC,4,9 extracellular secretion of miR-483-5p, and greater serum levels in patients with ACC. These findings are consistent with studies that demonstrated active cellular secretion of miRNAs via exosomes.18
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