PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 6867348

Non-functioning adrenal adenomas discovered incidentally on computed tomography.

J S Mitnick·M A Bosniak·A J Megibow·D P Naidich
View original source ↗Export metadata ↓

Abstract

Eighteen patients with unilateral non-metastatic, non-functioning adrenal masses were studied with computed tomography (CT). Pathological examination in 6 cases revealed benign adrenal adenoma. The others were followed up with serial CT scans and found to show no change in tumor size over a period of six months to three years. On the basis of these findings, the authors suggest certain criteria of a benign adrenal mass, including (a) diameter less than 5 cm, (b) smooth contour, (c) well-defined margin, and (d) no change in size on follow-up. Serial CT scanning can be used as an alternative to surgery in the management of many of these patients.

Explore related subjects

AdenomaAdrenal Gland NeoplasmsAgedFemaleHumansMaleMiddle AgedTomography, X-Ray ComputedJournal Article

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

J S Mitnick, M A Bosniak, A J Megibow, D P Naidich. 1983. Non-functioning adrenal adenomas discovered incidentally on computed tomography.. https://doi.org/10.1148/radiology.148.2.6867348

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2009

HMGA proteins up-regulate CCNB2 gene in mouse and human pituitary adenomas.

The high mobility group As (HMGAs) belong to a family of nonhistone nuclear proteins that orchestrate the assembly of nucleoprotein complexes. Through a complex network of protein-DNA and protein-protein interaction, they play important roles in gene transcription, recombination, and chromatin structure. This protein family is involved, through different mechanisms, in both benign and malignant neoplasias. We have recently reported that transgenic mice carrying the Hmga1 or Hmga2 genes under transcriptional control of the cytomegalovirus promoter develop pituitary adenomas secreting prolactin and growth hormone. We have shown that the mechanism of the HMGA2-induced pituitary adenoma is based on the increased E2F1 activity. The expression profile of mouse normal pituitary glands and adenomas induced in HMGA transgenic mice revealed an increased expression of the ccnb2 gene, coding for the cyclin B2 protein, in the neoplastic tissues compared with the normal pituitary gland. Here, we show, by electrophoretic mobility shift assay and chromatin immunoprecipitation, a direct binding of HMGA proteins to the promoter of ccnb2 gene, whereas luciferase assays showed that HMGAs are able to up-regulate ccnb2 promoter activity. Finally, we report an increased CCNB2 expression in human pituitary adenomas of different histotypes that is directly correlated with HMGA1 and HMGA2 expression. Because cyclin B2 is involved in the regulation of the cell cycle, these results taken together indicate that HMGA-induced cyclin B2 overexpression gives an important contribution to experimental and human pituitary tumorigenesis.

Adenoma↗
PubMed2007

Inhibition of lung carcinogenesis by 1alpha,25-dihydroxyvitamin D3 and 9-cis retinoic acid in the A/J mouse model: evidence of retinoid mitigation of vitamin D toxicity.

9-cis-Retinoic acid (9cRA) and 1alpha,25-dihydroxyvitamin D3 (1,25D) show promise as potential chemopreventive agents. We examined 9cRA and 1,25D, alone and in combination, for their potential to inhibit carcinogen (NNK)-induced lung carcinogenesis in A/J mice. A/J mice (n=14/group) were treated with 9cRA (7.5, 15, or 30 mg/kg diet), 1,25D (2.5 or 5.0 microg/kg diet), or a combination of 9cRA (15 mg/kg diet) plus 1,25D (2.5 microg/kg diet) for 3 weeks before and 17 weeks after carcinogen injection. Lung tumor incidence, tumor multiplicity, plasma 1,25D levels and kidney expression of vitamin D 24-hydroxylase (CYP24) were determined. Compared to carcinogen-injected controls, mice receiving 9cRA supplementation had significantly lower tumor multiplicity at all doses (decreased 68-85%), with body weight loss at the higher doses of 9cRA. Mice receiving 1,25D supplementation had significantly lower tumor incidence (decreased 36 and 82%) and tumor multiplicity (decreased 85 and 98%), but experienced significant body weight loss, kidney calcium deposition, elevated kidney CYP24 expression and decreased fasting plasma 1,25D levels. Although, there was no apparent influence on chemopreventive efficacy, addition of 9cRA to 1,25D treatment effectively prevented the weight loss and kidney calcification associated with 1,25D treatment alone. These data demonstrate that 9cRA and 1,25D, alone or combined, can inhibit lung tumor promotion in the A/J mouse model. Combining 1,25D with 9cRA has the potential to mitigate the toxicity of 1,25D, while preserving the significant effect of 1,25D treatment against lung carcinogenesis. The underlying mechanism behind this effect does not appear to be related to retinoid modulation of vitamin D catabolism.

Adenoma↗
PubMed2007

A weighted logistic regression model for estimation of recurrence of adenomas.

In a colorectal polyp prevention trial, some participants might have their follow-up colonoscopy conducted before the scheduled time (i.e. at the end of the trial). This results in variable follow-up lengths for participants and the data of recurrence status at the end of the trial can be considered as current status data. In this paper, we use a weighted logistic regression model to estimate recurrence rate of adenoma data at the end of the trial. The weights are used to adjust for variable follow-up. We show that logistic regression tends to underestimate recurrence rate. In a simulation study, we show that Kaplan-Meier estimator derived from the right endpoint of the current status data tends to overestimate recurrence rate in contrast to logistic regression and the weighted logistic regression method can produce reasonable estimates of recurrence rate even under a high non-compliance rate compared to conventional logistic regression and Kaplan-Meier estimator. The method described here is illustrated with an example from a colon cancer study.

Adenoma↗