National Cancer Institute®
Last Modified: February 1, 2002
UI - 11769530
AU - Taniguchi S; Ikuyama S; Hiramatsu S; Shiokawa S; Hata T; Sato F; Imagawa
TI - M; Nomura Y; Sasano H; Nishimura J [Aldosterone and cortisol-producing adrenal tumor]
SO - Nippon Naika Gakkai Zasshi 2001 Nov 10;90(11):2291-4
AD - Department of Clinical Immunology and Medicine, Medical Institute of Bioregulation, Kyushu University, Beppu.
UI - 11800650
AU - Wang L; Cornford ME
TI - Coincident choroid plexus carcinoma and adrenocortical carcinoma with elevated p53 expression: a case report of an 18-month-old boy with no family history of cancer.
SO - Arch Pathol Lab Med 2002 Jan;126(1):70-2
AD - Department of Pathology, Los Angeles County-University of Southern California Medical Center, Los Angeles, CA 90033, USA. firstname.lastname@example.org
We describe a young patient with no known family history of cancer who presented at 18 months with 2 advanced primary tumors, choroid plexus carcinoma and adrenal cortical carcinoma. Immunohistochemical studies demonstrated high levels of nuclear p53 protein expression in both tumors, as well as in the adjacent normal-appearing adrenal cortical cell nuclei of the adrenal gland. The immunohistologic distribution of elevated p53 expression suggests that this individual has a de novo germline mutation affecting p53 gene expression.
UI - 11556748
AU - Gupta D; Shidham V; Holden J; Layfield L
TI - Value of topoisomerase II alpha, MIB-1, p53, E-cadherin, retinoblastoma gene protein product, and HER-2/neu immunohistochemical expression for the prediction of biologic behavior in adrenocortical neoplasms.
SO - Appl Immunohistochem Mol Morphol 2001 Sep;9(3):215-21
AD - Magee Women's Hospital and University of Pittsburgh, Pennsylvania, USA.
Prediction of biologic behavior in adrenocortical neoplasms is difficult because of the lack of availability of reliable clinical, biochemical, and pathologic prognostic markers. Reliable objective markers predictive of clinical outcome in adrenocortical neoplasms are needed to assign optimal treatment of potentially malignant tumors. In the current article, the authors evaluated a set of molecular markers (topoisomerase II alpha (Topo II alpha), MIB-1, p53, human epithelial cadherin (E-cadherin), retinoblastoma gene protein product, and HER-2/neu) and correlated their expression with histologic diagnosis and clinical outcome. Paraffin-embedded, formalin-fixed tissue blocks from 30 cases of adrenocortical neoplasms (15 benign and 15 malignant) were obtained from the surgical pathology archives at the University of Utah Health Sciences Center (Salt Lake City, UT) and the Medical College of Wisconsin (Milwaukee, WI). Age, gender, recurrence, tumor size and weight, hemorrhage, necrosis, pleomorphism, mitotic count, capsular and lymphovascular invasion, hyaline globules, intranuclear inclusions, and immunohistochemical expression of Topo II alpha, p53, MIB-1, E-cadherin, retinoblastoma gene protein product, and HER-2/neu were studied. Clinical data were obtained from the clinical charts, or communication with the treating physician, or both. Adrenocortical neoplasms with hemorrhage, necrosis, large size (>5 cm), weight more than 100 g, nuclear pleomorphism, lymphovascular invasion, and brisk mitotic rate (more than 5 per 30 high-power fields) were more likely to behave in a malignant fashion (P approximately 0.001-0.009). The difference in proliferation indices in benign and malignant neoplasms was statistically significant (P < 0.001). The difference in p53 staining in benign and malignant neoplasms also was statistically significant (P < 0.001). Higher p53 labeling index (>20%) was present in 73% (11/15) of malignant lesions but was found in only 1 of 15 (6.6%) benign lesions. The difference in retinoblastoma staining between benign and malignant neoplasms was statistically significant (P = 0.004). There was no significant difference in staining pattern of E-cadherin expression between benign and malignant lesions. HER-2/neu overexpression was not observed in any of the benign or malignant adrenocortical neoplasms.
UI - 11719878
AU - Muensterer OJ; Till H; Schwarz HP; Joppich I
TI - Testosterone-producing adrenocortical neoplasm in a 6-year-old boy.
SO - Eur J Pediatr Surg 2001 Oct;11(5):354-7
AD - Department of Paediatric Surgery, Dr. von Haunersches Kinderspital, University of Munich, Munich, Germany. email@example.com
Adrenal tumours that predominantly secrete testosterone are virtually unknown in prepubertal male patients.We present the case of a 6-year-old boy with premature sexual development and markedly elevated serum testosterone, but normal urinary steroid levels. Diagnostic imaging demonstrated a spherical tumour of the left adrenal gland. Surgical excision led to normalisation of testosterone levels, and postoperative serial low hormone measurements ruled out tumour recurrence.Although extremely rare, this case illustrates that testosterone-producing adrenal adenomas may be encountered in boys without urinary steroid elevation. Surgical excision promises a definite cure. Testosterone is a useful tumour marker in these patients until the beginning of puberty.
UI - 11711511
AU - Egidy G; Baviera E; Ciuffo G; Corvol P; Pinet F
TI - Localization of the endothelin system in aldosterone-producing adenomas.
SO - Hypertension 2001 Nov;38(5):1137-42
AD - INSERM Unit 36, College de France, Paris, France.
Endothelin-1 (ET-1) could play a role in the regulation of aldosterone secretion of the human adrenal gland. The presence of the endothelin-converting enzyme 1 (ECE-1) and ET-1 suggests that there is a local ET system in the adrenal cortex, but the in situ synthesis of ET-1 remains to be confirmed. The cellular distribution of the whole ET system was evaluated in 20 cases of aldosterone-producing adenomas. Polymerase chain reaction studies gave strong signals for ECE-1 mRNA and the mRNAs for endothelin type A (ET(A)) and B (ET(B)) receptors and faint signals for prepro-ET-1 mRNA. In situ hybridization showed ET(A) receptors scattered throughout the adenoma, in both secretory cells and vascular structures (score, +). There were more ET(B) receptors (score, ++), but they were restricted mainly to the endothelium. ECE-1 mRNA and protein were ubiquitous and abundant in secretory cells (score, +++) and vascular structures (score, ++); the enzyme was active on big ET-1. There was no prepro-ET-1 mRNA in the cortex, except in the thickened precapillary arterioles present in only 30% of the aldosterone-producing adenomas studied. ET-1 immunoreactivity was detected in vascular structures (score, +), probably bound to receptors, suggesting that ET-1 has an endocrine action. The low concentrations of ET-1 could also indicate that it acts in a paracrine-autocrine fashion to control adrenal blood flow. The discrepancy between the concentrations of ECE-1 and its substrate suggests that ECE-1 has another role in the adrenal secretory cells. Our data indicate that ET probably is not a primary cause of the development or maintenance of the adenoma.
UI - 11603574
AU - Choi KM; Park IB; Kim NH; Lee JB; Choi DS; Baik SH
TI - A case of adrenocortical tumor coexisted with paragangliomas.
SO - Endocr J 2001 Aug;48(4):499-502
AD - Department of Internal Medicine, Korea University College of Medicine, Seoul.
We report a case of adrenocortical tumor that coexisted with paragangliomas. A 35-year-old woman was admitted to the hospital because of left upper abdominal pain. A palm-sized mass was palpated at left upper quadrant. Hormonal studies revealed the features of pheochromocytoma. An emergency operation was performed because hemorrhage of the tumor was suspected. A 10 cm diameter ruptured mass was found in the left adrenal area and other tumors were also noted adjacent to inferior vena cava (IVC). The pathologic report revealed that the adrenal mass was an adrenocortical tumor with hemorrhagic necrosis and that the tumors adjacent to IVC were paragangliomas. This was the first case of adrenocortical tumor with paragangliomas in our Medline search result, hence we report the case with a review of the literature.
UI - 11793196
AU - Liu AM; Maeda S; Hosone M; Azuma K; Katayama H; Yokoyama M; Naito Z;
TI - Sugisaki Y; Asano G Use of electron microscopic evaluation for the diagnosis of adrenal cortical carcinoma in fine needle aspiration cytology: a case report and review of the literature.
SO - Med Electron Microsc 2001 Sep;34(3):190-7
AD - Central Institute for Electron Microscopic Research, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan. Liu_Aiminfirstname.lastname@example.org
Bilateral adrenal tumors were detected in a 72-year-old man who had a history of hepatic inflammatory pseudotumor. Computet tomography (CT)-guided fine needle aspiration cytology (FNAC) of the adrenal glands was performed. The cytologic findings were similar to the previous diagnosis of "inflammatory pseudotumor" in the liver. However, the origin of some aggregated large atypical cells observed in the adrenal FNAC specimens was not known. Immunocytochemically, these large atypical cells were positive for vimentin and negative for cytokeratin and chromogranin A. An electron-microscopic study showed that these large atypical cells contained mitochondria with tubulovesicular cristae and smooth endoplasmic reticulum arranged in whorled and laminated patterns, and these findings confirmed diagnosis of primary adrenal cortical carcinoma. The histopathological diagnosis of the resected bilateral adrenal tumor was adrenal cortical carcinoma. The patient died 7 months after surgery, with recurrence of the bilateral adrenal cortical carcinoma and extensive metastases. A diagnosis of primary adrenal cortical carcinoma with extensive metastases was finally demonstrated by autopsy. Retrospectively, the previous liver tumor was determined to be a metastatic lesion.
UI - 11832743
AU - Takahashi S; Minowada S; Tomita K; Katumata N; Tanaka T; Kitamura T
TI - Massive adrenocortical adenoma following long-term treatment of 21-hydroxylase deficiency.
SO - J Urol 2002 Mar;167(3):1390-1
AD - Department of Urology, Faculty of Medicine, The University of Tokyo and International Medical Center of Japan, and National Children's Medical Research Center, Tokyo, Japan.
The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.