Table of Contents
1
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.
2
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.
lwang61@hotmail.com
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.
3
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.
4
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.
oliver.muensterer@kk-i.med.uni-muenchen.de
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.
5
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.
6
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.
7
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_Aimin/emlab@nms.ac.jp
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.
8
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.
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