Table of Contents
1
UI - 11701664
AU - Koch CA; Chrousos GP
TI -
Editorial: Is the diminuto/dwarf1 gene involved in physiologic
adrenocortical size regulation and tumor formation?
SO - J Clin Endocrinol Metab 2001 Nov;86(11):5127-9
2
UI - 11712085
AU - Forneris M; Gottardo L; Albertin G; Malendowicz LK; Nussdorfer GG
TI -
Expression and function of adrenomedullin and its receptors in Conn's
adenoma cells.
SO - Int J Mol Med 2001 Dec;8(6):675-9
AD - Department of Human Anatomy and Physiology, Section of Anatomy,
University of Padua, I-35121 Padua, Italy.
Adrenomedullin (ADM) is a hypotensive peptide, that derives from the
proteolytic cleavage of pro(p)ADM and acts through two subtypes of
receptors, called L1-receptor (L1-R) and calcitonin receptor-like
receptor (CRLR). CRLR may function as a calcitonin gene-related peptide
or a selective ADM receptor depending on the expression of the subtype 1
or the subtypes 2 and 3 of a family of proteins, named receptor-activity
modifying proteins (RAMPs). Reverse transcription (RT)-polymerase chain
reaction (PCR) allowed the detection of pADM mRNA in dispersed cells of
eight Conn's adenomas (aldosteronomas). These cells also expressed
peptidyl-glycine alpha-amidating monooxigenase, the enzyme converting
immature ADM to the mature form, and contained sizeable amounts of
ADM-immunoreactivity as measured by radioimmunoassay. RT-PCR also
demonstrated the presence in aldosteronoma cells of the specific mRNAs
of L1-R, CRLR and RAMPs 1-3. ADM (10(-8) M) inhibited angiotensin-II
(10(-9) M)-simulated aldosterone secretion from cultured aldosteronoma
cells, without affecting basal production. ADM (10(-8) M) also enhanced
basal proliferation rate of cultured cells, as estimated by the
5-bromo-2'-deoxyuridine immunocytochemical technique. Both effects of
ADM were annulled by the ADM-receptor selective antagonist ADM22-52
(10(-7) M). In conclusion, our study provides evidence that
aldosteronoma cells express both ADM and ADM22-52-sensitive receptors.
These findings, coupled with the demonstration that ADM exerts an
aldosterone antisecretagogue action and a proliferogenic effect on
cultured aldosteronoma cells, make it likely that endogenous ADM system
plays a potentially important role in the paracrine or autocrine
functional control of Conn's adenomas.
3
UI - 11808146
AU - Ichikawa T; Ito H
TI -
[Adrenocortical carcinoma]
SO - Nippon Rinsho 2001 Nov;59 Suppl 7():393-400
AD - Department of Molecular Oncology, Graduate School of Medicine, Chiba
University.
4
UI - 11837629
AU - Yarman S; Gurbuz L; Tanakol R; Kapran Y; Alagol F
TI -
Association of Fallot Tetralogy with Carney's complex.
SO - Ir Med J 2001 Nov-Dec;94(10):305-7
AD - Department of Internal Medicine, Istanbul Faculty of Medicine, Turkey.
esyarman@hotmail.com
The Carney complex is an inherited, autosomal disease of multicentric
tumors in many organs. Some components of Carney's complex are cardiac
myxoma, spotty pigmentation, and endocrine overactivity. Primary
pigmented nodular adrenocortical dysplasia (PPNAD) is an exceedingly
rare cause of Cushing's syndrome in infants, children, and young adults.
PPNAD occurs sporadically or as part of a familial syndrome called
Carney's complex. Up to our knowledge, the association of Fallot
Tetralogy with Carney's complex has not been previously reported. We
presented, a 20-year-old woman, who had been operated for Fallot
Tetralogy at the age of 3 years, had Carney's complex, i.e. left atrial
myxoma, two facial spotty pigmented areas, and PPNAD.
5
UI - 11602999
AU - Becherer A; Vierhapper H; Potzi C; Karanikas G; Kurtaran A; Schmaljohann
TI -
J; Staudenherz A; Dudczak R; Kletter K
FDG-PET in adrenocortical carcinoma.
SO - Cancer Biother Radiopharm 2001 Aug;16(4):289-95
AD - Department of Nuclear Medicine, University of Vienna, Austria.
alexander.becherer@univie.ac.at
Adrenal cortical carcinoma (ACC) is a rare malignant neoplasm with a
poor prognosis. Radical surgery of the primary tumor and of local as
well as of distant recurrence is the only effective treatment, and
requires accurate and early localization of recurrent tumors. In this
regard, we prospectively scanned 10 patients with ACC, 8 during
follow-up and 2 at primary work-up. In all patients PET scans from the
neck to the upper thighs were obtained 45 minutes after injection of 370
MBq [18F]FDG. Reading was done visually, with the investigator blinded
to the results of other diagnostic modalities. All known sites of ACC
lesions showed markedly increased FDG uptake. In 3 patients, previously
unknown lesions were identified by PET in the lung (one lesion), the
abdomen (3 lesions), and the skeleton (multiple), respectively. One
false positive liver focus was shown by PET aside from the true positive
lung metastases in the same patient. The sensitivity/specificity of PET
based on different organs was 100/97%, that based on the number of
PET-detected lesions (N = 23) was 100/95%. PET altered or influenced the
tumor stage in 3/10 patients, modifying the subsequent therapeutic
management in 2/10 patients. We conclude that FDG-PET is highly useful
in ACC and should be included in the work-up for initial staging as well
as for follow-up.
6
UI - 11825112
AU - Loy TS; Phillips RW; Linder CL
TI -
A103 immunostaining in the diagnosis of adrenal cortical tumors: an
immunohistochemical study of 316 cases.
SO - Arch Pathol Lab Med 2002 Feb;126(2):170-2
AD - Department of Pathology, University of Missouri Health Sciences Center,
1 Hospital Drive, Columbia, MO 65212, USA. loyts@health.missouri.edu
CONTEXT: The monoclonal antibody A103 recognizes an antigen on melanoma
cells known as Melan-A or MART-1. Recent studies have shown that A103
also reacts with adrenal cortical cells and may be useful in the
diagnosis of adrenal cortical tumors. However, only small numbers of
some of the tumors in the differential diagnosis of adrenal cortical
neoplasms have been studied. OBJECTIVE: To study the specificity of A103
immunohistochemistry in a large number of tumors in the differential
diagnosis of adrenal cortical neoplasms. DESIGN: Formalin-fixed,
paraffin-embedded tissue from 21 adrenal cortical tumors, 16 cases of
metastatic carcinoma to the adrenal, 10 pheochromocytomas, and 269
extra-adrenal carcinomas was evaluated for A103 immunoreactivity using a
commercially available antibody (Novocastra, Newcastle, UK). RESULTS:
Positive staining was seen in all of the adrenal cortical tumors but in
none of the adrenal metastases or pheochromocytomas. In the 269
extra-adrenal carcinomas, A103 immunoreactivity was limited to a single
ovarian serous carcinoma. CONCLUSION: A103 immunostaining is useful in
distinguishing adrenal cortical neoplasms from other carcinomas and
pheochromocytoma.
7
UI - 11844815
AU - Stojadinovic A; Ghossein RA; Hoos A; Nissan A; Marshall D; Dudas M;
TI -
Cordon-Cardo C; Jaques DP; Brennan MF
Adrenocortical carcinoma: clinical, morphologic, and molecular
characterization.
SO - J Clin Oncol 2002 Feb 15;20(4):941-50
AD - Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York,
NY 10021, USA.
PURPOSE: To define multimolecular phenotypes of adrenocortical carcinoma
(ACC) and to correlate outcome with morphologic and molecular
parameters. PATIENTS AND METHODS: Clinical data were analyzed for 124
patients, histopathologic slides for 67 primary tumors, and tissue
specimens for 74 patients (38 primary and 36 metastatic tumors) with ACC
and for 38 normal adrenal tissue samples. Molecular expression profiles
were investigated by immunohistochemistry. The prognostic significance
of 12 gross and histologic parameters in 67 primary ACCs was evaluated.
Morphologic and protein expression patterns were correlated with
disease-specific survival (DSS). Univariate influence of prognostic
factors on DSS was analyzed by log-rank test and multivariate analysis
by Cox regression. RESULTS: The median follow-up period was 4.7 years.
Significant predictors of DSS included distant metastasis at time of
initial presentation; venous, capsular, and adjacent organ invasion;
tumor necrosis, mitotic rate, atypical mitosis, and mdm-2
overexpression. Five-year DSS by number (one to six) of adverse
histologic parameters was as follows: one to two, 84%; three to four,
37%; more than four, 9% (P =.005).The phenotype
Ki-67(-)p53(-)mdm-2(+)cyclinD1(-)Bcl-2(-)p21(-)p27(+) was observed in
83% of normal and 3% of malignant adrenal tissue (P =.01). Molecular
phenotypic expression was more heterogeneous in malignant than in normal
(10 v five phenotypes) adrenal tissue. CONCLUSION: Meticulous
morphologic evaluation, mitotic count, and tumor stage are essential in
determining prognosis for patients with ACC. Multimolecular phenotyping
demonstrates that the molecular complexity and heterogeneity of these
neoplasms are such that targeted therapy needs to be patient specific.
8
UI - 11809538
AU - Vierhapper H
TI -
Adrenocortical tumors: clinical symptoms and biochemical diagnosis.
SO - Eur J Radiol 2002 Feb;41(2):88-94
AD - Department of Internal Medicine III, Division of Endocrinology and
Metabolism, University of Vienna, Wahringer Gurtel 18-20, A-1090,
Vienna, Austria.
Patients who are suspected clinically to suffer from hypersecretory
disorders of their adrenal(s) should undergo an appropriate
endocrinological investigation to confirm or exclude the presence of
such disorders prior to any radiological investigation. In those
patients in whom an adrenal mass is found 'incidentally' on imaging
clinical symptoms of hormonal activity should be carefully followed up.
Asymptomatic patients should be screened biochemically for latent
hormonal hypersecretion syndromes including pheochromocytoma (urine
catecholamine excretion), hypercortisolism (overnight dexamethason
suppression test) and aldosteronism (blood pressure and serum
potassium). These investigations are mandatory in all patients scheduled
for surgery. The decision to refer patients with inactive adrenal tumors
to surgery is, in the absence of valid biochemical markers of
malignancy, mainly influenced by tumor size but remains arbitrary.
Patients who are not at first treated by surgery should be operated if
follow-up indicates a progression in tumor size.
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.
About OncoLink Contact OncoLink Privacy statement Disclaimer Link to OncoLink Home