Table of Contents
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UI - 20250166
AU - Razavi B; O'Toole J; Schilling M; Razavi M
TI -
Cryptococcal meningitis, an endocrine emergency?
SO - Lancet 2000 Apr 22;355(9213):1426
AD - Department of Medicine, University of Iowa, Iowa City 52242, USA.
Razavib@mail.medicine.uiowa.edu
2
UI - 20520899
AU - Kuruvilla A
TI -
Cryptococcal meningitis and Cushing's syndrome.
SO - Lancet 2000 Jul 22;356(9226):342-3
3
UI - 21281570
AU - Bartley GB; Campbell RJ; Salomao DR; Bradley EA; Marsh WR; Bite U
TI -
Adrenocortical carcinoma metastatic to the orbit.
SO - Ophthal Plast Reconstr Surg 2001 May;17(3):215-20
AD - Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota 55905,
USA.
PURPOSE: To describe the clinical course and histopathologic features of
a patient with adrenocortical carcinoma metastatic to the orbit.
METHODS: Case report and literature review. RESULTS: A 24-year-old man
first came to medical attention because of symptoms referable to a
4.47-kg, nonfunctioning carcinoma of the left adrenal cortex. Several
metastases ensued, including a large tumor to the right superior lateral
bony orbit with extension to the brain, temporalis fossa, and orbit
proper. The tumor was resected with the use of a combined neurosurgical,
ophthalmic, and craniofacial approach. The patient died of widespread
metastatic disease 15 months after the orbital operation. CONCLUSIONS:
Metastasis to the orbit from adrenocortical carcinoma is rare. Surgical
resection is the treatment of choice, with adjunctive radiation therapy
and chemotherapy in some cases. The prognosis is poor.
4
UI - 21382634
AU - Kardar AH
TI -
Rupture of adrenal carcinoma after biopsy.
SO - J Urol 2001 Sep;166(3):984
AD - Department of Urology, King Faisal Specialist Hospital and Research
Centre, Riyadh, Saudi Arabia.
5
UI - 21382635
AU - Kurek R; Von Knobloch R; Feek U; Heidenreich A; Hofmann R
TI -
Local recurrence of an oncocytic adrenocortical carcinoma with ovary
metastasis.
SO - J Urol 2001 Sep;166(3):985
AD - Departments of Urology and Pathology, Philipps-University, Marburg,
Germany.
6
UI - 21407839
AU - Wachenfeld C; Beuschlein F; Zwermann O; Mora P; Fassnacht M; Allolio B;
TI -
Reincke M
Discerning malignancy in adrenocortical tumors: are molecular markers
useful?
SO - Eur J Endocrinol 2001 Sep;145(3):335-41
AD - Schwerpunkt Endokrinologie, Medizinische Universitatsklinik Wurzburg,
Wurzburg, Germany.
OBJECTIVE: Adrenocortical carcinoma (ACC) is a rare neoplasm with poor
prognosis. Discerning ACCs from benign adenomas histologically may be
difficult if invasion into surrounding tissues or metastases are
missing. DESIGN: In order to establish molecular markers for malignancy,
we analyzed seven normal adrenals, three massive macronodular
ACTH-independent adrenocortical hyperplasias (MMAHs), 30 adrenocortical
adenomas (ACAs) and ten ACCs. METHODS: All tissues were studied for the
presence of alterations in the p53 tumor suppressor gene using the PAb
1801 antibody, which detects mutant p53 protein and the pYNZ22
microsatellite marker to show loss of heterozygosity (LOH) at 17p, for
expression of the proliferation-associated antigen Ki67 using the MIB1
antibody, for the rate of apoptotic tumor cells with the TdT-mediated
dUTP biotin nick end labeling (TUNEL) method, and for LOH of 11q13
(menin gene locus) with the D11S956 microsatellite marker. RESULTS: 0/3
MMAH, 1/28 ACA and 3/10 ACC revealed immunopositive staining for p53.
LOH for pYNZ22 was observed in 1/3 MMAH, 1/23 informative ACA and 6/6
informative ACC. The rate of apoptotic cells was significantly higher in
ACC (P<0.0001 by ANOVA) than in ACA but there was some overlap between
groups. The Ki67 index (% immunopositive cells) was 1.9+/-1.30%
(mean+/-s.d.) in normal adrenals, 3.47+/-1.37% in MMAH, and 2.11+/-1.01%
in ACA. ACC had the highest Ki67 index of 11.94+/-7.58% distinguishing
all ACC from the ACA and MMAH studied with a cut-off level of 5%. LOH
for 11q13 was detected in 2/3 MMAH, 5/26 ACA and 6/8 ACC. CONCLUSIONS:
We conclude that a Ki67 index above 5% is a sensitive and specific
indicator of ACC and may be useful in the differentiation of adenomas
from carcinomas.
7
UI - 21455236
AU - Vassilopoulou-Sellin R; Schultz PN
TI -
Adrenocortical carcinoma. Clinical outcome at the end of the 20th
century.
SO - Cancer 2001 Sep 1;92(5):1113-21
AD - Department of Endocrine Neoplasia and Hormonal Disorders, University of
Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
BACKGROUND: Adrenocortical carcinoma remains a rare and lethal neoplasm.
Effective therapies have not emerged in recent decades. However, medical
advances have improved diagnostic techniques and supportive measures;
these changes may have a beneficial impact on the natural history of the
disease. METHODS: The authors retrospectively analyzed the clinical
outcomes of patients with adrenocortical carcinoma registered at the
University of Texas M.D. Anderson Cancer Center focusing on patients who
received their diagnosis since 1980 and comparing data from those
patients with earlier reports. RESULTS: Since 1980, 139 patients have
registered at M.D. Anderson Cancer Center with the diagnosis of
adrenocortical carcinoma. One-third had evidence of hormone
hypersecretion, and one-third had localized disease at diagnosis. Men
were affected as frequently as women but tended to be older and have
larger tumors at diagnosis. The 5-year survival rate was 60%
(Kaplan-Meier analysis). The 30 patients with the longest survival (> 5
years) and the 30 patients with the shortest survival (< 11 months) had
no significant differences in age, gender, tumor size, or functionality.
However, long-term survivors had significantly less extensive disease. A
comparison with patients reviewed in earlier reports from the same
institution showed no significant differences in gender predilection,
tumor function, or extent of disease. Despite these similarities,
patients whose disease was diagnosed since 1980 lived much longer than
patients observed in earlier decades. CONCLUSIONS: Despite the lack of
significant improvements in early diagnosis and effective therapies,
patients with adrenocortical carcinoma are living longer (5-year
survival rate, 60%). It is important to revise assumptions regarding the
clinical outcomes of patients with this disease. Copyright 2001 American
Cancer Society.
8
UI - 21434005
AU - Stratakis CA; Kirschner LS; Carney JA
TI -
Clinical and molecular features of the Carney complex: diagnostic
criteria and recommendations for patient evaluation.
SO - J Clin Endocrinol Metab 2001 Sep;86(9):4041-6
AD - Unit on Genetics and Endocrinology, Developmental Endocrinology Branch,
National Institute of Child Health and Human Development, National
Institutes of Health, Bethesda, Maryland 20892-1862, USA.
stratakc@cc1.nichd.nih.gov
Carney complex is a multiple neoplasia syndrome featuring cardiac,
endocrine, cutaneous, and neural tumors, as well as a variety of
pigmented lesions of the skin and mucosae. Carney complex is inherited
as an autosomal dominant trait and may simultaneously involve multiple
endocrine glands, as in the classic multiple endocrine neoplasia
syndromes 1 and 2. Carney complex also has some similarities to
McCuneAlbright syndrome, a sporadic condition that is also characterized
by multiple endocrine and nonendocrine tumors. Carney complex shares
skin abnormalities and some nonendocrine tumors with the lentiginoses
and certain of the hamartomatoses, particularly Peutz-Jeghers syndrome,
with which it shares mucosal lentiginosis and an unusual gonadal tumor,
large-cell calcifying Sertoli cell tumor. Careful clinical analysis has
enabled positional cloning efforts to identify two chromosomal loci
harboring potential candidate genes for Carney complex. Most recently,
at the 17q22-24 locus, the tumor suppressor gene PRKAR1A, coding for the
type 1alpha regulatory subunit of PKA, was found to be mutated in
approximately half of the known Carney complex kindreds. PRKAR1A acts a
classic tumor suppressor gene as demonstrated by loss of heterozygosity
at the 17q22-24 locus in tumors associated with the complex. The second
locus, at chromosome 2p16, to which most (but not all) of the remaining
kindreds map, is also involved in the molecular pathogenesis of Carney
complex tumors, as demonstrated by multiple genetic changes at this
locus, including loss of heterozygosity and copy number gain. Despite
the known genetic heterogeneity in the disease, clinical analysis has
not detected any corresponding phenotypic differences between patients
with PRKAR1A mutations and those without. This article summarizes the
clinical manifestations of Carney complex from a worldwide collection of
affected patients and also presents revised diagnostic criteria for
Carney complex. In light of the recent identification of mutations in
the PRKAR1A gene, an estimate of penetrance and recommendations for
genetic screening are provided.
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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.
UI - 21443288
AU - Gicquel C; Bertagna X; Gaston V; Coste J; Louvel A; Baudin E; Bertherat
TI -
J; Chapuis Y; Duclos JM; Schlumberger M; Plouin PF; Luton JP; Le Bouc Y
Molecular markers and long-term recurrences in a large cohort of
patients with sporadic adrenocortical tumors.
SO - Cancer Res 2001 Sep 15;61(18):6762-7
AD - Laboratoire d'Explorations Fonctionnelles Endocriniennes, Hopital
Trousseau, AP-HP, 75012 Paris, France.
christine.gicquel@trs.ap-hop-paris.fr
Genetic alterations, such as loss of heterozygosity (LOH) at the 17p13
and 11p15 loci and overexpression of the insulin-like growth factor
(IGF)-II gene, are associated with the malignant phenotype in sporadic
adrenocortical tumors. A high risk of recurrence after surgery for
adrenocortical tumors is predicted in cases with regional invasion or
distant metastases. However, patients with localized tumors also have a
high risk of recurrence. Reliable prognostic markers are required to
identify subjects at high risk of recurrence. The aim of this study was
to assess the prognostic value of three molecular markers (17p13 LOH,
11p15 LOH, and overexpression of the IGF-II gene) by assessing
disease-free survival in a large series of adult patients with sporadic
adrenocortical tumors. Adult patients (114) were prospectively followed
was initially diagnosed in 18 patients (McFarlane stage III: n = 1 and
stage IV: n = 17). The remaining 96 patients with localized adrenal
disease at diagnosis (stage I: n = 60 and stage II: n = 36) were at risk
of recurrence. Histological grade was assessed according to Weiss
criteria, and tumors were classified into two groups (Weiss score
UI - 21459479
AU - Serrano R; Rodriguez-Peralto JL; Santos-Briz A; de Agustin P
TI -
Fine needle aspiration cytology of metastatic hepatic adrenocortical
carcinoma mimicking hepatocellular carcinoma: a case report.
SO - Acta Cytol 2001 Sep-Oct;45(5):768-70
AD - Department of Pathology, Hospital Doce de Octubre, Madrid, Spain.
BACKGROUND: Adrenocortical carcinoma (AC) is a rare neoplasm, usually
considered one of the most morbid and lethal human tumors. It occurs
primarily in children and young adults and often presents with advanced
and/or metastatic disease. CASE: A 9-year-old boy with a previous
diagnosis of adrenocortical carcinoma underwent computed tomography
(CT)-guided fine needle aspiration (FNA) for preoperative investigation
of a hepatic mass. All smears revealed abundant groups of cells
surrounding an interconnective, thin-walled, central vascular core.
These cells showed finely vacuolated, large cytoplasm with eccentrically
placed nuclei. Occasionally, cells underwent a sudden, marked increase
in size, with prominent atypia. Multinucleated, atypical giant cells and
high mitotic rate were also evident. The cytologic findings resembled
the previous histologic adrenocortical carcinoma features. CONCLUSION:
The cytologic features of metastatic hepatic adrenocortical carcinoma
may mimic those of hepatocellular carcinoma. However, the presence of
atypical multinucleated and pleomorphic cells with microvacuolated
cytoplasm and eccentric nuclei as well as the absence of naked nuclei
and endothelial linings yield the diagnosis of adrenocortical carcinoma.
Nevertheless, other space-occupying liver lesions in children must also
be considered. This case demonstrates the usefulness of CT-localized FNA
biopsy in hepatic masses in children, and discusses the possible
cytologic differential diagnosis.
UI - 21466984
AU - Sworczak K; Babniska A; Stanek A; Lewczuk A; Siekierska-Hellmann M;
TI -
Blaut K; Drobinska A; Basinski A; Lachnski AJ; Czaplinska-Kalas H; Gruca
Z
Clinical and histopathological evaluation of the adrenal incidentaloma.
SO - Neoplasma 2001;48(3):221-6
AD - Department of Internal Medicine, Endocrinology and Hemostatic Disorders,
Medical University of Gdansk, Poland.
Clinically silent adrenal masses (incidentaloma) are incidentally
discovered lesions, when noninvasive imaging methods (USG, CT, MRI) are
performed for reasons other than known or suspected adrenal disease.
Most studies report on a prevalence of adrenal incidentaloma range
between 1% and 10% in radiological series. Between 1994 and 1999 we
observed in our Department 57 patients with incidentalomas of adrenal
glands. After endocrinological evaluation silent Cushing's syndrome was
found in 2 cases (3.5%). Fifty two patients were qualified for surgery.
Adrenocortical adenoma was diagnosed in 73.1%; adrenocortical carcinoma
in 7.7%; pheochromocytoma in 7.7% and less frequent adrenal lesions in
11.5%. All adrenal carcinomas and malignant pheochromocytomas (11.5%)
were found in tumors with diameter over 4 cm.
UI - 21288572
AU - Jamieson A; Ingham DG; Dominiczak AF; Connell JM
TI -
Not the usual cause of superior vena cava obstruction.
SO - Scott Med J 2001 Apr;46(2):51-2
AD - Department of Medicine and Therapeutics, MRC Blood Pressure Unit,
Western Infirmary, Glasgow. ajamieson.qmh@yahoo.co.uk
Superior vena cava obstruction has a classical association with
bronchial carcinoma. In the presence of cortisol excess, the diagnosis
of small-cell carcinoma and ectopic ACTH production seems likely. We
present a case where the clinical features did not accurately reflect
the underlying pathology.
UI - 21295730
AU - Makino S; Oda S; Saka T; Yasukawa M; Komatsu F; Sasano H
TI -
A case of aldosterone-producing adrenocortical adenoma associated with
preclinical Cushing's syndrome and hypersecretion of parathyroid
hormone.
SO - Endocr J 2001 Feb;48(1):103-11
AD - Department of Internal Medicine, Osaka Gyomeikan Hospital, Japan.
A rare case of aldosterone-producing adrenocortical adenoma with
preclinical Cushing's syndrome and hypersecretion of parathyroid hormone
(PTH) is described. A 64-year-old male patient had a history of
hypertension for two decades and hypokalemia for 4 years. He suffered
from left hemiparesis and aphasia due to cerebral hemorrhage, but his
appearance was not Cushingoid. His plasma renin activity was below the
normal range, while plasma aldosterone concentration was high. They did
not respond to furosemide-upright test. His plasma cortisol level in the
morning was at the upper limit of the normal range, but it did not show
a diurnal rhythm nor was it suppressed by 1 mg and 8 mg of
dexamethasone. Computed tomography showed a low density tumor in the
right adrenal gland. An adrenal scintigram under dexamethasone treatment
revealed an uptake of the tracer on the right side, and plasma
aldosterone and cortisol concentrations in the adrenal vein were higher
on the right side than on the opposite. The diagnosis of right
aldosterone-producing adrenal adenoma with an autonomous production of
cortisol was confirmed by right adrenalectomy. Histological findings
showed an adenoma consisting mostly of clear cells, but that the nests
of compact cells were scattered. Analysis of an extract from the adenoma
revealed that the adenoma contained an excess amount of aldosterone and
that the cortisol/corticosterone ratio was higher than that of
aldosterone-producing adenoma. Both serum calcium and PTH levels
remained high one year after adrenalectomy. Ultrasonography revealed the
swelling of a parathyroid gland on the left side, indicating the
coexistence of an autonomous hyperparathyroidism.
UI - 21339047
AU - Takahashi K; Totsune K; Murakami O; Shibahara S
TI -
Expression of urotensin II and urotensin II receptor mRNAs in various
human tumor cell lines and secretion of urotensin II-like
immunoreactivity by SW-13 adrenocortical carcinoma cells.
SO - Peptides 2001 Jul;22(7):1175-9
AD - Department of Molecular Biology and Applied Physiology, Tohoku
University School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi
980-8575, Japan. ktaka-md@mail.cc.tohoku.ac.jp
Urotensin II is the most potent vasoconstrictor peptide identified so
far. Expression of urotensin II and urotensin II receptor mRNAs was
studied in various human tumor cell lines by reverse transcriptase
polymerase chain reaction (PCR) method. Secretion of urotensin II by
these tumor cells was studied by radioimmunoassay. The tumor cell lines
studied were T98G glioblastoma cells, IMR-32 neuroblastoma cells, NB69
neuroblastoma cells, BeWo choriocarcinoma cells, SW-13 adrenocortical
carcinoma cells, DLD-1 colorectal adenocarcinoma cells and HeLa cervical
cancer cells. Urotensin II mRNA was expressed in 6 tumor cell lines
except for NB69 neuroblastoma cells. Urotensin II receptor mRNA was
expressed in all 7 tumor cell lines. A significant amount of urotensin
II-like immunoreactivity was detected only in the culture medium of
SW-13 adrenocortical carcinoma cells by radioimmunoassay. Sephadex G-50
column chromatography showed that the urotensin II-like immunoreactivity
in the culture medium extract was eluted earlier than synthetic human
urotensin II, suggesting that SW-13 cells secreted higher molecular
weight materials, perhaps partially processed forms of the urotensin II
precursor. Reverse phase high-performance liquid chromatography (HPLC)
showed three immunoreactive peaks, one of which was eluted in the
position of urotensin II. The present study has shown for the first time
expression of urotensin II and urotensin II receptor mRNAs in various
tumor cell lines and the secretion of urotensin II-like immunoreactivity
by SW-13 adrenocortical carcinoma cells.
UI - 21486612
AU - Latronico AC; Pinto EM; Domenice S; Fragoso MC; Martin RM; Zerbini MC;
TI -
Lucon AM; Mendonca BB
An inherited mutation outside the highly conserved DNA-binding domain of
the p53 tumor suppressor protein in children and adults with sporadic
adrenocortical tumors.
SO - J Clin Endocrinol Metab 2001 Oct;86(10):4970-3
AD - Hospital das Clinicas, Disciplina de Endocrinologia e Metabologia,
Faculdade de Medicina da Universidade de Sao Paulo, Sao Paulo CEP:
01060-970, Brazil. anacl@usp.br
Mutations of the p53 tumor suppressor gene are the single most common
genetic alterations in human cancers. Recently, a distinct nucleotide
substitution was identified in exon 10 of the p53 gene, leading to an
Arg337His mutation in 97% of children with adrenocortical tumors from
Southern Brazil. In the present study, we investigated the presence of
this mutation in a larger series of 55 patients (37 adults and 18
children) with benign and malignant sporadic adrenocortical tumors. None
of the patients had family cancer histories that conformed to the
criteria for Li-Fraumeni syndrome. Twenty-one asymptomatic close
relatives of patients with p53 mutations and 60 normal unrelated
individuals were also studied. The missense Arg337His mutation was
identified in 19 patients (14 children and 5 adults), and 8 of 11 cases
studied had LOH. Among the 19 patients with the Arg337His mutation, only
one boy and three adults showed fatal evolution or recurrent metastases.
This mutation was also identified in heterozygous state in asymptomatic
first-degree relatives of the patients, indicating that Arg337His
mutation was inherited in most cases. In contrast, this mutation was not
found in 120 alleles of normal unrelated controls. In conclusion, the
germ line Arg337His mutation of p53 protein is present at a high
frequency (77.7%) in children with benign or malignant sporadic
adrenocortical tumors, but it is not restricted to the pediatric group,
since 13.5% of adults with adrenocortical tumors also had this mutation.
The presence of this mutation was related to unfavorable prognosis in
most of the adults, but not in the children with adrenocortical tumors.
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