1
UI - 11914473
AU - Sasano H; Suzuki T; Moriya T
TI -
Discerning malignancy in resected adrenocortical neoplasms.
SO - Endocr Pathol 2001 Winter;12(4):397-406
AD - Department of Pathology, Tohoku University School of Medicine, 2-1
Seiryou-machi, Aoba-ku, Sendai, Japan 980-0872.
hsasano@patholo2.med.tohoku.ac.jp
Differential diagnosis between adenoma and carcinoma in resected human
adrenocortical neoplasms may be one of the most problematic and
difficult areas of surgical pathology practice. This is especially true
in cases of relatively small adrenocortical tumors not associated with
obvious signs of malignancy such as necrosis and/or hemorrhage. In
addition, the numbers of these small adrenocortical neoplasms are
increasing owing to the widespread application of sophisticated computed
tomography and/or magnetic resonance imaging scans. No single parameter
can be effective in this differential diagnosis of resected
adrenocortical tumor. Histopathologic evaluation using a multivariate
scoring system is considered most effective in discerning malignancy and
biologic behavior of resected adrenocortical neoplasms. Molecular and
cellular findings of adrenocortical carcinoma have been inconsistent
except for the increased cell proliferation associated with
adrenocortical malignancy. Therefore, an assessment of neoplastic cell
proliferation using immunostains of cell cycle-associated nuclear
antigen such as Ki-67 is the only useful auxiliary method of evaluating
malignancy in resected adrenocortical neoplasms at present.
2
UI - 11949624
AU - Erickson LA; Jin L; Sebo TJ; Lohse C; Pankratz VS; Kendrick ML; van
TI -
Heerden JA; Thompson GB; Grant CS; Lloyd RV
Pathologic features and expression of insulin-like growth factor-2 in
adrenocortical neoplasms.
SO - Endocr Pathol 2001 Winter;12(4):429-35
AD - Department of Laboratory Medicine and Pathology, Mayo Clinic/Foundation,
200 First Street SW, Rochester, NY 55905, USA.
We analyzed a series of adrenocortical neoplasms to compare the
clinicopathologic features and the expression of insulin-like growth
factor-2 (IGF-2) in adrenocortical adenomas and carcinomas. IGF-2 is a
growth factor commonly expressed in many tumors including adrenal
cortical and medullary neoplasms. Formalin-fixed paraffin-embedded
tissues from 64 adrenocortical adenomas and 67 adrenocortical carcinomas
were analyzed. The carcinomas were histologically graded from 1 to 4
based on mitotic activity and necrosis. Tumor weight, size, and
follow-up information were obtained by chart review. Expression of IGF-2
was detected by immunohistochemistry with the avidin-biotin-peroxidase
complex method and a monoclonal antibody against IGF-2. Adrenocortical
carcinomas were larger (mean: 13.1 cm, 787 g) than adenomas (mean: 4.2
cm, 52 g) (p < 0.001). Inpatients with adrenocortical carcinomas, high
tumor grade (3 or 4) (p = 0.01) was associated with decreased survival.
Expression of IGF-2 was higher in adrenocortical carcinomas than in
adenomas (p < 0.001). These results show that tumor size and weight
along with expression of IGF-2 protein are useful features to assist in
distinguishing between adrenocortical adenomas and carcinomas, and that
high tumor grade is a predictor of survival in adrenocortical
carcinomas. However, single immunohistochemical markers such as IGF-2 or
single histopathologic features cannot by themselves separate
adrenocortical adenomas from carcinomas, and a combination of clinical,
gross, and microscopic features are needed to establish the diagnosis in
difficult cases.
3
UI - 11817708
AU - Grossrubatscher E; Vignati F; Possa M; Lohi P
TI -
The natural history of incidentally discovered adrenocortical adenomas:
a retrospective evaluation.
SO - J Endocrinol Invest 2001 Dec;24(11):846-55
AD - Endocrine Unit, Ospedale Niguarda Ca Granda, Milan, Italy.
Adrenal adenoma is the most frequent lesion among adrenal
incidentalomas. The present retrospective study was undertaken to
investigate medium-term evolution of supposed or ascertained
adrenocortical adenomas in a group of 53 subjects (16 males and 37
females, aged 31-83 yr), with bilateral (no.=8) or monolateral (no.=45)
incidentally discovered adrenal masses (size 10-50 mm, median 25 mm),
who were followed-up for 6-78 months (median 24 months). Diagnosis of
adenoma was based on size and morphovolumetric aspect of the lesion at
computed tomography (CT), scintigraphic pattern using NP59 as a tracer,
and it was histologically confirmed in 7 patients. After an extensive
hormonal investigation including morning (no.=53) and midnight (no.=28)
serum cortisol, plasma ACTH (no.=50), serum DHEAS (no.=51), daily
urinary free cortisol excretion (no.=52), post-dexamethasone (1 mg)
cortisol (no.=42) and ACTH stimulation test for 17-hydroxyprogesterone
(17-OHP) response (no.=48) at the time of diagnosis, patients were
periodically re-evaluated for hormonal function and radiological aspect
of the lesion(s) by CT. Seven patients underwent surgery 6-42 months
after incidentaloma demonstration, with histological diagnosis of
adrenal adenoma. During follow-up an increase in the size of the lesion
was demonstrated in 22 patients (41.5%); the increase was greater than
10 mm in 8 cases. In 3 patients with unilateral mass, a contralateral
lesion appeared 10-52 months after first demonstration. Six patients
(11.3%) showed reduction or disappearance of the lesions. On the basis
of the hormonal evaluation 3 patients were considered to have
subclinical Cushing's syndrome and 10 patients exhibited 17-OHP
hyperresponse to ACTH test consistent with partial 21 -hydroxylase
deficiency. A significant difference in the size of the lesions was
observed between patients with or without 17-OHP hyperresponse to ACTH
test (31.1 1.9 vs 24.1 +/- 1.2 mm; p<0.01). No significant changes in
the hormonal parameters were observed in the patients, when retested. In
conclusion, although none of the patients of the present series
exhibited evolution to hypersecretion or to aberrant growth, in more
than 40% of patients an increase in the size of the mass was observed,
even after a long period of "quiescence". This suggests that a
radiological re-evaluation of lesions should be periodically undertaken.
4
UI - 11827421
AU - Al Saad KO; Chan NH
TI -
Test and teach. Surgically correctable hypertension. Conn's syndrome and
spironolactone bodies.
SO - Pathology 2001 Nov;33(4):508-10
AD - Department of Pathology and Laboratory Medicine, King Fahad National
Guard Hospital, Riyadh, Kingdom of Saudi Arabia.
khaledalsaad@hotmail.com
5
UI - 10874904
AU - Lang M; Sinn HP; Heilmann P; Klar E; Ziegler R; Seibel MJ
TI -
[Female pseudohermaphroditism in congenital adrenogenital syndrome as an
incidental intraoperative finding in a 68 year old patient]
SO - Dtsch Med Wochenschr 2000 May 26;125(21):660-4
AD - Abteilung Innere Medizin I (Endokrinologie und Stoffwechsel),
Universitat Heidelberg.
HISTORY AND CLINICAL FINDINGS: A 68-year-old man of small stature,
previously always healthy and with a grown-up daughter, was suspected of
having carcinoma of the colon with metastasis to the right kidney. At
laparotomy internal female genitalia with cancerous changes were
unexpectedly discovered in the left adnexae. The colon carcinoma, the
right adrenocortical tumour and left adnexae were resected.
INVESTIGATIONS: Histological examination revealed adenocarcinoma of the
colon, right adrenocortical adenoma and a Brenner tumour of the left
female adnexae. Postoperative tests showed increased levels of
17-OH-progesterone (3192 ng/dl), 21-desoxycortisol (1856 ng/dl) and of
adrostenedione (745 ng/dl), while the concentrations of 17-OH
pregnenolone, testosterone and mineralocorticoids were within normal
limits. Chromosome analysis demonstrated karyotype 46 XX. DIAGNOSIS,
TREATMENT AND COURSE: As far as could be ascertained, this is the first
documented case in the German-speaking region of female
pseudohermaphroditism diagnosed in an elderly person with uncomplicated
virilizing congenital adrenogrenital syndrome due to 21-hydroxylase
deficiency (deletion of CYP21 gene). To avoid a cortisone deficiency
crisis the patient was regularly given hydrocortisone and he quickly
recovered. But he died 6 months later of sequelae of the carcinoma of
the colon. CONCLUSION: An adrenogenital syndrome should be excluded in a
case of bilateral adrenocortical tumour. As this is usually benign,
conservative treatment should be attempted. This case demonstrates the
necessity of thorough examination which could have given an early
indication of the underlying condition.
6
UI - 11846094
AU - Thomopoulos GN; Kyurkchiev S; Perbal B
TI -
Immunocytochemical localization of NOVH protein and ultrastructural
characteristics of NCI-H295R cells.
SO - J Submicrosc Cytol Pathol 2001 Jul;33(3):251-60
AD - Aristotle University, School of Sciences, Department of Biology,
Thessaloniki, Greece.
In this study we present biochemical and immunocytochemical results on
NOVH protein secretion and localization in NCI-H295R cells, as well as
results on the ultrastructural characteristics of NCI-H295R cells.
NCI-H295R cells were characterized by small quantities of rough and
smooth endoplasmic reticulum, many free ribosomes, large nuclei with
prominent nucleoli, numerous elongated mitochondria, a few Golgi
complexes, and a small number of lipid droplets. Large numbers of coated
pits and coated vesicles were present, but no secretory granules or
exocytotic profiles were seen. Best ultrastructural preservation of
NCI-H295R cells was achieved when fixation was done directly on the
culture dishes and the cells were detached by scraping. Our biochemical
results showed that NCI-H295R cells secreted large amounts of NOVH
protein. The immunocytochemical localization of NOVH protein showed that
the protein was localized in the cytoplasm, the plasma membrane and the
nuclear envelope. This localization pattern, along with the
ultrastructural and biochemical findings raise interesting questions on
the function(s) and the mode of secretion of NOVH protein.
7
UI - 12057116
AU - Boushey RP; Dackiw AP
TI -
Adrenal cortical carcinoma.
SO - Curr Treat Options Oncol 2001 Aug;2(4):355-64
AD - Department of Surgical Oncology, Section of Endocrine Surgery, Princess
Margaret Hospital, University of Toronto, 610 University Avenue, Suite
3-130, Toronto, Ontario, Canada M5G 2M9.
Adrenal cortical carcinoma is a rare endocrine tumor, and complete
surgical resection is the only potentially curative treatment. Accurate
preoperative biochemical and radiographic evaluation of the patient who
presents with an adrenal mass optimizes patient management and
facilitates a complete margin-negative resection of the primary
tumor--the most important prognostic variable for long-term survival.
Response to mitotane or chemotherapy is modest in patients with advanced
disease. It is hoped that an improved understanding of the molecular
pathogenesis of this challenging tumor will lead to the development of
novel treatment strategies.
8
UI - 12061373
AU - Zuboy J
TI -
Radiofrequency ablation used to treat select renal and adrenal tumors.
SO - Curr Treat Options Oncol 2000 Jun;1(2):93-4
9
UI - 12094420
AU - Causeret S; Monneuse O; Mabrut JY; Berger N; Peix JL
TI -
[Adrenocortical carcinoma: prognostic factors for local recurrence and
indications for reoperation. A report on a series of 22 patients]
SO - Ann Chir 2002 May;127(5):370-7
AD - Service de chirurgie, hopital de l'Antiquaille, 69321 Lyon, France.
STUDY AIMS: The aim of this retrospective study was to identify
prognostic factors on local recurrence in patients with adrenocortical
carcinoma and to assess the effect of reoperations. METHODS: From 1985
to 2001, 22 patients were operated for adrenocortical carcinoma. We
evaluated the correlation between actuarial survival without local
recurrence and tumor staging, Weiss criteria, mitotic index, extensive
resection and Op'DDD therapy by univariate analysis. Then we evaluated
the effect of reoperations on survival. RESULTS: Local recurrence was
observed in 7 patients and the 5-years actuarial survival without local
recurrence was 50%. Tumor stage (I et II versus III et IV), Weiss
criteria (< or = 6 criteria versus > 6) and mitotic index (< or = 20
mitoses/50 HPF versus > 20) affected survival without local recurrence.
Extensive resection could reduce local recurrence rate. Op'DDD therapy
was ineffective in prolonging survival without local recurrence. Four
patients underwent repeat resections: 2 patients were still alive with
disease free, 54 and 8 months after reoperations and 2 patients died, 19
and 25 months after reoperations. Three patients did not have repeat
resection. They rapidly died within 8 months. CONCLUSION: Pathologic
features (tumor staging and mitotic index) affected local recurrence
prognostic. But extensive resection to adjacent organs could facilitate
complete resection tumor and reduce the local recurrence rate. Complete
repeat resection of local recurrence can improve survival. The disabling
effects of Op'DDD were important and its efficacy was not clear.
10
UI - 11848245
AU - van Grevenstein WM; de Krijger RR; de Herder WW; Tilanus HW; Bonjer HJ
TI -
Abdominal wall metastasis after open resection of an adrenocortical
carcinoma.
SO - Eur J Surg 2001 Nov;167(11):871-3
AD - Department of Surgery, University Hospital Rotterdam, The Netherlands.
vangrevenstein@hotmail.com
11
UI - 12016808
AU - Huang J; Zhou Z; Chao C
TI -
[Clinical analysis of 17 patients with adrenal "incidentaloma"]
SO - Hunan Yi Ke Da Xue Xue Bao 1999;24(3):282-4
AD - Department of Endocrinology, Second Affiliated Hospital, Hunan Medical
University, Changsha 410008.
This paper reports 17 cases of adrenal "incidentaloma", discovered by
B-mode ultrasonography, computed tomography and/or magnetic resonance
imaging scan and identified by operation and pathological examination.
Seven of them were pathologically diagnosed as adrenocortical adenoma, 4
pheochromocytoma, 2 adrenal cyst, and 1 mixed cell adenoma, 1 leiomyoma,
1 adrenocortical carcinoma, and 1 gangliocytoma. Adrenal shows
hormone-secreting function in 17 patients with adrenal "incidentaloma".
The diagnosis and management of this disorder are discussed.
12
UI - 12085205
AU - Bernini GP; Moretti A; Viacava P; Bonadio AG; Iacconi P; Miccoli P;
TI -
Salvetti A
Apoptosis control and proliferation marker in human normal and
neoplastic adrenocortical tissues.
SO - Br J Cancer 2002 May 20;86(10):1561-5
AD - Department of Internal Medicine, University of Pisa, Via Roma 67, 56100
Pisa, Italy. g.bernini@med.unipi.it
We evaluated by immunohistochemistry the expression of the Bcl-2 and p53
proteins, as markers of apoptosis control, and of MIB-1, as a marker of
cell proliferation, in a series of normal and neoplastic adrenocortical
tissues. The specimens were 13 normal adrenals, 13 aldosterone-producing
adenomas, 13 non-functioning adenomas and 16 carcinomas. Results were
calculated as percentage of immunostained cells by using specific
antibodies. No p53 protein was detected in any of the adrenocortical
adenomas (functioning and non functioning) or normal adrenals, while p53
was overexpressed in 15 out of 16 carcinomas. In particular, 10 adrenal
cancer specimens (62.5%) showed strong staining in a high percentage
(range 10-50%) of the malignant cells. The percentage of Bcl-2 positive
cells was higher (P<0.05 or less) in non-functioning adenomas
(8.1+/-1.9%) and in carcinomas (14.9+/-5.6%) than in normals
(2.9+/-0.9%) and aldosterone-producing adenomas (5.3+/-1.3%) since four
specimens of the non-functioning adenomas-group (30.7%) and six of the
carcinomas-group (37.5%) showed over 10% positivity (cut-off for normal
values, set at 90th percentile of our controls). MIB-1 positivity was
0.50+/-0.36% in normals, 0.54+/-0.08% in non-functioning adenomas and
0.54+/-0.08% in aldosterone-producing adenomas. MIB-1 was expressed in
all carcinomas with values (13.7+/-3.1%) significantly (P<0.0006) higher
than in the other groups. In conclusion, the present data indicate that
the apoptosis control and proliferation activity evaluated by the p53
and MIB-1 proteins are impaired in adrenal carcinomas but preserved in
adenomas, independently of their functional status. Therefore, these
immunohistochemical markers, overexpressed in carcinomas only, may be
useful in the diagnosis of malignancy in adrenocortical tumours. Whether
Bcl-2 positivity found in some carcinomas and non-functioning adenomas
may constitute, in the latter, a negative prognostic marker is still
unknown. comCopyright 2002 Cancer Research UK
13
UI - 12107267
AU - Sidhu S; Marsh DJ; Theodosopoulos G; Philips J; Bambach CP; Campbell P;
TI -
Magarey CJ; Russell CF; Schulte KM; Roher HD; Delbridge L; Robinson BG
Comparative genomic hybridization analysis of adrenocortical tumors.
SO - J Clin Endocrinol Metab 2002 Jul;87(7):3467-74
AD - Cancer Genetics, Kolling Institute of Medical Research, Royal North
Shore Hospital, St. Leonards, New South Wales 2065, Australia.
Comparative genomic hybridization (CGH) is a molecular cytogenetic
technique that allows the entire genome of a tumor to be surveyed for
gains and losses of DNA copy sequences. A limited number of studies
reporting the use of this technique in adult adrenocortical tumors have
yielded conflicting results. In this study we performed CGH analysis on
13 malignant, 18 benign, and 1 tumor of indeterminate malignant
potential with the aim of identifying genetic loci consistently
implicated in the development and progression of adrenocortical tumors.
Tissue samples from 32 patients with histologically proven
adrenocortical tumors were available for CGH analysis. CGH changes were
seen in all cancers, 11 of 18 (61%) adenomas, and the 1 tumor of
indeterminate malignant potential. Of the adrenal cancers, the most
common gains were seen on chromosomes 5 (46%), 12 (38%), 19 (31%), and 4
(31%). Losses were most frequently seen at 1p (62%), 17p (54%), 22
(38%), 2q (31%), and 11q (31%). Of the benign adenomas, the most common
change was gain of 4q (22%). Mann-Whitney analysis showed a highly
significant difference between the cancer group (mean changes, 7.6) and
the adenoma group (mean changes, 1.1) for the number of observed CGH
changes (P < 0.01). Logistic regression analysis showed that the number
of CGH changes was highly predictive of tumor type (P < 0.01). This
study has identified several chromosomal loci implicated in
adrenocortical tumorigenesis. Activation of a protooncogene(s) on
chromosome 4 may be an early event, with progression from adenoma to
carcinoma involving activation of oncogenes on chromosomes 5 and 12 and
inactivation of tumor suppressor genes on chromosome arms 1p and 17p.
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