PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ADRENAL CORTEX NEOPLASMS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed2000

Myxoid neoplasms of the adrenal cortex: a rare histologic variant.

The myxoid variant of adrenocortical carcinoma is a rare neoplasm described previously in only two case reports. Because of the rarity of these lesions, the presence of myxoid changes in adrenal cortical neoplasms usually raises the possibility of malignancy. We studied the histopathologic features of 14 cases of myxoid adrenocortical neoplasms, including six adenomas and eight carcinomas. All patients with adenomas with sufficient follow-up (n = 5) were alive with no recurrence of their tumors or evidence of metastatic disease. Four patients with carcinomas died of their disease, two were alive with metastatic disease, and one was alive with no evidence of recurrence or metastatic disease. Histologically, the 14 tumors varied in their myxoid composition, ranging from 10% to 95%. The myxoid foci stained positively with Alcian blue and were usually negative with periodic acid-Schiff and mucicarmine stains. As a group, the immunophenotype of the lesions was typical of other adrenal cortical neoplasms, with positive immunostaining for vimentin, synaptophysin, and alpha-inhibin. One tumor was focally positive for keratin. Myxoid adrenal cortical neoplasms should be included in the differential diagnosis of myxoid retroperitoneal neoplasms. Myxoid changes in adrenal cortical neoplasms may be present in both adenomas and carcinomas, and the usual clinical and histopathologic features for adrenocortical neoplasms should be used to diagnose these neoplasms.

Adolescent↗
PubMed1990

Mortality in patients with familial adenomatous polyposis.

The authors identified 132 patients who died with a documented diagnosis of familial adenomatous polyposis (FAP). A review of the medical records, autopsy reports, and in-depth discussion with local physicians and well-informed family members was performed. It was impossible, even after the review, to ascertain the exact cause of death in 22 patients. In the remaining patients, the cause of death was as follows: metastatic colorectal carcinoma, 64 patients (58.2 percent), (colon, 49 [44.5 percent], rectal, 15 [13.6 percent]); desmoid tumors, 12 (10.9 percent); periampullary carcinoma, 9 (8.2 percent); brain tumors, 8 (7.3 percent); perioperative mortalities, 5 (4.5 percent); adrenal carcinoma, 1 (0.9 percent); and abdominal carcinomatosis, 1 (0.9 percent). Ten patients died of causes not related to FAP. The major causes of death in 36 patients who underwent prophylactic colectomy were desmoid tumor and periampullary malignancy. This finding underscores the importance of lifelong surveillance and periodic endoscopic evaluation in patients with FAP.

Abdominal Neoplasms↗
PubMed1997

Expression patterns of the c-myc gene in adrenocortical tumors and pheochromocytomas.

Abundant c-myc gene expression in neoplasms has been often linked to poor prognosis. As c-myc mRNA is expressed and hormonally regulated in human adrenals, we examined the c-myc gene expression in adrenal tumors by RNA analysis and immunohistochemistry to find out the possible role of c-myc in adrenal neoplasms. The abundant expression of the c-myc gene in normal adrenals was localized to the zona fasciculata and zona reticularis, with much lower expression in the zona glomerulosa and adrenal medulla. In hormonally active adrenocortical carcinomas (n = 6) and in virilizing adenomas (n = 4), c-myc mRNA levels were approximately 10% of those in normal adrenals (n = 11). In contrast, adrenal adenomas from patients with Cushing's (n = 4) and Conn's (n = 9) syndrome, non-functional adenomas (n = 2), adrenocortical hyperplasias (bilateral, n = 5; nodular, n = 4), and non-functional adrenocortical carcinomas (n = 3) expressed c-myc mRNA to the same extent as normal adrenals. The c-myc mRNA abundance in benign adrenal pheochromocytomas (n = 19) was similar to that in normal adrenal medulla. However, in malignant adrenal pheochromocytomas (n = 6), the average c-myc mRNA levels were approximately threefold that in benign adrenal pheochromocytomas. There was a good correlation between c-myc mRNA expression and immunohistochemical reactivity in both normal and pathological adrenal tissues. Southern blot analysis revealed no amplification or rearrangement of the c-myc gene in any of the adrenal tumors. In conclusion, c-myc expression localized to zona fasciculata and reticularis in normal adrenals. Virilizing adenomas and hormonally active adrenocortical carcinomas expressed c-myc mRNA clearly less than the other adrenal neoplasms and normal adrenal tissue. On the other hand, malignant pheochromocytomas contained more c-myc mRNA than benign ones. Further studies are required to clarify the mechanisms and significance for the distinct expression pattern of the c-myc gene in different adrenal neoplasms.

Adrenal Cortex Neoplasms↗
PubMed1993

Absent ras gene mutations in human adrenal cortical neoplasms and pheochromocytomas.

A variety of human tumors have been studied for ras mutations to date. However, little is known about the prevalence and significance of ras gene activation in adrenal neoplasms. Recently, a study of 10 primary human pheochromocytomas found no evidence for ras mutations. To our knowledge no survey of ras mutations in adrenocortical neoplasms has been reported. Therefore, we analyzed deoxyribonucleic acid (DNA) from 17 archival tumors (8 adrenocortical carcinomas, 6 pheochromocytomas, 2 adrenal adenomas, 1 aldosteronoma, 2 fresh pheochromocytomas and 1 fresh benign adrenal gland) for activating mutations at the 12, 13 and 61 codons of N-ras, H-ras and K-ras. DNA was extracted from archival tissues using 3 different methods: a simplified boiling method, a proteinase-K-phenol chloroform extraction and a novel heat-stable protease Thermus rt41A technique. The boiling and heat-stable protease methods provided for more consistent polymerase chain reaction amplifications than the more laborious phenol chloroform method. This heat-stable protease Thermus rt41A method had not been reported previously for use in archival DNA extraction. Polymerase chain reaction amplified the ras gene regions of interest, and mutations were screened by mutation-specific oligonucleotide probe hybridization of Southern and slot blots. Polymerase chain reaction-generated mutation-specific positive and negative controls were used in the hybridization protocol. With these controlled conditions no definite mutations were detected at codons 12, 13 or 61 of N, H or K-ras. Ras activation via point mutations at these codons rarely, if ever, occurs in adrenal neoplasms.

Adrenal Cortex Neoplasms↗
PubMed1997

Adrenal neoplasms in children.

Neuroblastoma is the most common extracranial neoplasm of childhood. Although it most commonly occurs in the adrenal gland, it may be found anywhere along the sympathetic chain. The characteristic clinical and imaging features of neuroblastoma are discussed in this article. Less common neoplasms of the adrenal gland, adenoma, adrenocortical carcinoma, and pheochromocytoma are also discussed.

Adrenal Cortex Neoplasms↗
PubMed1995

Pathology of adrenal neoplasms.

The use of immunohistochemistry and electron microscopy enables the strict separation of adreno-cortical and adreno-medullary tumors in every case, as tumors of the medulla are generally positive for neuroendocrine markers (chromogranin A, synaptophysin) and negative for D11 whereas those of the cortex are stained with D11 and are negative with the other markers. Our surgical collection of cortical tumors and tumor-like lesions (n = 104) covers adenomas (39%), carcinomas (15%), microadenomatosis (2%), macronodular hyperplasia (4%), hemangioma (1%), myelolipoma (2%), hematoma (1%), pseudocysts (2%), and metastases (6%). The often difficult interpretation of dignity was aided by a point system of criteria. Isolated nodules were differentiated from adenomas by their size (ie less than 3 cm), the histological pattern and the lack of cellular atypia. Correlations of the lesions with the endocrine functions were presented. The tumors of the medulla (n = 42) were differentiated in pheochromocytomas (88%), malignant pheochromocytomas (7%), neuroblastomas (2%), and ganglioneuroblastomas (2%). 8-10% of pheochromocytomas are malignant, but with the exception of invasion of the capsule or of the veins or the demonstration of metastases, no other reliable criteria for malignancy exist. The lack of S100-protein-immunoreacting satellite cells may indicate a malignant growth. 89% of pheochromocytomas in our collection were shown to be endocrine active secreting catecholamines and in one case additionally ACTH.

Adrenal Cortex Neoplasms↗
PubMed1995

[Diagnostic and therapeutic approach to incidentally detected adrenal tumors].

The authors report their experience relative to 12 cases of adrenal "incidentaloma" surgically treated. All masses removed had a main diameter larger than 3 cm. In all patients an anterior median transperitoneal incision was performed. They didn't record postoperative mortality and the postoperative morbidity rate was 15%. In 6 cases a nonfunctioning cortical adenoma was diagnosed. No malignant neoplasm was detected in their series.

Adenoma↗
PubMed1979

Massive adrenal haemorrhage complicating adrenal neoplasm.

Two patients presented to hospital with clinical features of acute retroperitoneal haemorrhage. In each case, laparotomy revealed massive adrenal haemorrhage, and histological evidence of underlying neoplasia was eventually found.

Adrenal Cortex Neoplasms↗
PubMed1996

Diagnosis and management of adrenal tumors.

Tumors of the adrenal gland are not uncommon. Patients with these tumors usually demonstrate symptoms associated with the biochemical substance or hormone produced by the tumor. Tumors of the adrenal cortex, whether benign or malignant, are often associated with excess production of steroids, whereas tumors of the medulla are generally associated with overproduction of catecholamines. With the ubiquitous use of computed tomographic imaging, many asymptomatic adrenal lesions are discovered, presenting a management problem for the clinician. The algorithm for investigating so-called adrenal "incidentalomas" in the current era of cost containment continues to evolve. This review addresses current trends in the clinical evaluation, biochemical testing, and nuclear and radiologic imaging in the diagnostic work-up of these neoplasms. The mainstay of treatment is still surgical extirpation, the only curative modality. However, advances have occurred in adjuvant therapies, perhaps best typified by the neoadjuvant use of 131I-methyl iodobenzylguanidine in the treatment of neuroblastoma.

Adrenal Cortex Neoplasms↗
PubMed1976

In vitro synthesis of steroids by a feminising adrenocortical carcinoma: effect of prolactin and other protein hormones.

The study describes the effects of ACTH, prolactin and other protein hormones on the synthesis and secretion of steroid hormones by tissue from a feminising adrenocortical carcinoma removed from a post-menopausal female. Steroid production by the tissue was determined by high resolution-mass fragmentography and by radioimmunoassay. Prolactin and ACTH stimulated the synthesis of estrogens by the tissue whereas GH, LH and ACTH were more effective than prolactin in stimulating androgen synthesis. The effect of protein hormones, other than ACTH, on adenylate cyclase activity of this tumour tissue indicated a lack of specificity of the membrane receptor sites.

Adenylyl Cyclases↗
PubMed1990

Mortality and tumour incidence of Han:SPRD rats.

In a longevity study a total of 394 Han:SPRD rats (200 males and 194 females) were kept in a barrier type animal quarter from weaning until their natural death. The mean life span of males was 29.6 +/- 5 months, that of females 27.6 +/- 6.2 months. The most frequent neoplasms in females were mammary gland tumours (63.4%). Neoplasms of endocrine organs were common in animals of both sexes. Thyroid neoplasms, predominantly of C-cell origin, occurred in 60% of the males and 51.5% of the females. Pituitary gland tumours were observed in 53% of male and 45.1% of female rats. Further frequent tumours of the endocrine system included phaeochromocytomas (23% in males, 15.5% in females), adrenal cortex neoplasms (6% in males, 13.5% in females) and tumours of islet cells of the pancreas (20.8% in males, 8.2% in females). An uncommonly high incidence of squamous cell neoplasms (16% in males; 9.3% in females) of the preputial and clitoral gland was observed in this stock. Further organs frequently affected by neoplasms were the skin/subcutis and brain.

Animals↗
PubMed1984

Diagnosis of adrenal tumors with radionuclide imaging.

The development of radiolabeled cholesterols in 1969 as precursors of adrenocortical steroid production allowed the first noninvasive imaging of the adrenal cortices. FDA-NDA approval in 1984 should allow routine use of these agents in most hospitals. NP-59 is most commonly used in the diagnosis and management of Cushing syndrome; the second most common use is in the diagnosis of primary aldosteronism. It is also helpful in the differential diagnosis of adrenal and ovarian hyperandrogenism and hirsutism, and is the only noninvasive method of detecting unilateral adrenocortical hypofunction. The newest and most popular use is in the differential diagnosis of asymptomatic masses in the region of the adrenal gland discovered incidentally with CT scan ("incidentalomas"). In this situation, the NP-59 scan can define whether the tumor is in the adrenal gland and if it is functional or nonfunctional. We believe that, in the future, radiolabeled enzyme inhibitors might offer better diagnostic imaging of the adrenal cortex, although these agents will probably not be available for routine use for some time. Our development of a radioiodinated guanethidine analog, 131I-MIBG, has allowed differentiation of normal adrenal medullary function from bilateral adrenal medullary hyperplasia before the development of hypertension or tachycardia, diagnostic increases in plasma or urinary catecholamines, or abnormal CT scans. The search for a pheochromocytoma should begin with 131I-MIBG scintigraphy. While over 90% of primary pheochromocytomas occur in the abdomen, neither a survey of the abdomen nor the finding of a single tumor should conclude the search. Whereas the CT scan can only detect a mass, the MIBG scan not only detects the mass but proves whether the mass is a pheochromocytoma. We have detected small or recurrent pheos when all other localizing studies were normal. Present drug and X-ray therapy is relatively ineffective in treating metastatic cancer of the adrenal medulla. Preliminary results in five patients indicate that, for the first time, a complex organic molecule can carry 131I into adrenal neoplasms reproducibly and in therapeutically effective doses of irradiation. We may also be able to select which patients will respond to therapeutic doses of 131I-MIBG and which patients will not respond.

Adenoma↗
PubMed1997

[Diagnostic guidelines for adrenal gland nodules: typing, assessment of biological potential and prognosis, molecular pathogenesis].

The aim of morphological tumour diagnosis is to answer clinical questions on type, biological potential, prognosis and aetiology of individual neoplasms. The limitations and perspectives of different methods used in the diagnosis of adrenal tumours, ranging from histology to molecular genetic DNA analyses, are described. When surgical specimens from adrenal neoplasms cannot be typed on the basis of histology and/or with clinica data (e.g. endocrine symptoms and history) as adrenocortical tumours, phaeochromocytomas or metastases to the adrenal, immunohistological investigations with a panel of different antibodies are necessary. After identification of the tissue derivation of an individual adrenal tumour, its biological potential must be assessed. Among adrenocortical neoplasms, adenomas and carcinomas can be distinguished by evaluation of various histological parameters (including structural features and signs of invasion) according to defined algorithms. In addition, conventional histology (by estimation of mitotic activity) allows the discrimination of tumours with especially high malignant potential from other adrenocortical carcinomas. In contrast, among adrenomedullary tumours even the combined use of histological, immunohistological and DNA cytophotometric techniques only allows the definition of risk groups (benign versus suggestive of malignancy), while reliable recognition of an individual malignant phaeochromocytoma is so far impossible. The question as to whether a particular phaeochromocytoma represents a sporadic tumour or a neoplasm inherited as one feature of a defined syndrome cannot be answered with the above methods, but only by the application of molecular genetic techniques.

Adrenal Cortex Neoplasms↗
PubMed2004

Cystic adrenal neoplasms.

BACKGROUND: Cystic lesions of the adrenal gland are uncommon and demonstrate a spectrum of histologic changes and may vary from pseudocysts to malignant cystic neoplasms. METHODS: The authors analyzed a series of primary cystic lesions of the adrenal gland to evaluate the clinicopathologic features and histologic spectrum and to determine features that are helpful in distinguishing benign from malignant cystic adrenal tumors. RESULTS: A total of 41 cases of macroscopically cystic lesions among patients who underwent surgery at the Mayo Clinic were identified over a 25-year period. Of these 41 cases, 32 were pseudocysts, 8 were endothelial cysts, and 1 was an epithelial cyst. Of the 32 pseudocysts, 6 were associated with adrenal neoplasms, including 2 adrenal cortical carcinomas, 2 adrenal cortical adenomas, and 2 pheochromocytomas. One pheochromocytoma case was identified in association with an endothelial cyst. Both patients with cystic adrenal cortical carcinomas died of disease. CONCLUSIONS: Adrenal neoplasms, including adrenal cortical carcinomas, may be associated with benign-appearing cysts. Extensive pathologic sampling of resected tissues is important to rule out malignancy in patients with cystic adrenal lesions.

Adolescent↗
PubMed1995

[Morphological typing, evaluation of tumor dignity and prognosis and etiologic classification of adrenomedullary and adrenocortical neoplasias].

The aim of morphological tumour diagnosis is to answer clinical questions on type, biological potential, prognosis and aetiology of individual neoplasms. The limitations and perspectives of different methods used in the diagnosis of adrenal tumours, ranging from histology to molecular genetic DNA analyses, are described. When surgical specimens from adrenal neoplasms cannot be typed on the basis of histology and/or with clinica data (e.g., endocrine symptoms and history) as adrenocortical tumours, phaeochromocytomas or metastases to the adrenal, immunohistological investigations with a panel of different antibodies are necessary. After identification of the tissue derivation of an individual adrenal tumour, its biological potential must be assessed. Among adrenocortical neoplasms, adenomas and carcinomas can be distinguished by evaluation of various histological parameters (including structural features and signs of invasion) according to defined algorithms. In addition, conventional histology (by estimation of mitotic activity) allows the discrimination of tumours with especially high malignant potential from other adrenocortical carcinomas. In contrast, among adrenomedullary tumours even the combined use of histological, immunohistological and DNA cytophotometric techniques only allows the definition of risk groups (benign versus suggestive of malignancy), while reliable recognition of an individual malignant phaeochromocytoma is so far impossible. The question as to whether a particular phaeochromocytoma represents a sporadic tumour or a neoplasm inherited as one feature of a defined syndrome cannot be answered with the above methods, but only by the application of molecular genetic techniques.

Adrenal Cortex↗
PubMed1996

Expression of the steroidogenic acute regulatory protein mRNA in adrenal tumors and cultured adrenal cells.

The steroidogenic acute regulatory protein (StAR) has recently been shown to be a factor necessary for cholesterol transport into adrenal and gonadal mitochondria, which is the regulated, rate-limiting step in steroidogenesis. We show here that StAR mRNA is highly expressed in normal adult adrenals (n = 9), adrenocortical adenomas (n = 16), adrenal hyperplasias (n = 6), adrenocortical carcinomas (n = 6) and adrenals adjacent to tumor tissues (n = 9). There was a good correlation between the expression of StAR and the cholesterol side-chain cleavage enzyme/20,22-desmolase (P450 scc) mRNAs both in normal (r = 0.93; P < 0.01) and in tumor (r = 0.97; P < 0.001) tissues. No StAR mRNA was detected in Northern blots of liver, kidney, breast, parathyroid or phaeochromocytoma RNAs. In cultured adrenocortical cells, adrenocorticortropin (ACTH), (Bu)2cAMP, and cholera toxin increased StAR and P450 scc mRNA accumulation 6- to 18-fold, dose- and time-dependently. StAR (and P450 scc) mRNA increased relatively slowly in response to ACTH treatment, with the maximal increment at 24 h, while the mRNA of the early response gene c-fos peaked within 2 h. The protein kinase inhibitor H-7 inhibited basal and ACTH-induced StAR mRNA expression. Our results show that StAR mRNA is expressed at high levels in normal human adrenals and adrenocortical neoplasms. It is up-regulated in parallel with P450 scc by ACTH in adult adrenocortical cells, which suggests that ACTH is at least one of the key regulators of adrenal StAR expression.

Adenoma↗
PubMed1997

Adrenomedullin gene expression and its different regulation in human adrenocortical and medullary tumors.

Adrenomedullin (ADM) is a polypeptide originally discovered in a human pheochromocytoma and is also present in normal adrenal medulla. It has been proposed that ADM could be involved in the regulation of adrenal steroidogenesis via paracrine mechanisms. Our aim was to find out if ADM gene is expressed in adrenocortical tumors and how ADM gene expression is regulated in adrenal cells. ADM mRNA was detectable by Northern blotting in most normal and hyperplastic adrenals, adenomas and carcinomas. The average concentration of ADM mRNA in the hormonally active adrenocortical adenomas was about 80% and 7% of that in normal adrenal glands and separated adrenal medulla respectively. In adrenocortical carcinomas, the ADM mRNA concentration was very variable, but on average it was about six times greater than that in normal adrenal glands. In pheochromocytomas, ADM mRNA expression was about ten times greater than that in normal adrenals and three times greater than in separated adrenal medulla. In primary cultures of normal adrenal cells, a protein kinase C inhibitor, staurosporine, reduced ADM mRNA accumulation in a dose- and time-dependent fashion (P < 0.01), whereas it simultaneously increased the expression of human cholesterol side-chain cleavage enzyme (P450 scc) gene (a key gene in steroidogenesis). In cultured Cushing's adenoma cells, adrenocorticotropin, dibutyryl cAMP ((Bu)2cAMP) and staurosporine inhibited the accumulation of ADM mRNA by 40, 50 and 70% respectively (P < 0.05), whereas the protein kinase C activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA), increased it by 50% (P < 0.05). In primary cultures of pheochromocytoma cells, treatment with (Bu)2cAMP for 1 and 3 days increased ADM mRNA accumulation two- to threefold (P < 0.05). Our results show that ADM mRNA is present not only in adrenal medulla and pheochromocytomas, but also in adrenocortical neoplasms. Both protein kinase A- and C-dependent mechanisms regulate ADM mRNA expression in adrenocortical and pheochromocytoma cells supporting the suggested role for ADM as an autocrine or paracrine (or both) regulator of adrenal function.

8-Bromo Cyclic Adenosine Monophosphate↗