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PubMed1988

A compound adrenal medullary tumor (pheochromocytoma and ganglioneuroma) and a cortical adenoma in the ipsilateral adrenal gland. A case report with enzyme histochemical and immunohistochemical studies.

Neoplasms of all the adrenal parenchymatous elements [i.e., a compound adrenal medullary tumor (MT) consisting of pheochromocytoma (Pheo) and ganglioneuroma (GN) and a cortical adenoma] were found in the right adrenal gland of a 53-year-old man. A mature GN element was predominant in the MT, and nodules of small polygonal Pheo cells were scattered in GN. No neuroblastomatous element or malignant Pheo was found. The cortical adenoma consisted of compact cells and clear cells; it showed 3 beta hydroxysteroid dehydrogenase, glucose-6-phosphate dehydrogenase, and succinate dehydrogenase activity. The nonneoplastic cortex was slightly atrophic and showed weaker activity of the enzymes, suggesting that the adenoma was cortisol-producing. The cortex surrounding the MT was invaded and replaced by either GN or Pheo. In some places, however, hypertrophic compact cells constituted the cortex and were in contact with ACTH-immunoreactive chromaffin cells. A few of the latter were also positive for other proopiomelanocortin (POMC)-derived peptides. Pheo cells in the other parts were negative for POMC-derived peptides.

Adenoma↗
PubMed1990

Immunocytochemical differential diagnosis of adrenocortical neoplasms using the monoclonal antibody D11.

The monoclonal antibody D11 is a valuable aid in the accurate typing of adrenal tumours as, in formalin-fixed, paraffin-embedding material, strong nuclear D11 positivity was observed only in adrenocortical cells in 190 neoplasms (including 100 adrenal tumours). This pattern was demonstrated for all zona glomerulosa cells in 27 normal adrenals and for the neoplastic cells of 15 adrenocortical adenomas derived from that zone, as judged from clinically evident hyperaldosteronism. Normal cells of zona fasciculata and reticularis also showed strong diffuse D11 immunostaining and the same nuclear plus cytoplasmic D11 reactivity was evident in 15 benign and malignant adrenocortical neoplasms derived from these zones, documented by hypercortisolism. Cytoplasmic and/or nuclear D11 staining made topohistogenetic typing possible in 15 non-functioning cortical tumours. D11 immunostaining gave negative results in 50 specimens containing normal, hyperplastic and neoplastic adrenomedullary cells. In addition, absence of D11 reactivity was recorded in 4 adrenal metastases of extra-adrenal carcinomas, 5 paragangliomas, 25 primary renal carcinomas and 59 of 60 primary thyroid carcinomas. D11 immunocytochemistry allows the accurate typing of benign and malignant adrenocortical neoplasms, irrespective of histology and function. With this method, primary adrenocortical tumours can be separated from carcinomas metastatic to the adrenal gland, including secondary tumours of similar phenotype (such as renal carcinomas). By exclusion, D11 negativity provides evidence of the medullary origin of primary adrenal tumours even in the absence of clinical, structural, histochemical and conventional immunohistochemical indicators of phaeochromocytoma.

Adenoma↗
PubMed1992

Studies on pathological morphology, clinical features and nuclear DNA contents by flow cytometry in adrenal neoplasms.

Pathological morphology, clinical features and nuclear DNA contents determined by flow cytometry (FCM) were studied in 11 cases of normal adrenals and 41 cases of adrenal neoplasms. It was found that despite differences in clinical manifestations and in degrees of cellular atypia of the adenomas their DNA contents were the same as in normal adrenals. On the other hand, the pheochromocytomas were benign in nature, but most of them (16/19) showed DNA aneuploidy and the DNA indices were correlated with their clinical and morphological features.

Adenoma↗
PubMed2000

Adrenocortical carcinoma in children. Review and recent innovations.

Adrenocortical carcinoma in childhood is a rare potentially fatal disease. Despite its often dramatic presentation, there typically has been a distressingly long delay between the onset of symptoms and the time of diagnosis. This delay undoubtedly has contributed to the historically poor prognosis in these children by permitting the disease to reach an advanced stage before treatment is started. It is imperative that the physician recognizes the endocrine manifestations of these tumors early and has a high index of suspicion. Although biochemical and histologic evaluations are helpful, they often cannot differentiate benign lesions from malignant neoplasms and should not unduly delay intervention. Aggressive complete surgical resection continues to be the mainstay of treatment and is the best prognosticator of overall survival. The role of adjuvant therapy and chemotherapy continues to evolve. Molecular studies have increased understanding of cancer biology and may provide possible novel therapeutic approaches in the future. It is hoped that increased familiarity with this unusual tumor will result in earlier detection, prompt intervention, and improved survival for children with adrenocortical carcinoma.

Adrenal Cortex Neoplasms↗
PubMed1975

Adrenocortical neoplasms. Prognosis and morphology.

The clinical data and morphologic findings in 16 cases of adrenocortical carcinoma were compared with those in 11 cases of surgically removed functional adenomas and 12 cases of nonfunctional adenomas found at autopsy. Histopathologic changes of architectural disarray, pleomorphism, increased mitotic activity, vascular invasion, hemorrhage, or necrosis were generally reliable criteria for diagnosis of malignancy. However, weight was the parameter that most consistently correlated with outcome, since all patients with tumors under 50 Gm. survived and all lesions of 95 Gm. or over proved to be malignant.

Adenoma↗
PubMed1994

Adrenal carcinoma.

Adrenal cortical carcinoma is an uncommon but highly malignant tumor. Functioning tumors are detected earlier than nonfunctioning neoplasms such that patients with functioning tumors are younger and the tumors smaller than in patients with nonfunctioning tumors. Most tumors are quite large by presentation and are easily detected by imaging studies. CT is the primary imaging modality and can be used to stage most patients accurately. MR may be employed to clarify equivocal findings, especially the delineation of venous extension. Surgery is the only effective treatment, so precise tumor delineation is essential. Chemotherapy with ortho para DDD provides some palliation, but the prognosis remains poor.

Adolescent↗
PubMed2002

The molecular pathogenesis of hereditary and sporadic adrenocortical and adrenomedullary tumors.

Modern imaging modalities lead to frequent detection of adrenal masses, most of them incidental findings. Although the majority of adrenocortical and adrenomedullary tumors are benign, there are no reliable clinical and laboratory markers to distinguish most of them from malignant neoplasms. The molecular mechanisms underlying the pathogenesis of these tumors have recently begun to be unraveled. A fruitful avenue for the elucidation of tumorigenesis has been the study of adrenal tumors that are manifestations of hereditary or postzygotic genetic syndromes, because one knows the "first hit", i.e. the primary gene defect. In contrast, in sporadic adrenal tumors the first hit, possibly a somatic mutation of a tumor-related gene, is unknown, and therefore the sequence of genetic alterations is difficult to establish. In this article we review in addition to our own work the literature on molecular aspects of adrenocortical and adrenomedullary tumorigenesis.

Adrenal Cortex Neoplasms↗
PubMed1996

[Adrenal gland carcinoma--status of diagnostic and therapeutic possibilities].

Innovations in diagnosis and therapy of adrenal neoplasms require a discussion about these tumors. Especially, the articles deal with the radiologic evaluation of the adrenal gland, technical as well as perioperative considerations of adrenalectomy, and adrenocortical carcinoma. Several conclusions can be drawn from our own results and a review of the literature. Firstly, the diagnostic accuracy should improve with advances in magnetic resonance imaging. Secondly, all asymptomatic nonfunctional adrenal masses about 3 cm require removal. Thirdly, adrenocortical carcinomas are generally curable only if small and localized. Fourthly, among the adrenal tumors, pheochromocytomas--especially malignant pheochromocytomas--deserve a careful approach: adequate preparation and early ligation of the adrenal vein after transabdominal access are the main goals. Finally, adjuvant treatment regimens for more advanced adrenocortical carcinomas using mitotane and conventional multiagent chemotherapy need to be evaluated in randomized trials.

Adrenal Cortex Neoplasms↗
PubMed1987

Lipid degeneration in pheochromocytomas mimicking adrenal cortical tumors.

A case of bilateral adrenal pheochromocytomas with unusual morphologic features is reported in a 27-year-old man with a family history of von Hippel-Lindau disease. In both glands, the medulla was replaced by neoplasms with two distinct gross and microscopic appearances. There was typical pheochromocytoma in areas of dusky red tissue. The yellow nodules noted on gross examination were microscopically composed of large cells with vacuolated cytoplasm. Fat stains confirmed the presence of lipid in these areas. Immunohistochemistry revealed positivity for neuron-specific enolase and chromogranin in the cytoplasm of pheochromocytes, as well as in the perinuclear cytoplasm and processes of cells scattered in the yellow nodules. Ultrastructural examination of the yellow lesions showed characteristics of pheochromocytoma and an extensive accumulation of lipid. Although gross and light-microscopic examination of the yellow tissue suggested adrenal cortical nodules, immunohistochemistry and electon microscopy elucidated lipid degeneration within pheochromocytoma, a finding not previously described.

Adrenal Cortex Neoplasms↗
PubMed1999

Detection of Ob-receptor in human adrenal neoplasms and effect of leptin on adrenal cell proliferation.

Leptin, a hormone mainly secreted from adipose tissue, communicates a metabolic signal to the adrenal gland. Ob-Receptor (Ob-R) expression was reported in rat, mice and human adrenal glands. This study intended to investigate possible differences in the Ob-R expression and distribution of Ob-R protein in human adrenal tumors as compared to normal adrenal tissue. Proliferative effects of leptin were analyzed in the human adrenocortical carcinoma cell line (NCI-H295). The full length Ob-R mRNA and the isoforms B219.1 and B219.3 could be demonstrated by RT-PCR in all adrenal tumors (n=8), the tumor cell line (NCI-H295) and normal tissue. In contrast the Ob-R isoform B219.2 was absent in the carcinoma cell line and in most of the adrenal tumors (n=5), whereas it was present in normal adrenals. The Ob-R protein could be demonstrated in benign and malignant adrenocortical tumors. Pheochromocytomas showed only a weak immunostaining with the human Ob-R antibody. Human leptin did not affect the proliferation or variability of adrenal tumor cells as demonstrated by [3H]-thymidine assay and WST-1 test. In conclusion, although functional leptin receptors are expressed in human adrenal tumors, leptin does not regulate tumor cell proliferation.

Adenoma↗
PubMed1994

Calcium-dependent protein kinase-C activity in human adrenocortical neoplasms, hyperplastic adrenals, and normal adrenocortical tissue.

The calcium- and phospholipid-dependent protein kinase-C (PKC) is a critical enzyme of cellular signal transduction. In this report we studied calcium-dependent total PKC activity in eight adrenocortical carcinomas (group 1), nine adrenocortical adenomas (group 2), six hyperplasias (group 3), and five human normal adrenal tissues (group 4). The PKC activity assay was based on phosphorylation of a specific synthetic peptide from myelin basic protein. The specificity of the assay was confirmed by using an inhibitor peptide common to alpha-, beta-, and gamma-isoenzymes of PKC. The median value in group 1 was 1.15 pmol 32P/min.micrograms protein (range, 0.55-2.19), that in group 2 was 1.2 (range, 0.74-2.7), that in group 3 was 0.915 (range, 0.6-1.7), and that in group 4 was 1.22 (range, 0.6-3.95). The calcium-dependent total PKC activity was similar in the four groups studied. We did not find any correlation between urinary total cortisol, serum cortisol, testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, androstenedione, aldosterone, and estradiol concentrations and PKC activity. These findings suggest that the calcium-dependent PKC activity is not elevated in adrenocortical tumors and is not a useful marker of adrenocortical malignancy.

Adolescent↗
PubMed1998

Experience gained from operation of 103 adrenal incidentalomas.

BACKGROUND: Adrenal incidentaloma poses a perplexing problem for physicians. The challenge is to identify the rare functioning or malignant adrenal tumor that should be removed. PATIENTS AND METHODS: From 1970 until December 1996, we managed 579 patients with adrenal hyperplasia or neoplasm. Of these, 110 were followed without any operation and 469 were operated on. The histology from the operated patients revealed 145 pheochromocytomas, 72 Cushing's syndrome, 98 aldosteronomas, 21 virilizing tumors, 3 feminizing tumors, 98 non-functioning adrenalomas, 17 metastases, 7 cysts, and 15 miscellaneous tumors. RESULTS: Among the 98 non-functioning adrenal tumors, 79 were incidentalomas. Histological examination of 103 operated incidentalomas found 55 adenomas (5 functioning=aldosteronomas), 12 benign pheochromocytomas, 3 malignant or suspicious pheochromocytomas, 8 cystic lymphangiomas, 4 metastases, 4 angiomas, 3 ganglioneuromas, 4 myelolipomas, 1 hyperplasia, 2 hematomas, 2 cysts, and 5 adreno-cortical carcinomas. Among the non-operated incidentalomas, the most frequent findings were adenomas, metastases, hematomas, cysts and pseudotumoral hyperplasia; three disappeared spontaneously. No patients died of unrecognized adrenocortical carcinoma. CONCLUSION: Our experience confirms that in case of incidentaloma, the first concern is a nonfunctional pheochromocytoma (15%), and the less common occurrence is adreno-cortical carcinoma (2%). We recommend a restrictive surgical approach in the setting of adrenal incidentalomas.

Adenoma↗
PubMed1980

Management of intravenous extensions of endocrine tumors and prognosis after surgical treatment.

The capacity of endocrine neoplasms to give rise to intravenous tumor extensions is a feature that is recognized preoperatively by the use of venography employed primarily for tumor localization. A series of adrenocortical tumors, a pheochromocytoma and an extraadrenal chromaffin tumor are reported in which the intravenous tumor component was recognized and the surgical approach was modified to include extirpation of the intravascular tumor. Although intravenous tumor propagation has implied a grave prognosis because of the possibility of blood-borne metastases from the intravascular tumor or physiologic disruption from clot or tumor embolus, resection designed for cure, including distal venous control and tumor thrombectomy, was carried out in each patient. Wider application of preoperative venography enables recognition of these intravenous neoplastic extensions from endocrine tumors; the results of surgical management suggest that this invasive feature should not be a grave prognostic indicator that inhibits attempt at operative eradication of the primary tumor and its intravenous extension.

Adolescent↗
PubMed1994

Clonal composition of human adrenocortical neoplasms.

The mechanisms of tumorigenesis of adrenocortical neoplasms are still not understood. Tumor formation may be the result of spontaneous transformation of adrenocortical cells by somatic mutations. Another factor stimulating adrenocortical cell growth and potentially associated with formation of adrenal adenomas and, less frequently, carcinomas is the chronic elevation of proopiomelanocortin-derived peptides in diseases like ACTH-dependent Cushing's syndrome and congenital adrenal hyperplasia. To further investigate the pathogenesis of adrenocortical neoplasms, we studied the clonal composition of such tumors using X-chromosome inactivation analysis of the highly polymorphic region Xcen-Xp11.4 with the hybridization probe M27 beta, which maps to a variable number of tandem repeats on the X-chromosome. In addition, polymerase chain reaction amplification of a phosphoglycerokinase gene polymorphism was performed. After DNA extraction from tumorous adrenal tissue and normal leukocytes in parallel, the active X-chromosome of each sample was digested with the methylation-sensitive restriction enzyme HpaII. A second digestion with an appropriate restriction enzyme revealed the polymorphism of the region Xcen-Xp11.4 and the phosphoglycerokinase locus. Whereas in normal polyclonal tissue both the paternal and maternal alleles are detected, a monoclonal tumor shows only one of the parental alleles. A total of 21 female patients with adrenal lesions were analyzed; 17 turned out to be heterozygous for at least one of the loci. Our results were as follows: diffuse (n = 4) and nodular (n = 1) adrenal hyperplasia in patients with ACTH-dependent Cushing's syndrome, polyclonal pattern; adrenocortical adenomas (n = 8), monoclonal (n = 7), as well as polyclonal (n = 1); adrenal carcinomas (n = 3), monoclonal pattern. One metastasis of an adrenocortical carcinoma showed a pattern most likely due to tumor-associated loss of methylation. In the special case of a patient with bilateral ACTH-independent macronodular hyperplasia, diffuse hyperplastic areas and a small nodule showed a polyclonal pattern, whereas a large nodule was monoclonal. We conclude that most adrenal adenomas and carcinomas are monoclonal, whereas diffuse and nodular adrenal hyperplasias are polyclonal. The clonal composition of ACTH-independent massive macronodular hyperplasia seems to be heterogeneous, consisting of polyclonal and monoclonal areas.

Adenoma↗
PubMed1978

Adrenocortical carcinoma in two children with subsequent primary tumors.

Two 13-month-old children with adrenocortical carcinoma were treated surgically; each developed a second primary tumor, four and seven years later, and died shortly thereafter. Adrenocortical carcinoma is a rare childhood tumor. Second primary tumors in children are also uncommon. The coupling of two unusual events in each child is thought to represent genetic predisposition since potentially carcinogenic therapeutic modalities were not employed in treating their original tumors and neither patient exhibited an immune defense deficit.

Adrenal Cortex Neoplasms↗