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Results for “Adrenal Cortex Neoplasms”

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At least 19 recordsLinked to original sources
PubMed1977

Rare urologic pathology presenting as abdominal masses in children.

The key to correct diagnosis of abdominal masses in children is awareness of all the possibilities. Three children with abdominal masses of uncommon urologic origin are described. The lesions were adrenal cortical carcinoma, a pancake pelvic kidney and a non-functioning hydronephrotic segment of a horseshoe kidney. Management of these patients is discussed and the literature is reviewed.

Abdominal Neoplasms↗
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↗
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↗
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↗
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↗
PubMed1977

Virilizing adrenal cortical carcinoma.

A 43-year-old man with a 36-year history of virilization due to an adrenal carcinoma is presented. The initial presentation at age 7 with precocious puberty and epiphyseal bone fusion suggested increased androgen effect at a very early age. The patient's 36-year course before his death suggested either a very slow growing adrenal carcinoma or untreated congenital adrenal hyperplasia that progressed to an adrenal carcinoma. Endocrine evaluation showed markedly increased DHEA and DHEA-sulfate levels. These were associated with elevated plasma and urinary estradiol levels and suppressed LH and FSH plasma concentrations. The 24-hour mean levels of cortisol and testosterone were normal. Studies of the circadian periodicity of cortisol showed a disturbed temporal pattern but a normal 24-hour mean concentration that correlated with a normal cortisol production rate. The 24-hour LH secretory pattern showed a decrease in the normal episodic fluctuation of this hormone over the 24-hour period.

Adrenal Cortex Neoplasms↗
PubMed1978

Genetic and pathologic findings in a kindred with hereditary sarcoma, breast cancer, brain tumors, leukemia, lung, laryngeal, and adrenal cortical carcinoma.

A familial cancer aggregation comprising sarcomas, brain tumors, leukemias, and carcinomas of breast, larynx, lung, adrenal, cortex, and other sites has been studied from a pathologic--genetic standpoint. Based upon sibships segregating for cancer, the genetic segregation parameter is estimated to be 45.6 +/- 11% which is compatible with that expected for a rare deleterious autosomal gene showing complete dominance. Pathologic review of 16 tumors by bright field microscopy revealed variable occurrences of intranuclear cytoplasmic invaginations, intranucleolar bodies, and acidophilic intracytoplasmic inclusions in eight lesions. Two tumors showed both intranuclear cytoplasmic invaginations and intranucleolar inclusions. Morphological findings coupled with the observed pattern and distribution of cancer in the subject kindred suggest that the cancer-prone genotype interacts with one or more exogenous factors in causing this familial tumor association.

Adolescent↗
PubMed1978

Rat adrenocortical carcinoma 494: an integrated structural, stereological, and biochemical analysis.

Snell adrenocortical tumor 494 was implanted into male Sprague-Dawley rats and recovered 7, 14, 21, 28 or 35 days following initial detection by palpation (7-10 days following transplantation). Electron microscopic, stereological and biochemical analyses of the tumor were compared to adrenals of normal animals to serve as a baseline for further studies of the effects of chemotherapeutic agents on tumor cells. Tumor cells possessed oval or elongated mitochondrial profiles with tubular cristae, one or two very large (greater than 5 micrometer) lipid droplets, abundant ribosomes and coated vesicles, and sparse rough and smooth endoplasmic reticulum. Stereologic evaluation revealed that tumor lipid volume was 41% and mitochondrial volume 29% that of the normal adrenal controls. Tumor nuclei were 2.5 times larger than adrenocortical nuclei while cellular volumes were similar. On a net weight basis, tumor cholesterol was 55%, cholesterol ester 2.2%, and lipid phosphate 25% of respective mean values for normal adrenal glands. The tumor cholesterol: cholesterol ester ratio progressively decreased with time but remained 18-fold greater than the normal adrenal. Plasma corticosterone levels in tumor-bearing rats were elevated 3-fold by 14 days and initial detection. The adrenals of the tumor-bearing host exhibited marked involution, the extent of which was directly related to tumor size.

Adrenal Cortex Neoplasms↗