Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report 50 examples of an uncommon type of renal adenoma from the files of the Armed Forces Institute of Pathology. They appear to be benign tumors with no malignant potential, and their chief importance is related to the fact that they are most often misinterpreted as renal cell carcinoma or epithelial Wilms' tumor. They predominated in females by well over 2:1. The mean age of the patients was 41 years, with a range of 5 to 83 years, and the mean size was 5.5 cm, with a range of 0.3 to 15.0 cm. Presenting signs and symptoms included pain in 11, hematuria in five, and palpable mass in five. In 20 patients the tumors were found incidentally during evaluation for other problems, and in six the other problem was polycythemia. This finding establishes a higher incidence of polycythemia in renal adenoma than in other previously reported renal diseases. Also of preoperative importance is the fact that these tumors are more commonly calcified than other renal neoplasms. Microscopically, these tumors consist of very small epithelial cells that form very small acini in an acellular stroma. Less often, they form tubular, glomeruloid, or polypoid and papillary formations. Most also show evidence of regression in the form of scarring and calcification. These lesions seem histogenetically related to epithelial Wilms' tumor, and, in fact, the two may occur together. They are histologically very similar to the metanephric hamartomatous element of nephroblastomatosis.
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PMID:Metanephric adenoma. Clinicopathological study of fifty patients. 757 69

The development of renal cell neoplasms ranging from adenoma to metastatic carcinoma is the most serious complication of acquired cystic kidney disease (ACKD). A comprehensive review of the pertinent literature shows that there is up to 50-fold increased risk of renal cell carcinoma in ACKD compared to the general population. The ACKD-associated renal cell carcinoma is seen predominantly in males, occurs approximately 20 years earlier than in the general population, and is frequently bilateral (9%) and multicentric (50%). Acquired cystic kidney disease-associated renal cell carcinoma is frequently asymptomatic (86%), but may be associated with bleeding, abrupt changes in hematocrit, fever, and flank pain or rarely with hypoglycemia, hypercalcemia, or metastases at presentation. Computed tomography seems to provide a better diagnostic yield than sonography or magnetic resonance imaging; nevertheless, large (up to 8 cm) tumors not visualized by any imaging techniques have been reported. It is generally agreed that there is a need for regular screening of symptomatic ACKD patients for early detection of renal cell carcinoma; however, whether screening is needed for asymptomatic patients remains controversial. Nephrectomy is indicated for tumors larger than 3 cm. Management for tumors smaller than 3 cm with persistent symptoms, such as back pain or hematuria, remains controversial, but nephrectomy may be recommended since many of these tumors turn out to be unequivocal renal cell carcinoma. Asymptomatic tumors smaller than 3 cm should be serially screened, and tumor enlargement may be an indication for nephrectomy. Acquired cystic kidney disease-associated renal cell carcinoma accounts for approximately 2% of deaths in renal transplant patients. A median length of survival of approximately 14 months and a 5-year survival rate of 35% are comparable to the same data for renal cell carcinoma in the general population. Successful renal transplant probably decreases the risk of renal cell carcinoma in ACKD patients, but this preliminary observation needs confirmation. The development of ACKD-associated renal carcinoma is a continuous process with evolving phenotypic expression, including damaged renal tubule, simple cyst, cyst with atypical lining, adenoma, and, finally, carcinoma. The pathogenesis of this continuous process is not entirely known, but growth factor-induced compensatory growth of tubular epithelium initiated by the changes of end-stage kidney disease, and probably perpetuated by activation of proto-oncogenes, seems to be the most significant factor.
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PMID:Renal neoplasm in acquired cystic kidney disease. 761 Dec 40

Cytopathologic smears and/or imprints of human adrenal cortex (9 cases) and its disorders were examined, including adrenocortical nodule (3 cases), adrenocortical adenoma (23 cases), carcinoma (8 cases), and renal cell carcinoma (6 cases). Immunocytochemistry directed against 3 beta-hydroxysteroid dehydrogenase and adrenal-4-binding protein (Ad4BP), a transcription factor in steroidogenesis, was also performed. There were no cytologic differences between normal adrenal and adrenocortical nodules. Large nuclei with prominent nucleoli were observed predominantly in adrenocortical neoplasms. Cellular atypia or pleomorphism and the degree of cohesiveness were unreliable criteria in differentiating between adrenocortical adenoma and carcinoma. Mitosis and necrotic materials were observed only in adrenocortical carcinoma. These cytologic findings were considered contributory, but not diagnostic when evaluating adrenocortical disorders because of marked intra-tumoral heterogeneity. There were no reliable cytologic criteria in differentiating adrenocortical and renal cell carcinoma. Immunocytochemistry of 3 beta-hydroxysteroid dehydrogenase and especially Ad4BP was demonstrated to aid greatly in the differential diagnosis between these carcinomas by identifying adrenocortical parenchymal cells.
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PMID:Adrenocortical cytopathology. 763 90

Renal cell carcinoma can have solitary adrenal metastasis years or even decades after resection of the primary tumor. The difficulty in distinguishing an adrenocortical adenoma from a solitary metastasis of a renal cell carcinoma prompted us to study 10 adrenal adenomas, 11 primary renal cell carcinomas, and three renal cell carcinomas metastatic to the adrenal gland by immunohistochemical stains and flow cytometry to determine if these techniques could help make the distinction. Immunohistochemical staining was performed for detection of cytokeratin, vimentin, and epithelial membrane antigen (EMA). Cytokeratin, vimentin, and EMA were detected in 10/11, 9/11, and 11/11 primary renal cell carcinomas, respectively, and 1/3, 2/3, and 3/3 metastatic renal cell carcinomas, respectively. All cases of adrenal adenoma were negative for the three antigens. DNA content analysis by flow cytometry showed no evidence of an abnormal DNA stemline in any of the cases except one renal cell carcinoma. We conclude that staining for EMA is consistently strongly positive in primary and metastatic renal cell carcinomas and consistently negative in adrenal adenomas, proving to be a useful distinguishing marker. Cytokeratin and vimentin, although uniformly absent in adrenal adenomas, are variably and often only weakly positive in renal cell carcinomas, and therefore of less help in making the distinction. Flow cytometry analysis has no discriminatory value in these cases.
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PMID:Adrenal cortical adenoma and adrenal metastasis of renal cell carcinoma: immunohistochemical and DNA ploidy analysis. 767 35

To examine the indication of nephron sparing operations, we searched 31 nephrectomized kidneys with renal cell carcinoma for small associated lesions in the normal-appearing portion of these kidneys. The diameter of the predominant tumors was between 15 and 50 mm. The kidneys were serially sectioned at 5-mm intervals, and all sections were examined microscopically. Two of the 31 kidneys had a small renal cell carcinoma, and four had a small adenoma in the normal-appearing portion. We recommend that the nephron-sparing operation should be is performed limitedly and that radical nephrectomy is yet a standard operation in the presence of a normal contralateral kidney.
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PMID:[A clinico-pathological study of renal cell carcinoma with a diameter of less than 5 cm]. 770

Rats carrying the Eker tumor-susceptibility mutation (Eker rats) are predisposed to developing renal cell carcinoma. Rats heterozygous for the Eker mutation develop spontaneous multiple bilateral renal cell tumors by the age of 1 yr. In a previous study, Eker-mutation carrier and noncarrier rats were exposed to the renal carcinogen dimethylnitrosamine (DMN), and male rats carrying the Eker mutation exhibited a 70-fold increase in the induction of renal adenomas and carcinomas when compared with noncarrier rats. In this study, spontaneous and DMN-induced rat renal cell tumors (adenomas and carcinomas) were analyzed for mutations of the p53 gene by direct sequencing of cDNA polymerase chain reaction products. There were no mutations in p53 cDNA derived from renal tumors from six untreated rats. Mutations were found in one of 15 of the DMN-induced tumors: a transition at codon 140, CCT-->CTT, in a renal adenoma. Additionally, seven cell lines derived from spontaneous renal cell tumors did not contain mutations in p53. The low frequency of p53 mutations (one of 21 renal cell tumors and none of seven cell lines derived from renal cell tumors) indicates that the development of both spontaneous and carcinogen-induced renal tumors involved a non-p53-dependent pathway. As p53 is infrequently mutated in human renal cell carcinomas and in rat renal mesenchymal tumors, it is likely that a tumor suppressor gene or genes other than p53 are involved in the development of renal cancer.
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PMID:p53 status in spontaneous and dimethylnitrosamine-induced renal cell tumors from rats. 772 45

A case of a rare renal tumor showing characteristic histologic features is presented. The patient was a 54 year old female, whose renal tumor was incidentally detected on abdominal ultrasound (US) examination. Ultrasound, computed tomography and angiography findings were consistent with a diagnosis of renal cell carcinoma of the hypovascular type. Left nephrectomy was performed. The tumor, which measured 2.6 x 2.6 x 2.5 cm, was located in the left renal cortex, and had a uniformly whitish-yellow cut surface and well-defined margin. Histologically, the tumor was characterized by its monomorphous growth pattern and was composed of uniformly small cells arranged in a tubular or rosette-like pattern. The tumor cells had scant cytoplasm and the nuclei were small, round and regular. These histologic features resembled the epithelial elements of a metanephric hamartoma in the nephroblastomatosis complex in infants. However, there was no mitosis and cellular atypia was minimal, suggesting benignity. According to these histologic features, the diagnosis of metanephric adenoma was made. Its clinicopathologic features are discussed.
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PMID:Metanephric adenoma of the kidney. 774 28

The differential diagnosis of bilateral solid multifocal intrarenal and perirenal lesions includes neoplastic, infiltrative, inflammatory, and vascular disorders. In a retrospective study 560 solid lesions were examined with cross-sectional imaging modalities (computed tomography (CT), ultrasonography (US), and magnetic resonance imaging (MRI). The results suggest that focal inflammatory disease can often be recognized because the lesions are poorly defined and may show a rather characteristic peripheral rim enhancement following the administration of intravenous contrast. Angiomyolipomas can be accurately diagnosed with CT, MR and US imaging. Because of their unique histomorphology they show fat-equivalent attenuation values at CT, hyperintense signal on T1 and hypointense signal on T2-weighted MR images, and appear homogeneous and hyperchoic with smooth margins at US. By the radiologic appearance alone renal metastases cannot be distinguished from lymphoma or renal cell carcinoma or adenoma. However, when multiple bilateral solid intrarenal or perirenal lesions are found with synchronous metastatic involvement of other organs or occur in the setting of a known primary tumour, the diagnosis of renal metastases is very likely. In the absence of these additional findings, malignant lymphoma has a higher probability. Infiltration of perinephric fat and thickening of the perinephric fascia may occur in inflammatory disease and lymphoma. CT remains the most suitable imaging technique to screen for these additional perirenal and extrarenal findings because of ready availability and relatively short scanning time as compared to MR imaging.
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PMID:Bilateral solid multifocal intrarenal and perirenal lesions: differentiation with ultrasonography, computed tomography and magnetic resonance imaging. 774 16

To elucidate the mechanisms of abnormal steroid production in hyperfunctioning and non-hyperfunctioning adrenal tumors, we examined both the activities and amounts of steroidogenic cytochromes P450 in the tumor and non-tumor portions of these adrenals at the posttranslational (protein) level. Adrenals from 5 patients with primary aldosteronism, 5 with Cushing's syndrome, 1 with deoxycorticosterone (DOC)-producing adenoma, 10 with non-hyperfunctioning adrenal adenoma, and 5 subjects with normal control adrenals (obtained from patients with renal cell carcinoma) were used in our studies. Activities of P450scc, P45011 beta and P450aldo, and P450C21 and P-45017 alpha were assayed in a reconstituted enzyme system using 20 alpha-hydroxycholesterol, DOC, and progesterone, respectively, and the substrate and the extracted products were analyzed by HPLC. Enzyme amounts were determined by immunoblot analysis with anti-bovine P450scc, P45011 beta, and P450C21 IgG, and anti-porcine P45017 alpha IgG. Human P450aldo was only detected in the tumor portion of primary aldosteronism adrenals, with both activities and amounts of other P-450s similar to those in the non-tumor portion of primary aldosteronism and normal controls. In Cushing's syndrome, both activities and amounts of P45017 alpha and P450C21 were significantly increased in the tumor compared with those in the non-tumor portion of Cushing's syndrome and normal controls. In DOC-producing adenoma, both activities and amounts of P45017 alpha and P45011 beta in the tumor portion of the adenoma decreased compared with normal control, while those of other P450s were similar to normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Significance of steroidogenic enzymes in the pathogenesis of hyperfunctioning and non-hyperfunctioning adrenal tumor. 779 14

Solid renal masses are being increasingly detected incidentally in individuals with no urologic symptoms. Contemporary imaging modalities allow the diagnosis of RCC to be established with 85% to 90% accuracy. Some solid renal masses with radiographic characteristics of RCC will ultimately prove to be a benign adenoma or oncocytoma. Recent data suggest that radical nephrectomy and nephron-sparing surgery each provide effective curative treatment for patients with a single, small, unilateral, localized RCC. The long-term renal functional advantage of nephron-sparing surgery with a normal opposite kidney remains unproven. Radical nephrectomy remains the treatment of choice for patients with larger (> 4 cm) or multiple localized renal cell carcinomas.
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PMID:Management of the incidentally detected solid renal mass. 785 59


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