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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review discusses the impact of molecular genetics on the diagnosis and prognosis of renal cell tumours as well as the genetic changes in renal cell tumours associated with von Hippel-Lindau disease and end-stage kidney disease. The use of molecular techniques enables the division of renal cell tumours into genetically and biologically well defined entities. The new classification system distinguishes between papillary renal cell tumours, including papillary renal cell adenoma and papillary renal cell carcinoma, nonpapillary renal cell carcinoma, chromophobe renal cell carcinoma and renal oncocytoma. The advantage of the new classification system is that genetic markers, in contrast to the tumour phenotype, are constant during tumour progression and allow a precise diagnosis even from a small biopsy specimen.
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PMID:Molecular genetics of human renal cell tumours. 904 31

Advances in operative, diagnostic and post-operative care technique have rendered liver resections safe. Consecutively, indications for operative interventions in primary and secondary liver tumors have changed. A current state of the art is presented. Focal nodular hyperplasia, if found incidentally during laparotomy, should be removed en-passant. Large or central lesions should be biopsied and can be observed if they remain asymptomatic and stable in size. Symptomatic or growing FNH should be removed. If the diagnosis is evasive resection should be favored. Most patients with hepatocellular adenoma are symptomatic and the lesion should therefore be removed. Hemangiomas are rarely causing symptoms. In case they truly are, or if they cause complications they should be excised. Anatomical resections for hepatocellular carcinoma are only feasible in non-cirrhotic livers or in patients with cirrhosis and compensated liver function. Other patients are candidates for liver transplantation if the cancer is stage I or II. Stage III and IVa lesions are subject of current studies. Surgical resection remains the only potentially curative treatment for intrahepatic cholangiocellular carcinoma. Because of their dismal prognosis these patients are not candidates for transplantation. Resection continues to be the most effective therapy for colorectal metastases to the liver. Patients with non-colorectal, non-neuroendocrine metastases are usually only candidates for surgical palliation. Cure can be achieved in patients with renal cell carcinoma or Wilms' tumor. Additionally, neuroendocrine metastases to the liver can be resected in curative intent if extrahepatic disease was excluded. In the few symptomatic patients in whom extrahepatic disease was excluded, symptomatic treatment has failed, and the lesions are not resectable, liver transplantation can provide a reasonable therapeutic choice.
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PMID:[Surgical therapy of primary and secondary liver tumors]. 906 25

The MN/CA9 protein is a tumor-associated antigen that has been shown to have diagnostic utility in identifying cervical dysplasia and carcinoma. MN/CA9 expression is limited to very few normal tissues. We have now extended those observations to further investigate expression of the MN/CA9 protein in histological sections and fine-needle aspiration biopsy smears of normal kidney, benign renal cell lesions, all categories of renal cell carcinomas (clear/granular/spindle cell, chromophilic cell, chromophobic cell, and collecting duct cell RCCs), metastatic RCCs, and non-renal cell clear cell adenocarcinomas. We have found that high levels of MN/CA9 expression is seen in all primary RCCs, cystic RCCs, and metastatic RCCs, with the exception of two cases of the chromophobe cell type, which were MN/CA9 negative. Identical MN/CA9 immunostaining was also observed in the aspiration cytological smears. In contrast, all benign lesions, including pyelonephritis, renal cysts, adenomas, oncocytomas, and normal kidney, did not express the MN/CA9 protein. Thus, we conclude that MN/CA9 protein expression could serve as a valuable adjunct to the cytological and histological diagnosis of benign renal cysts versus cystic RCC, adenoma versus RCC, and oncocytoma versus granular cell RCC. Diffuse membraneous staining of all RCCs (with the exception of chromophobic cell RCC) suggests that MN/CA9 protein expression might have an important clinical utility in the early detection and treatment of RCC. Absence of MN/CA9 expression in non-renal cell clear cell adenocarcinoma also indicates that MN/CA9 protein expression may be used as a differential diagnostic biomarker of metastatic clear cell RCC.
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PMID:Identification of the MN/CA9 protein as a reliable diagnostic biomarker of clear cell carcinoma of the kidney. 923 Jan 82

Papillary renal cell carcinomas (RCCs) traditionally have been defined histologically as tumors with at least 50% true papillae. However, these tumors also have characteristic immunohistochemical and genetic features that separate them from other RCCs. We identified six tumors composed of solid sheets of cells without true papillae but that otherwise resembled papillary RCCs, which we feel represent solid variants of papillary RCCs. All six tumors were primary lesions of the kidney, all were strongly reactive for epithelial membrane antigen, cytokeratin 7, and callus keratin, and all were negative for the high molecular weight keratin antibody 34BE12. Four of four tumors tested showed trisomies for chromosome 7, chromosome 17, or both by either cytogenetic analysis or fluorescence in situ hybridization. Four cases were composed of solid sheets of cells containing distinct micronodules that in some cases resembled abortive papillae. The cells composing the micronodules had abundant eosinophilic cytoplasm, open chromatin, and in some cases prominent nucleoli. The intervening cells had similar nuclei, but the amount of cytoplasm was variable. In three of these micronodular cases, multiple tumors diffusely replaced the kidney; in the fourth case two typical clear cell RCCs and a typical papillary RCC were also present in the same kidney, but the micronodular tumor was unifocal. The two remaining cases were solitary tumors consisting of solid sheets of cells forming ill-defined tubules. These cells had scant clear cytoplasm and small round to elongate nuclei with occasional nuclear grooves but only rare small nucleoli. Limited follow-up has shown no evidence of disease in any patient thus far. The differential diagnosis includes "renal adenoma," renal adenomatosis, metanephric adenoma, and clear/granular cell RCC. We conclude that solid variants of papillary RCCs lack true papillae but have characteristic histologic, immunohistochemical, and genetic features.
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PMID:Solid variants of papillary (chromophil) renal cell carcinoma: clinicopathologic and genetic features. 933 Dec 93

Trisomy 7 and 17 with deletion of Y is typical of papillary renal cell adenoma (PRCA), and additional alterations occur in the putative genetic progression toward papillary renal cell carcinoma (PRCC). Our study correlated aneuploidy with clinicopathologic features in PRCCs. We used fluorescence in situ hybridization to assess copy number for chromosomes 7, 8, 10, 12, 16, 17, and Y in 16 PRCCs and surrounding benign tubular parenchyma from 15 patients by use of alpha satellite (centromere) probes on deparaffinized tissue sections. We then compared the pattern of monosomy/nullisomy or trisomy/polysomy/hemidisomy to clinicopathologic parameters. Nine tumors (58% Group 1) showed the numeric aberrations typical of PRCAs and PRCCs, with gains of 7 and 17 and loss of Y. We also identified four trisomies of 12 and 16 and one of 8 in Group 1. The remaining seven cases (Group 2) were cytogenetically atypical. Two displayed borderline loss of chromosome 7, although trisomy 17 was present in both. Five had trisomy 7, but none exhibited chromosome 17 alterations, and two exhibited a gain of Y. Neoplasms in Group 2 were less often multicentric than were Group 1 tumors, and they contained foamy macrophage infiltrates less often. One chromophilic carcinoma with abundant clear cells and another with oncocytic features exhibited Group 2 chromosomal profiles. One patient (nuclear grade 4) died from disease, and 14 had no evidence of carcinoma at the last follow-up. We concluded that PRCCs represent a histologically and genotypically heterogeneous group of tumors. If PRCAs consistently exhibit +7, +17, and -Y, it is uncertain whether PRCCs always evolve directly from such lesions. The presence of genotypic heterogeneity might reflect histologic variants of PRCCs, which overlap with other types of RCC. PRCC is generally an indolent neoplasm, despite a high frequency of chromosomal aneuploidy.
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PMID:Clinicopathologic and interphase cytogenetic analysis of papillary (chromophilic) renal cell carcinoma. 938 66

This paper presents the conclusions of a workshop entitled 'Impact of Molecular Genetics on the Classification of Renal Cell Tumours', which was held in Heidelberg in October 1996. The focus on 'renal cell tumours' excludes any discussion of Wilms' tumour and its variants, or of tumours metastatic to the kidneys. The proposed classification subdivides renal cell tumours into benign and malignant parenchymal neoplasms and, where possible, limits each subcategory to the most commonly documented genetic abnormalities. Benign tumours are subclassified into metanephric adenoma and adenofibroma, papillary renal cell adenoma, and renal oncocytoma. Malignant tumours are subclassified into common or conventional renal cell carcinoma; papillary renal cell carcinoma; chromophobe renal cell carcinoma; collecting duct carcinoma, with medullary carcinoma of the kidney; and renal cell carcinoma, unclassified. This classification is based on current genetic knowledge, correlates with recognizable histological findings, and is applicable to routine diagnostic practice.
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PMID:The Heidelberg classification of renal cell tumours. 939 23

We report two cases of metanephric adenoma in 40 and 48 year-old women. These rare kidney tumors were composed of cuboidal epithelial cells forming tubules, glomeruloid structures and sheets. Ultrastructural and immunohistochemical studies revealed that the tumor cells are similar to epithelial cells of developing nephrons. These features differentiate the metanephric adenoma from tubulo-papillary renal carcinoma, nephroblastoma, and cortical adenoma. According to its invariably benign course, the metanephric adenoma treatment could be restricted to a simple tumorectomy.
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PMID:Metanephric adenoma of the kidney. A clinicopathologic, immunohistochemical and electron microscopic study of two cases. 960 64

Renal adenoma indistinguishable from renal cell carcinoma preoperatively in a 34-year-old male is reported. The tumor found by CT-scan was located in the middle portion of the left kidney. Renal cell carcinoma was diagnosed preoperatively by total diagnostic imaging. Simple nephrectomy was conducted, and the pathological specimen was a renal adenoma.
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PMID:[A renal adenoma: a case report and review of diagnostic imaging]. 971 40

In the assessment of incidentally discovered adrenal masses the detection of hormonal activity and the evaluation of benignity or malignity, either primary or metastatic, constitute the most important issues. This article reports 9 asymptomatic adrenal masses: The histopathological diagnosis consisted of cortical adenoma in 5 cases, adrenal metastatic mass in 2, respectively from a pulmonary microcytoma and from a renal carcinoma, a myelolipoma with leukemic infiltration and an hemorrhagic pseudocyst in the remnants. Evaluation of biochemical activity showed no endocrinological abnormality in all patients except in two cases of adenoma: the positivity of the 1 mg dexamethasone test, the low serum DHEAS levels and a concordant scintigraphic uptake were consistent with the pre-Cushing syndrome in the first case, whereas the ACTH inhibition revealed by low serum DHEAS levels without other hormonal alterations were the biochemical pattern in the second. Ultrasonography has been helpful in the diagnosis of adrenal mass in 6 cases, whereas CT scan allowed an etiopathogenetic diagnosis in 8 cases. All patients were submitted to adrenalectomy through the conventional surgical accesses; in 4 cases the adrenalectomy was performed as a associated intervention during vascular or gastrointestinal surgery. No postoperative death occurred. At follow-up ranging from 3 to 6 years, we recorded 4 deaths: the causes were represented by the progression of the primary malignancy in 2 patients that have been operated on for adrenal metastatic tumors, by hemorrhagic shock from an aorto-duodenal fistula and by systemic infectious complications respectively in the remnant two cases. The other patients were well and the endocrinological assessment showed normal findings. The Authors, according with data from literature, suggest an essential biochemical screening to evaluate the adrenal function in case of incidentally discovered mass: it is characterized by determination of plasma and urinary electrolytes, catecholamines, serum DHEAS and 17-OH progesterone levels, dexamethasone suppression test. In case of asymptomatic mass suspect for pheochromocytoma we advocate the MIBG scintigraphy.. The adrenocortical scintigraphy (NP 59) provides both anatomical and functional characterization of the adrenal glands: the concordant or discordant imaging patterns are useful in the diagnosis of benignity or malignancy. Although the management of patients with incidentally discovered masses remain controversial, we advocate adrenalectomy when they are hormonally hypersecreting, increasing in the diameter or malignant and in association with other abdominal operation.
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PMID:[Incidentaloma of the adrenal glands: analysis of 9 surgical cases]. 973 86

Proliferative activity in renal cell carcinomas seems to be a significant predictor of prognosis independent of tumor stage and grade; its correlation with tumor type is not as well studied. We performed immunohistochemical analysis with antibodies directed against Ki67 (MIB1), cyclin A, and cyclin E on 44 renal tumors, including 2 metanephric adenomas, 9 oncocytomas, and 33 renal cell carcinomas, including 10 clear cell, 11 papillary, 6 chromophobe, and 6 sarcomatoid tumors. MIB1 and cyclin A stained between 0 and 23% of tumor nuclei. Reactivity for cyclin E was rare. There was a positive correlation between reactivity for MIB1 and for cyclin A (Spearman rank correlation r = .3587). Reactivity for either MIB1 or cyclin A did not correlate with tumor type, stage, or grade, but reactivity for MIB1 was significantly higher in patients older than 60 years than in patients 60 years of age or younger (P = .046). Proliferative activity as defined by either MIB1 or cyclin A is independent of tumor type, grade, or stage. The proliferative activity of benign renal tumors (metanephric adenoma and oncocytoma) was not significantly different than that seen in renal cell carcinoma.
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PMID:Cyclin A and MIB1 (Ki67) as markers of proliferative activity in primary renal neoplasms. 979 23


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