Sonography in the diagnosis of cervical recurrence in patients with differentiated thyroid carcinoma. (41/183)

OBJECTIVE: To determine the sensitivity of thyroglobulin (Tg), iodine scanning, and sonography in the diagnosis of cervical recurrence of thyroid cancer. METHODS: This prospective study assessed 81 patients with cervical metastases or extrathyroid invasion at first appearance who underwent clinical examination, scanning, measurement of Tg after thyroxine withdrawal, and sonography about 8 months after thyroidectomy followed by radioiodine treatment. Only patients without distant metastases and without anti-Tg antibodies were included. RESULTS: Fifty patients showed persistence of the disease in the cervical region, with only 16% of them having had a suspicion on clinical examination, 33 with Tg levels of 2 ng/mL or greater (66% sensitivity), and 29 with positive scan findings (58% sensitivity). A combination of the 2 methods detected disease in 40 (80%) of 50 patients but failed to show 20% of cases that were identified by sonography and confirmed by fine-needle aspiration. Sonography had sensitivity of 96%. Specificity values for Tg, iodine scanning, and sonography were 80.6%, 90.3%, and 87%, respectively. CONCLUSIONS: Classic follow-up methods may not detect cervical disease in some patients with differentiated thyroid carcinoma, and sonography is necessary even in patients apparently free of the disease.  (+info)

Eosinophilic and classic chromophobe renal cell carcinomas have similar frequent losses of multiple chromosomes from among chromosomes 1, 2, 6, 10, and 17, and this pattern of genetic abnormality is not present in renal oncocytoma. (42/183)

That chromophobe renal cell carcinoma has an uncommon eosinophilic variant has been recognized for more than a decade. In sections stained with hematoxylin and eosin, the eosinophilic variant of chromophobe renal cell carcinoma and renal oncocytoma are similar in appearance. While it is well established that chromophobe renal cell carcinoma and renal oncocytoma have different patterns of genetic anomalies, little is known of the genetics of the eosinophilic variant of chromophobe renal cell carcinoma. This study was undertaken to elucidate the genetic lesions of eosinophilic chromophobe renal cell carcinoma and to compare them with those found in classic chromophobe renal cell carcinoma and in renal oncocytoma. A total of 29 renal neoplasms--nine eosinophilic chromophobe renal cell carcinomas, 10 classic chromophobe renal cell carcinomas, and 10 oncocytomas--were investigated by fluorescence in situ hybridization on 5 microm paraffin-embedded tissue sections with centromeric probes for chromosomes 1, 2, 6, 10, and 17. Signals were counted in 100-200 neoplastic nuclei from each tumor. Chromophobe renal cell carcinomas frequently showed loss of chromosomes 1 (70% of classic, 67% of eosinophilic), 2 (90% classic, 56% eosinophilic), 6 (80% classic, 56% eosinophilic), 10 (60% classic, 44% eosinophilic), and 17 (90% classic, 78% eosinophilic); Among the classic chromophobe renal cell carcinomas, only one had no loss of any of the chromosomes, while 50% had loss of all five chromosomes. Among the eosinophilic chromophobe renal cell carcinomas, one of nine had no loss and 44% had loss of all five chromosomes. One oncocytoma had loss of chromosome 1. No other chromosomal loss was detected in the oncocytomas. In conclusion, losses of chromosomes 1, 2, 6, 10, and 17 are frequent in both eosinophilic and classic chromophobe renal cell carcinomas. Loss of chromosome 1 occurs occasionally in oncocytoma but losses of chromosomes 2, 6, 10, and 17 are not found in oncocytomas. When the differential diagnostic problem is oncocytoma vs eosinophilic chromophobe renal cell carcinoma, detection of losses of chromosomes 2, 6, 10, or 17 effectively excludes the diagnosis of oncocytoma and supports the diagnosis of chromophobe renal cell carcinoma.  (+info)

The incidence of thyroid carcinoma in multinodular goiter: retrospective analysis. (43/183)

Thyroid carcinoma (TC) is a relatively rare tumour, but it represents the most frequent form of cancer of the endocrine glands. Epidemiologically ascertained risk factors are ionising radiation, the presence of thyroid adenoma and multinodular goiter (MNG). Multinodularity of goiter should no longer be considered an indicator of probable benign disease. A retrospective analysis was performed on patients operated of MNG at the Unit of Otolaryngology, Sanremo Hospital (Italy) from January 1st 1995 to December 31st 2002, in order to establish the incidence of carcinoma. The results of this retrospective study, demonstrate that in 13.7% of the patients operated for goiter, the presence of a carcinoma was noticed in the definitive histopathologic examination. Such incidence percentage of MNG is in accordance with the data reported in published reports. Thus, the authors conclude that the risk of malignancy in MNG has not to be underestimated, and that a dominant nodule in MNG should be valued as if it were a solitary nodule in an otherwise normal gland.  (+info)

Assessment of proliferative activity of thyroid Hurthle cell tumors using PCNA, Ki-67 and AgNOR methods. (44/183)

We have undertaken an attempt to compare the application efficacy of the proliferative activity markers in differential diagnosis of thyroid Hurthle cell tumors (HCT) using the PCNA and Ki-67 labeling and AgNOR visualisation techniques. The present work is a retrospective analysis of 78 Hurthle cell tumors: 20 Hurthle cell carcinomas (HCC), 32 Hurthle cell adenomas (HCA) and 26 hyperplastic nodules with Hurthle cell metaplasia (HCM). Five microm sections were stained according to AgNOR technique and labeled with antibodies against PCNA and Ki-67. AgNOR dot count in the nucleus and proliferative index (PI - percentage of cells expressing PCNA and Ki-67) in randomly chosen nuclei (100 in case of AgNOR and over 1000 in case of PI) were evaluated in each slide. The mean values of AgNOR dot count, PI-PCNA and PI-Ki-67 in HCC, HCA and HCM were respectively: 5.1, 61.3 and 54.9; 3.4, 42.4 and 38.6 and 2.5, 39.3 and 34.3. Statistically significant difference was found in all the proliferative activity markers between malignant and benign tumors: HCC:HCA (p<0.01) and HCC:HCM (p<0.001). There was no statistically significant difference between HCA and HCM.  (+info)

Expression of aquaporins and PAX-2 compared to CD10 and cytokeratin 7 in renal neoplasms: a tissue microarray study. (45/183)

Diagnostic use of antibodies against aquaporin water channel proteins and PAX-2, a nuclear transcription factor in renal development, was tested in 202 renal neoplasms, using tissue microarray technique. Immunohistochemistry for aquaporin-1, aquaporin-2, PAX-2, CD10, and cytokeratin 7 was performed on 102 clear cell renal cell carcinomas, 44 papillary renal cell carcinomas (among them 34 type 1 and 10 type 2), 24 chromophobe renal cell carcinomas, three collecting duct carcinomas (carcinomas of the collecting ducts of Bellini), and 29 oncocytomas. Aquaporin-1 expression was found in clear cell renal cell carcinomas and papillary renal cell carcinomas of both types (78 and 73%, respectively), but not in chromophobe renal cell carcinomas, collecting duct carcinomas, and oncocytomas. Aquaporin-2 expression was not seen in any of the tested tumors. PAX-2 and CD10 was found in the majority of clear cell renal cell carcinomas (88 and 85%, respectively) but only in few papillary renal cell carcinomas, chromophobe renal cell carcinomas and oncocytomas. Decrease or loss of aquaporin-1 and PAX-2 was shown in higher grades compared to lower grades of clear cell renal cell carcinomas (P<0.0001 and <0.0245, respectively). Cytokeratin 7 was rarely seen in clear cell renal cell carcinomas, type 2 papillary renal cell carcinomas, and oncocytomas, but was found in the majority of type 1 papillary renal cell carcinomas (97.1%) and chromophobe renal cell carcinomas (88%). Aquaporin-1 and PAX-2 expression was found to correlate with nuclear grading for clear cell renal cell carcinomas but not for papillary renal cell carcinomas. No correlation of tumor stage and aquaporin-1 and PAX-2 expression was seen. Aquaporin-1 and PAX-2 are reliable markers for clear cell renal cell carcinomas of lower grades but not for higher grades. CD10 expression remains stable, independent of nuclear grading.  (+info)

De novo renal cell carcinoma of native kidney in renal transplant recipients. (46/183)

BACKGROUND: The 10-year risk of developing a solid malignancy is 20% for kidney transplant recipients. The goal of the current study was to investigate the epidemiology and the diagnostic and prognostic parameters associated with de novo malignancies of the native kidney among transplant recipients at the authors' institution (Department of Urology and Renal Transplantation, Hopital Salvator, Marseille, France). METHODS: The authors reexamined the follow-up of 933 consecutive transplant recipients at their institution between 1987 and 2003. Immunossupressive therapy was not modified in the event of malignant disease, nor was systematic radiologic monitoring of native kidneys performed. All de novo malignancies of the native kidney were included in the current analysis. RESULTS: Among the 933 patients examined, a combined total of 12 malignancies of the native kidney were diagnosed in 11 individuals. For these 11 individuals, the average ages at transplantation and diagnosis were 42.5 and 49.1 years, respectively. Ten malignancies were discovered fortuitously, whereas two were symptomatic. Among the 10 renal echographies performed, there was 1 false-negative result. Tomodensitometry was performed in 11 cases and yielded no false-negative results. The average tumor size was 37 mm. Nephrectomy was performed in 10 cases, and biopsy was performed in 1. Among the 12 kidney malignancies encountered in the current study, there were 7 conventional cell carcinomas, 3 basophilic papillary carcinomas, and 2 chromophobic renal cell carcinomas. Half of all tumors were Furhman Grade 3 lesions, and pT1aN0M0 tumors (2003 TNM staging system) also accounted for half of all malignancies in the current cohort. Two affected transplant recipients died (one due to disease), and the remaining nine are alive without recurrence and with normal renal functioning (median follow-up, 39 months). CONCLUSIONS: There appears to be an increased risk of malignancy of the native kidney in renal transplant recipients, with high-grade and papillary tumors being particularly common. Consequently, systematic radiologic follow-up of native kidneys must be performed for individuals who undergo kidney transplantation.  (+info)

Tumour induction in rats following exposure to short-term high dose aristolochic acid I. (47/183)

The purpose of this study was to assess the carcinogenic activity of aristolochic acid I (AAI) in short-term high doses. Forty-four female Sprague-Dawley rats were randomly assigned to two groups. A dose of 50 mg/kg/day AAI was administrated to rats in the experimental group by gavage consecutively for 3 days, while the control group received only distilled water, after which renal function and pathological changes were assessed. At day 8 post-treatment AAI had induced elevations of both plasma urea and creatinine, coupled with increased urine production, urinary proteins, glucose and N-acetyl-beta-glucosaminidase. At 1, 3 and 6 months post-treatment renal function and urinary parameters for the experimental group approached baseline values. However, tumours and preneoplastic proliferation were both observed at 6 months for the experimental group. The rate of occurrence of preneoplastic proliferation in the kidneys was 100% (14/14); the rate of occurrence of renal tumours was 28.6% (4/14), which included three mesenchymal tumours and one case of renal oncocytoma; the rate of occurrence of extrarenal tumours was 7.1% (1/14), which was a case of mammary duct carcinoma. Renal preneoplastic proliferation and renal tumours, as well as extrarenal tumours, were not observed in control rats during the 6 months. These results differ from previous reports in that tumours originating from both epithelial and mesenchymal tissues were found, which may be attributed to the duration of treatment and the dosage of the drug. These data indicate that AAI administered in an acute manner at high doses does in fact have carcinogenic properties.  (+info)

Kidney-specific cadherin, a specific marker for the distal portion of the nephron and related renal neoplasms. (48/183)

Renal cell neoplasms are presumably derived from different cell types of the nephron. Clear cell and papillary renal cell carcinoma (RCC) are thought to be of proximal tubular origin, whereas oncocytoma and chromophobe RCC are derived from intercalated cells of distal nephron. A few molecules, such as RCC marker and CD10, have been shown to be markers for clear cell RCC and papillary RCC. Such markers are not yet available for renal tumors presumably of the distal nephron. The expression of kidney-specific (Ksp) cadherin, a recently cloned gene thought to be transcribed exclusively in the kidney, was studied in normal human kidney, as well as in 105 primary renal neoplasms, including 42 clear cell RCC, 30 papillary RCC, 13 chromophobe RCC, and 20 oncocytomas. The expression patterns were compared with those of RCC marker. The Ksp-cadherin expression was noted preferentially in distal convoluted tubules with a basolateral membrane stain in normal kidney. All 13 chromophobe RCC and 19 of 20 oncocytomas showed diffuse and strong immunoreactivity for Ksp-cadherin, while only 14% clear cell RCC and 13% papillary RCC showed focal positivity. The RCC marker expression was detected in 85%, 98%, 15% and 0% of clear cell RCC, papillary RCC, chromophobe RCC, and oncocytoma, respectively. A few clear cell RCC and papillary RCC showed dual expression of both RCC marker and Ksp-cadherin, which appear to have distinct histologic features. These results demonstrated high sensitivity and specificity of Ksp-cadherin for distal convoluted tubules, which can be used as adjunct for diagnosis of chromophobe RCC.  (+info)