Immunohistochemical analysis for cytokeratin 7, KIT, and PAX2: value in the differential diagnosis of chromophobe cell carcinoma. (73/183)

Immunohistochemical staining for cytokeratin 7 (CK7), KIT, and PAX2 expression was performed on 91 renal neoplasms, 37 conventional (clear cell) renal cell carcinomas (CRCCs), 20 papillary RCCs (PRCCs), 11 chromophobe RCCs (ChCs), and 23 oncocytomas, with available karyotypes. All ChCs, 19 PRCCs, 2 CRCCs, and 1 oncocytoma were CK7+; all ChCs, 22 oncocytomas, 2 CRCCs, and no PRCCs expressed KIT; PAX2 was positive in 31 CRCCs, 17 PRCCs, 20 oncocytomas, and 1 ChC. The predominant expression profiles were as follows: CRCC, CK7-/KIT-/PAX2+ (26/37); PRCC, CK7+/KIT-/PAX2+ (17/20); ChC, CK7+/KIT+/PAX2- (10/11); and oncocytoma, CK7-/KIT+/PAX2+ (19/23). Cytogenetic analysis showed that the sole PAX2+ ChC had a retained chromosome 10, and all ChCs with chromosome 10 loss were PAX2-. These results identify specific staining patterns of the 4 major histologic subtypes of renal neoplasms and raise the question of a relationship between chromosome 10 loss and loss of PAX2 expression in ChC.  (+info)

Papillary renal cell carcinoma within a renal oncocytoma: case report of an incidental finding of a tumour within a tumour. (74/183)

The most common renal tumours are clear cell, papillary, chromophobe and collecting duct renal cell carcinomas (RCCs), and benign oncocytomas and angiomyolipomas. Tumours with hybrid features between some of these entities have been recognised; in particular, tumours with features of both chromophobe RCC and oncocytoma. Case reports describing one distinct type of primary renal tumour actually within another are very rare. The incidental finding of a papillary RCC located in an oncocytoma in a nephrectomy specimen from a 75-year-old man is described. Morphological criteria for each tumour type were completely satisfied and fluorescence in situ hybridisation detected the expected number of copies of chromosome 7 in the cells of each tumour type. The cells in the papillary tumour contained three copies, whereas the oncocytoma cells contained only two per nucleus. To our knowledge, this is the first report of a papillary RCC being identified within an oncocytoma.  (+info)

Claudin-7 is highly expressed in chromophobe renal cell carcinoma and renal oncocytoma. (75/183)

Claudin-7 has recently been suggested to be a distal nephron marker. We tested the possibility that expression of claudin-7 could be used as a marker of renal tumors originating from the distal nephron. We examined the immunohistochemical expression of claudin-7 and parvalbumin in 239 renal tumors, including 179 clear cell renal cell carcinoma (RCC)s, 29 papillary RCCs, 20 chromophobe RCCs, and 11 renal oncocytomas. In addition, the methylation specific-PCR (MSP) of claudin-7 was performed. Claudin-7 and parvalbumin immunostains were positive in 3.4%, 7.8% of clear cell RCCs, 34.5%, 31.0% of papillary RCCs, 95.0%, 80.0% of chromophobe RCCs, and 72.7%, 81.8% of renal oncocytomas, respectively. The sensitivity and specificity of claudin-7 in diagnosing chromophobe RCC among subtypes of RCC were 95.0% and 92.3%. Those of parvalbumin were 80.0% and 88.9%. The expression pattern of claudin-7 was mostly diffuse in chromophobe RCC and was either focal or diffuse in oncocytoma. All of the cases examined in the MSP revealed the presence of unmethylated promoter of claudin-7 without regard to claudin-7 immunoreactivity. Hypermethylation of the promoter might not be the underlying mechanism for loss of its expression in RCC. Claudin-7 can be used as a useful diagnostic marker in diagnosing chromophobe RCC and oncocytoma.  (+info)

Diagnostic utility of S100A1 expression in renal cell neoplasms: an immunohistochemical and quantitative RT-PCR study. (76/183)

S100A1 is a calcium-binding protein, which has been recently found in renal cell neoplasms. We evaluated the diagnostic utility of immunohistochemical detection of S100A1 in 164 renal cell neoplasms. Forty-one clear cell, 32 papillary, and 51 chromophobe renal cell carcinomas, and 40 oncocytomas, 164 samples of normal renal parenchyma adjacent to the tumors and 13 fetal kidneys were analyzed. The levels of S100A1 mRNA detected by quantitative RT-PCR analysis of frozen tissues from seven clear cell, five papillary, and six chromophobe renal cell carcinomas, four oncocytomas, and nine samples of normal renal tissues adjacent to neoplasms were compared with the immunohistochemical detection of protein expression. Clear cell and papillary renal cell carcinomas showed positive reactions for S100A1 in 30 out of 41 tumors (73%) and in 30 out of 32 (94%) tumors, respectively. Thirty-seven renal oncocytomas out of 40 (93%) were positive for S100A1, whereas 48 of 51 (94%) chromophobe renal cell carcinomas were negative. S100A1 protein was detected in all samples of unaffected and fetal kidneys. S100A1 mRNA was detected by RT-PCR in all normal kidneys and renal cell neoplasms, although at very different levels. Statistical analyses comparing the different expression of S100A1 in clear cell and chromophobe renal cell carcinomas observed by immunohistochemical and RT-PCR methods showed significant values (P<0.001), such as when comparing by both techniques the different levels of S100A1 expression in chromophobe renal cell carcinomas and oncocytomas (P<0.001). Our study shows that S100A1 protein is expressed in oncocytomas, clear cell and papillary renal cell carcinomas but not in chromophobe renal cell carcinomas. Its immunodetection is potentially useful for the differential diagnosis between chromophobe renal cell carcinoma and oncocytoma. Further, S100A1 protein expression is constantly detected in the normal parenchyma of the adult and fetal kidney.  (+info)

Differential expression of caveolin-1 in renal neoplasms. (77/183)

BACKGROUND: Caveolin-1 is a major component of membrane caveolae, which are specialized lipid raft microdomains on cell membrane that are implicated in molecular transport, cell adhesion, and signal transduction. The overexpression of caveolin-1 recently was associated with a poor outcome in patients with clear-cell renal cell carcinoma (CCRCC) and was proposed as a useful diagnostic marker. In the current study, the authors used immunohistochemistry to investigate the membranous and cytoplasmic expression of caveolin-1 and its correlation with other pathologic parameters in different subtypes of renal neoplasms. METHODS: A tissue microarray (TMA) was constructed from 60 normal kidneys, 22 CCRCCs, 20 papillary renal cell carcinomas (PRCCs), 16 chromophobe renal cell carcinomas (ChRCCs), and 19 oncocytomas (ONCs). The TMA was immunostained for caveolin-1 protein. Both membranous and cytoplasmic caveolin-1 expression levels were measured and were correlated with tumor size, Fuhrman nuclear grade, and pathologic stage. RESULTS: Caveolin-1 was expressed normally in distal convoluted tubules, collecting ducts, parietal cells of Bowman capsule, smooth muscle, and vascular endothelial cells. Membranous caveolin-1 expression was detected in 19 of 22 CCRCCs (86.4%), which was significantly higher than the membranous caveolin-1 expression detected in PRCCs (1 of 20 tumors; 5%), ChRCCs (0 of 16 tumors; 0%), and ONCs (1 of 19 tumors; 5.3%). Cytoplasmic caveolin-1 expression was detected in 16 of 22 CCRCCs (72.7%), in 13 of 20 PRCCs (65%), in 8 of 16 ChRCCs, (50%), and in 13 of 19 ONCs (68.4%). The percentage of tumors that expressed cytoplasmic caveolin-1 did not differ significantly among the different types of renal tumors (P = .1). Only membranous caveolin-1 expression was correlated with tumor size (Pearson correlation = 0.266; P = .043). There was no correlation between membranous or cytoplasmic caveolin-1 expression and other pathologic parameters, including Fuhrman nuclear grade and staging according to the American Joint Committee on Cancer tumor, lymph node, metastasis classification system. CONCLUSIONS: Caveolin-1 expression has 2 distinctive patterns in renal neoplasms: membranous and cytoplasmic. In the current study, membranous caveolin-1 expression was detected predominantly in CCRCCs and only rarely in other subtypes of renal neoplasms. Thus, the current results indicated that caveolin-1 expression may have potential both as a diagnostic marker in the differential diagnosis of renal tumors and as a therapeutic target, especially for CCRCC.  (+info)

Quantitative promoter methylation analysis of multiple cancer-related genes in renal cell tumors. (78/183)

BACKGROUND: Aberrant promoter hypermethylation of cancer-associated genes occurs frequently during carcinogenesis and may serve as a cancer biomarker. In this study we aimed at defining a quantitative gene promoter methylation panel that might identify the most prevalent types of renal cell tumors. METHODS: A panel of 18 gene promoters was assessed by quantitative methylation-specific PCR (QMSP) in 85 primarily resected renal tumors representing the four major histologic subtypes (52 clear cell (ccRCC), 13 papillary (pRCC), 10 chromophobe (chRCC), and 10 oncocytomas) and 62 paired normal tissue samples. After genomic DNA isolation and sodium bisulfite modification, methylation levels were determined and correlated with standard clinicopathological parameters. RESULTS: Significant differences in methylation levels among the four subtypes of renal tumors were found for CDH1 (p = 0.0007), PTGS2 (p = 0.002), and RASSF1A (p = 0.0001). CDH1 hypermethylation levels were significantly higher in ccRCC compared to chRCC and oncocytoma (p = 0.00016 and p = 0.0034, respectively), whereas PTGS2 methylation levels were significantly higher in ccRCC compared to pRCC (p = 0.004). RASSF1A methylation levels were significantly higher in pRCC than in normal tissue (p = 0.035). In pRCC, CDH1 and RASSF1A methylation levels were inversely correlated with tumor stage (p = 0.031) and nuclear grade (p = 0.022), respectively. CONCLUSION: The major subtypes of renal epithelial neoplasms display differential aberrant CDH1, PTGS2, and RASSF1A promoter methylation levels. This gene panel might contribute to a more accurate discrimination among common renal tumors, improving preoperative assessment and therapeutic decision-making in patients harboring suspicious renal masses.  (+info)

Thyroid cancer in toxic and non-toxic multinodular goiter. (79/183)

BACKGROUND: Many authors have claimed that hyperthyroidism protects against thyroid cancer and believed that the incidence of malignancy is lower in patients with toxic multinodular goiter (TMG) than in those with non-toxic multinodular goiter. But in recent studies, it was reported that the incidence of malignancy with TMG is not as low as previously thought. AIM: To compare the thyroid cancer incidence in patients with toxic and non-toxic multinodular goiter. SETTINGS AND DESIGN: Histology reports of patients treated surgically with a preoperative diagnosis of toxic and non-toxic multinodular goiter were reviewed to identify the thyroid cancer incidence. Patients having a history of neck irradiation or radioactive iodine therapy were excluded from the study. MATERIALS AND METHODS: We reviewed 294 patients operated between 2001-2005 from toxic and non-toxic multinodular goiter. One hundred and twenty-four of them were toxic and 170 were non-toxic. Hyperthyroidism was diagnosed by elevated tri-iodothyroinine / thyroxine ratios and low thyroid-stimulating hormone with clinical signs and symptoms. All patients were evaluated with ultrasonography and scintigraphy and fine needle aspiration biopsy. STATISTICAL ANALYSIS USED: Significance of the various parameters was calculated by using ANOVA test. RESULTS: The incidence of malignancy was 9% in the toxic and 10.58% in the non-toxic multinodular goiter group. Any significant difference in the incidence of cancer and tumor size between the two groups could not be detected. CONCLUSIONS: The incidence of malignancy in toxic multinodular goiter is not very low as thought earlier and is nearly the same in non-toxic multinodular goiter.  (+info)

20 years of RET/PTC in thyroid cancer: clinico-pathological correlations. (80/183)

The RET/PTC oncogene has been isolated almost twenty years ago. During these years, the research has given a final answer to several questions. In fact, it has been demonstrated that: a) RET/PTC is an early event in the process of thyroid carcinogenesis and has a critical role in the generation of the papillary carcinoma; b) RET/PTC activation is essentially restricted to the papillary histotype and to the Hurthle thyroid tumors; c) its incidence increases after exposure to radiations. However, some questions have not found a final answer yet: a) which is the real frequency of RET/PTC activation? Likely it is around 20%, but this point is still questionable; b) which other gene modifications are required to lead a thyroid cell carrying a RET/PTC oncogene to the malignant phenotype?, and c) is there any correlation between RET/PTC activation and clinical parameters? We hope that these questions will have a clear answer in the near future.  (+info)