microRNA expression profile in a large series of bladder tumors: identification of a 3-miRNA signature associated with aggressiveness of muscle-invasive bladder cancer.

The aim of this study was to evaluate the expression levels of microRNAs (miRNAs) in bladder tumors in order to identify miRNAs involved in bladder carcinogenesis with potential prognostic implications. Expression levels of miRNAs were assessed by quantitative real-time RT-PCR in 11 human normal bladder and 166 bladder tumor samples (86 non-muscle-invasive bladder cancer (NMIBC) and 80 muscle-invasive bladder cancer (MIBC)). The expression level of 804 miRNAs was initially measured in a well-defined series of seven NMIBC, MIBC and normal bladder samples (screening set). The most strongly deregulated miRNAs in tumor samples compared to normal bladder tissue were then selected for RT-PCR validation in a well-characterized independent series of 152 bladder tumors (validation set), and in six bladder cancer cell lines. Expression levels of these miRNAs were tested for their association with clinical outcome. A robust group of 15 miRNAs was found to be significantly deregulated in bladder cancer. Except for two miRNAs, miR-146b and miR-9, which were specifically upregulated in MIBC, the majority of miRNAs (n = 13) were deregulated in the same way in the two types of bladder tumors, irrespective of pathological stage : three miRNAs were upregulated (miR-200b, miR-182 and miR-138) and the other 10 miRNAs were downregulated (miR-1, miR-133a, miR-133b, miR-145, miR-143, miR-204, miR-921, miR-1281, miR-199a and miR-199b). A 3-miRNA signature (miR-9, miR-182 and miR-200b) was found to be related to MIBC tumor aggressiveness and was associated with both recurrence-free and overall survival in univariate analysis with a trend to significance in the multivariate analysis (p = 0.05). Our results suggested a promising individual prognostic value of these new markers.

Identification of CAD as an androgen receptor interactant and an early marker of prostate tumor recurrence.

Markers of prostate tumor recurrence after radical prostatectomy are lacking and highly demanded. The androgen receptor (AR) is a nuclear receptor that plays a pivotal role in normal and cancerous prostate tissue. AR interacts with a number of proteins modulating its stability, localization, and activity. To test the hypothesis that an increased expression of AR partners might foster tumor development, we immunopurified AR partners in human tumors xenografted into mice. One of the identified AR partners was the multifunctional enzyme carbamoyl-phosphate synthetase II, aspartate transcarbamylase, and dihydroorotase (CAD), which catalyzes the 3 initial steps of pyrimidine biosynthesis. We combined experiments in C4-2, LNCaP, 22RV1, and PC3 human prostate cell lines and analysis of frozen radical prostatectomy samples to study the CAD-AR interaction. We show here that in prostate tumor cells, CAD fosters AR translocation into the nucleus and stimulates its transcriptional activity. Notably, in radical prostatectomy specimens, CAD expression was not correlated with proliferation markers, but a higher CAD mRNA level was associated with local tumor extension (P=0.049) and cancer relapse (P=0.017). These results demonstrate an unsuspected function for a key metabolic enzyme and identify CAD as a potential predictive marker of cancer relapse.

SMARCB1/INI1 inactivation in renal medullary carcinoma.

AIMS: Renal medullary carcinoma (RMC), a rare and highly aggressive tumour which occurs in patients with sickle-cell disease, shares many clinicopathological features with collecting duct carcinoma (CDC). The molecular mechanisms underlying RMC and CDC are mainly unknown, and there is ongoing debate about their status as distinct entities. Loss of expression of SMARCB1/INI1, a chromatin remodelling regulator and repressor of cyclin D1 transcription, has been reported recently in RMC. The aim of our study was to investigate if such loss of expression is specific for RMC. SMARCB1/INI1 genetic alterations and cyclin D1 expression were also studied. METHODS AND RESULTS: Using immunochemistry, neoplastic cells showed complete loss of SMARCB1/INI1 expression in all six cases of RMC but in only one of 22 cases of CDC. In two RMC cases investigated, comparative genomic hybridization demonstrated complete loss of one SMARCB1/INI1 allele, with no other genomic imbalances, and no mutations were found on the remaining allele. Cyclin D1 was expressed in all RMCs, suggesting that SMARCB1/INI1 inactivation may result in increased cyclin D1 transcription. CONCLUSIONS: The specific SMARCB1/INI1 inactivation observed in RMCs suggests that RMC and CDC are different entities.

Clear-cell papillary renal cell carcinoma: 24 cases of a distinct low-grade renal tumour and a comparative genomic hybridization array study of seven cases.

AIMS: To report clinicopathological and genomic characteristics of (ccpRCC), a rare, recently characterized renal tumour entity. METHODS AND RESULTS: Twenty-four renal tumours identified as ccpRCC were collected. Data from comparative genomic hybridization on microarrays (array-CGH) were obtained for seven of these. Most tumours (58%) occurred in the absence of renal disease. Mean patient age was 58.1 years. Tumours were small (mean size: 2.4 cm) and classified as pT1. Histological characteristics consisted of tubules and papillae lined by a single layer of small clear cells harbouring low-grade nuclei (Fuhrman grades 1 or 2). Architectural variations, with compact areas (41% of cases) and a micro- or macrocystic pattern (67% of cases) were observed frequently. Immunostaining demonstrated diffuse, strong expression of cytokeratin 7 and vimentin, whereas CD10, racemase, RCC antigen, translocation factor E3, TFE3 and translocation factor EB were consistently negative. In seven tumours, array-CGH detected no chromosomal imbalances. CONCLUSIONS: Clear-cell papillary renal cell carcinoma (ccpRCC) were differentiated from other renal neoplasms by a specific constellation of histopathological and immunohistochemical features, without characteristic genomic imbalances. Clinical, histopathological and genomic data suggested that these tumours have a low potential for malignancy.

Somatic pairing of chromosome 19 in renal oncocytoma is associated with deregulated EGLN2-mediated [corrected] oxygen-sensing response.

Chromosomal abnormalities, such as structural and numerical abnormalities, are a common occurrence in cancer. The close association of homologous chromosomes during interphase, a phenomenon termed somatic chromosome pairing, has been observed in cancerous cells, but the functional consequences of somatic pairing have not been established. Gene expression profiling studies revealed that somatic pairing of chromosome 19 is a recurrent chromosomal abnormality in renal oncocytoma, a neoplasia of the adult kidney. Somatic pairing was associated with significant disruption of gene expression within the paired regions and resulted in the deregulation of the prolyl-hydroxylase EGLN2 [corrected] a key protein that regulates the oxygen-dependent degradation of hypoxia-inducible factor (HIF). Overexpression of EGLN2 [corrected] in renal oncocytoma increased ubiquitin-mediated destruction of HIF and concomitantly suppressed the expression of several HIF-target genes, including the pro-death BNIP3L gene. The transcriptional changes that are associated with somatic pairing of chromosome 19 mimic the transcriptional changes that occur following DNA amplification. Therefore, in addition to numerical and structural chromosomal abnormalities, alterations in chromosomal spatial dynamics should be considered as genomic events that are associated with tumorigenesis. The identification of EGLN2 as a significantly deregulated gene that maps within the paired chromosome region directly implicates defects in the oxygen-sensing network to the biology of renal oncocytoma.

Genomic expression and single-nucleotide polymorphism profiling discriminates chromophobe renal cell carcinoma and oncocytoma.

BACKGROUND: Chromophobe renal cell carcinoma (chRCC) and renal oncocytoma are two distinct but closely related entities with strong morphologic and genetic similarities. While chRCC is a malignant tumor, oncocytoma is usually regarded as a benign entity. The overlapping characteristics are best explained by a common cellular origin, and the biologic differences between chRCC and oncocytoma are therefore of considerable interest in terms of carcinogenesis, diagnosis and clinical management. Previous studies have been relatively limited in terms of examining the differences between oncocytoma and chromophobe RCC. METHODS: Gene expression profiling using the Affymetrix HGU133Plus2 platform was applied on chRCC (n = 15) and oncocytoma specimens (n = 15). Supervised analysis was applied to identify a discriminatory gene signature, as well as differentially expressed genes. High throughput single-nucleotide polymorphism (SNP) genotyping was performed on independent samples (n = 14) using Affymetrix GeneChip Mapping 100 K arrays to assess correlation between expression and gene copy number. Immunohistochemical validation was performed in an independent set of tumors. RESULTS: A novel 14 probe-set signature was developed to classify the tumors internally with 93% accuracy, and this was successfully validated on an external data-set with 94% accuracy. Pathway analysis highlighted clinically relevant dysregulated pathways of c-erbB2 and mammalian target of rapamycin (mTOR) signaling in chRCC, but no significant differences in p-AKT or extracellular HER2 expression was identified on immunohistochemistry. Loss of chromosome 1p, reflected in both cytogenetic and expression analysis, is common to both entities, implying this may be an early event in histogenesis. Multiple regional areas of cytogenetic alterations and corresponding expression biases differentiating the two entities were identified. Parafibromin, aquaporin 6, and synaptogyrin 3 were novel immunohistochemical markers effectively discriminating the two pathologic entities. CONCLUSIONS: Gene expression profiles, high-throughput SNP genotyping, and pathway analysis effectively distinguish chRCC from oncocytoma. We have generated a novel transcript predictor that is able to discriminate between the two entities accurately, and which has been validated both in an internal and an independent data-set, implying generalizability. A cytogenetic alteration, loss of chromosome 1p, common to renal oncocytoma and chRCC has been identified, providing the opportunities for identifying novel tumor suppressor genes and we have identified a series of immunohistochemical markers that are clinically useful in discriminating chRCC and oncocytoma.

Hybrid tumour 'oncocytoma-chromophobe renal cell carcinoma' of the kidney: a report of seven sporadic cases.

OBJECTIVES: To determine whether renal hybrid tumours (HT) appear as a specific clinical and radiological entity, as HT are characterized by the association of both oncocytes and chromophobe cells within the same tumour, and have been described in patients with oncocytosis and Birt-Hogg-Dube syndrome. PATIENTS AND METHODS: We reviewed the medical charts of 67 patients who had a partial or radical nephrectomy in our institution for renal oncocytoma (RO, 24), chromophobe renal cell carcinoma (CRCC, 36) and HT (seven), from January 2006 to October 2007. We report the clinical, radiological and pathological characteristics of the seven cases of HT. RESULTS: The mean (range) age of the patients was 56 (41-68) year. None of the seven patients had any suspicion of RO, based on computed tomography (CT). Two patients had a history of kidney cancer. Five patients had partial and two a radical nephrectomy. The mean (range) maximum tumour diameter was 5.5 (1.8-9) cm. Two tumours were pT1a, two were pT1b and three were pT2. Pathological analysis showed RO-like and CRCC-like cells intermixed (six patients) or distinct (one). After a median (range) follow-up of 20 (8-25) months, none of the patients had any evidence of disease recurrence. CONCLUSIONS: In a large series of patients with sporadic RO and CRCC, 10% of the tumours had hybrid morphological features, as described in oncocytosis and Birt-Hogg-Dube syndrome. We were unable to identify any specific clinical characteristic. Most importantly, none of these HT showed any of the radiological characteristics of RO.

Loss of chromosomes 9 and 11 may be recurrent chromosome imbalances in juxtaglomerular cell tumors.

Juxtaglomerular cell tumor (JGCT), first described in 1967, is a rare tumor of the kidney that derived from specialized smooth muscle cells of the wall of the glomerular afferent arteriole. Less than 100 cases have been published, mainly as isolated case reports or small series. JGCTs are considered benign, but the clinical follow-up is short in most reported cases. Only 1 metastatic case has been reported to date, raising the question of tumors of uncertain malignant potential rather than clearly benign neoplasms. Genomic features have been studied in only 2 cases that showed gain of chromosome 10 as well as loss of chromosomes 9, 11q, and X. The present work studied the genomic characteristics of 2 additional cases of JGCT by comparative genomic hybridization. Similarly to the 2 previously reported cases, these 2 tumors showed loss of chromosomes 9 and 11, suggesting recurrent chromosomal imbalances. In addition, 1 case showed gain and loss of entire chromosomes, similar to a previous case studied by karyotyping. Such an aneuploid karyotype may reflect a potential for malignancy as previously reported. Thus, JGCT might be better considered as a tumor of uncertain malignant potential and then necessitates a prolonged follow-up. Future clinicopathologic and genomic studies of large retrospective and prospective series may help to better understand the biology of this fascinating entity.

The association of vascular endothelial growth factor receptor-1 with the risk of cancer progression following radical prostatectomy.

In the current study, we analysed the prognostic value of vascular endothelial growth factor receptor-1 (VEGFR-1) in clinically-localized prostate cancer (PCa). Forty patients who had undergone radical prostatectomy (RP) for clinically-localized PCa were included. Two groups were compared: 17 patients who experienced cancer progression following RP (group 1) and 23 patients who remained free of recurrence after intervention (group 2). Paraffin-embedded sections obtained from the RP specimens of the 40 patients were used to build tissue microarrays. The expression of VEGFR-1 was examined in the RP specimens using immunohistochemistry and was compared between the groups of patients. The two groups had similar tumor characteristics in terms of PSA, Gleason score and pathological stage of cancer. The median intensity score of VEGFR-1 expression was significantly higher in pT3 tumors than in pT2 tumors. Nevertheless, the intensity scores of VEGFR-1 expression were similar in the two groups of patients. Our results suggest that VEGFR-1 expression is not associated with the risk of cancer progression following RP. Therefore, VEGFR-1 may not be of prognostic value in clinically-localized PCa.

The prognostic value of vascular endothelial growth factor (VEGF)-A and its receptor in clinically localized prostate cancer: a prospective evaluation in 100 patients undergoing radical prostatectomy.

OBJECTIVES: To study the prognostic value of vascular endothelial growth factor (VEGF)-A and its receptor VEGFR-1 in localized prostate cancer. METHODS: One hundred patients undergoing radical prostatectomy (RP) for clinically localized prostate cancer were prospectively included. Plasma levels of VEGF-A were measured preoperatively. After intervention, tissue microarrays were built from the RP specimens. VEGF-A and VEGFR-1 expressions in prostate cancer tissue were determined using immunochemistry. Then the associations between plasma levels of VEGF-A, VEGF-A and VEGFR-1 expressions in prostate cancer tissue, and the outcome of patients were analyzed. RESULTS: After a median follow-up of 22 months, 14 patients experienced biological recurrence of prostate cancer. There was no correlation between plasma VEGF-A and the risk of recurrence following RP. Moreover, there was no correlation between VEGF-A expression or VEGFR-1 expression in prostate cancer tissue and the risk of recurrence after RP. CONCLUSIONS: Plasma levels of VEGF-A, the expression of VEGF-A and that of VEGFR-1 in prostate cancer tissue did not affect patients outcome following RP. VEGF-A and its receptor VEGFR-1 may have no prognostic value in localized prostate cancer. Further studies with longer follow-up are mandatory to confirm these findings.

[Non clear cell renal cell carcinoma. 2008 update in renal tumor pathology]. / Les tumeurs du rein qui ne sont pas des carcinomes à cellules claires. Etat des lieux en 2008.

Non clear cell renal cell carcinomas represent almost 20% of all renal neoplasms. Their classification is continuously being adjusted according to new cytogenetic and molecular data. Since molecular techniques are expensive, diagnosis still relies on morphological and immuno-histochemical criteria detailed hereby. Papillary renal cell carcinomas are the most important group and its classification is more and more complex. It encompasses low-grade papillary carcinomas (type 1 papillary renal cell carcinoma, oncocytic papillary renal cell carcinoma) and high-grade papillary carcinomas (type 2 papillary renal cell carcinoma, juvenile papillary carcinoma corresponding to renal carcinoma associated with Xp11.2 translocations and unclassified carcinomas). Mucinous tubular and spindle cell carcinoma and tubulocystic carcinoma are new entities, actually considered by some authors as low-grade papillary carcinomas. The so-called carcinoma of collecting ducts of Bellini and renal medullary carcinoma should be considered as intrarenal urothelial carcinoma or as high-grade papillary or unclassified carcinoma. Sarcomatoid carcinoma derives from morphological progression of any type of renal cell carcinoma. The group of oncocytomas/chromophobe renal cell carcinomas can be considered as a spectrum from benign (oncocytoma) to malignant neoplasm (chromophobe renal cell carcinoma). They are sometimes encountered in oncocytomatosis or familial Birt-Hogg-Dubbe syndrome in which tumoral cells may have hybrid features. Angiomyolipoma is usually a benign mesenchymatous neoplasm, that can be sporadic or familial (tuberous sclerosis). In the latter situation, some cases of epithelioid angiomyolipoma (potentially malignant) have been described. Renal epithelial and stromal tumors (REST) is a new concept gathering two benign mixed mesenchymal and epithelial tumors: cystic nephroma and mixed epithelial and stromal tumors (MEST).

[Evaluation of p63 and p504s markers for the diagnosis of prostate cancer]. / Evaluation des marqueurs p63 et p504s dans le diagnostic du cancer de prostate.

Prostate cancer with 60,000 new cases a year is a public health problem which requires adapted and effective responses. The era of PSA screening dramatically increased the number of prostate biopsies that pathologists have to screen and consequently the number of difficult cases requiring analysis. Immunohistochemistry with anti-AMACR/p504s is useful for detecting prostate cancer in the full range of prostate specimens encountered in needle biopsies. In particular, studies to date with AMACR/p504s clearly demonstrate the ability of this marker to support a diagnosis of malignancy in prostate needle biopsies, combined with negative staining for a basal cell marker, such as p63. This study conducted by the Prostate Committee of the French Association of quality assurance in pathological anatomy and cytology (AFAQAP), reports the evaluation of the current practices with available anti-p63 and -p504s antibodies. The results of this investigation show a correct evaluation of the immunostaining procedure. Overall, from the 39/56 structures tested, the value of the test was positive in 85%. The best results were obtained after antigenic restoration with TRIS-EDTA pH 9, p504s (13H4, 1/200) and p63 (A4A, 1/100).

[Juxtaglomerular cell tumors: report of two cases with genomic analysis]. / Tumeur à rénine du rein : à propos de deux cas, avec analyse génomique.

Juxtaglomerular-cell tumor (JGCT), first described in 1967, is a rare tumor of the kidney that derives from specialized smooth-muscle cells of the wall of the glomerular afferent arteriole. Less than 100 cases have been published, mainly as single-case reports or small series. JGCTs are considered benign, but the clinical follow-up has been short in most reported cases. Only one metastatic case has been reported to date, raising the question of tumors of uncertain malignant potential rather than clearly benign neoplasms. Genomic features have been studied in only two cases that showed gains on chromosome 10 as well as deletions on chromosomes 9, 11q and X. The present work studied the genomic characteristics of two additional cases of JGCT by CGH. Similarly to the two previously reported cases, these two tumors showed losses on chromosomes 9 and 11, suggesting recurrent chromosomal imbalances. In addition, one case showed gains and losses of entire chromosomes similar to a previous case studied by karyotyping. Such an aneuploid karyotype may reflect a potential for malignancy as previously reported. Thus, JGCT might be better considered as a tumor of uncertain malignant potential consequently requiring a prolonged follow-up. Future clinicopathologic and genomic studies of large retrospective and prospective series may help to better understand the biology of this fascinating entity.

Tubulocystic carcinoma of the kidney: a new entity among renal tumors.

Tubulocystic carcinoma is a tumor entity, which is not yet included in the WHO-classification of renal tumors. We report a series of 11 cases of this tumor, 6 of which were examined in by immunohistochemistry using a panel of five antibodies (CK7, CK34betaE12, CK19, CD10 and P504S). All patients were men. Each had renal tumor stage of pT1N0M0, with a diameter of 1.7 to 7 cm (mean, 3.3 cm). None of the patients presented with recurrence or metastases. Grossly, tumors were microcystic masses with a bubble-wrap appearance. Histological features included cysts and small tubules, separated by delicate septa and lined by flat to columnar or hobnail cells. The cyst and tubule epithelium showed immunohistochemical characteristics of both proximal and distal tubules. Tubulocystic carcinoma is a distinctive kidney tumor, with noteworthy macroscopic and microscopic characteristics, which can be distinguished from other cystic kidney tumors, including cystic nephroma, multilocular cystic renal cell carcinoma and some solid tumors with extensive cystic changes. More cases are needed to ascertain its prognosis. Tubulocystic carcinoma should be considered as a new subtype of renal cell carcinoma in the next revision of the WHO classification.

Plasma levels and expression of vascular endothelial growth factor-A in human localized prostate cancer.

Although the impact of vascular endothelial growth factor (VEGF) is clearly established in advanced prostate cancer (PCa), its role in localized PCa remains to be determined. The aim of our study was to analyse the plasma levels of VEGF-A and the expression of VEGF-A in prostatic tissue in a population of patients with localized PCa. We measured the preoperative plasma levels of VEGF-A in 100 patients undergoing radical prostatectomy (RP) for clinically-localized PCa. After intervention, we determined the expression of VEGF-A in all RP specimens using immunohistochemistry. We found no association between plasma levels of VEGF-A and the established prognostic factors of PCa. Moreover, there was no association between plasma levels of VEGF-A and the expression of VEGF-A in prostatic tissue. On the contrary, there was a strong correlation between the expression of VEGF-A in PCa tissue and the Gleason score of cancer: the expression of VEGF-A was significantly higher in patients with a high Gleason score on RP specimen (p=0.01). Our results suggest that the expression of VEGF may have a prognostic impact in clinically-localized PCa.

[The low weight of the prostate is an independent risk factor for positive surgical margins on radical prostatectomy specimens]. / Le faible poids de la prostate est un facteur de risque indépendant de marges chirurgicales positives sur pièce de prostatectomie radicale.

OBJECTIVE: The presence of positive surgical margins (PSM) on radical prostatectomy specimen is predictive of biological recurrence. Our objective was to analyze the influence of prostate weight on surgical margins status after radical prostatectomy. PATIENTS AND METHODS: A cohort of 295 patients operated consecutively between 1998 and 2004 at our institution was prospectively studied. The variables significantly associated with the surgical margins status in univariate analysis were used for multivariate analysis. RESULTS: The overall rate of PSM was 23% (9% for pT2 patients). Parameters significantly associated with surgical margins status were preoperative PSA (p = 0.02), number of positive biopsy cores (p = 0.04), pathological stage (p < 0. 001), and Gleason score on radical prostatectomy specimen (p < 0. 001). In addition, patient age and surgical specimen weight were conversely associated with surgical margins status (p = 0.008 and p = 0.001, respectively). In multivariate analysis, only three parameters were found to be independent factors of PSM: the pathological stage (p < 0. 001), the patient age (p = 0. 02), and the surgical specimen weight (p = 0.02). PSM rates were 6% and 25% in patients with prostate > 70g and < 70g, respectively (p = 0.008), and 15% and 28% in those with prostate weight > or = 50g and < 50g, respectively (p = 0.015). CONCLUSION: Low prostate weight is an independent risk factor of PSM. Patients with prostate weight > or = 70g should be considered at low risk of PSM, while those with prostate weight < 50g are at high risk of PSM.

Immunohistochemical expression of p63, p53 and MIB-1 in urinary bladder carcinoma. A tissue microarray study of 158 cases.

P63 is a member of the p53 family, which plays a role in the differentiation of urothelium and is supposed to play a role in urothelial carcinogenesis. P53 and MIB-1 are recognised in many studies as predictive markers of progression, but few studies in the literature have examined p63. The aims of our study were to explore the expression of p63 in bladder carcinomas and to compare this expression to p53 and MIB-1, as well as to stage and grade. Tissue microarrays were performed on 158 urothelial carcinomas (56 pTa, 45 pT1 and 57>or=pT2). Immunohistochemical studies were performed with p63, p53 and MIB-1 antibodies. In our study we observed that p63 immunostaining is present in all cell layers in papillary urothelial neoplasm of low malignant potential (PUNLMP), but partially lost in non-invasive papillary urothelial carcinoma low grade (NILGC) and in pT1/>or=pT2 bladder cancers. P53 and MIB-1 displayed lower expression in PUNLMP/NILGC vs non-invasive papillary urothelial carcinoma high grade (NIHGC)/pT1, but there was no correlation between the expression of p63, p53 and MIB-1. Our study demonstrates that p63 expression distinguishes between PUNLMP/NILGC and NIHGC/pT1 (p=4.10(5)). A statistical difference disserving pTa and pT1/>or=pT2 with a statistical significance (p<10(-6)) could also be observed. P63 should be considered as an additional biomarker that might help pathologists to classify their patients.

[Does transrectal MRI before radical prostatectomy modify the operative technique to decrease the positive margin rate?]. / L'IRM endorectale avant prostatectomie radicale modifie-t-elle la technique opératoire pour diminuer le taux de marges positives?

OBJECTIVE: To determine the value of magnetic resonance imaging (MRI) in the surgical management of prostate cancer patients. PATIENTS AND METHODS: 159 patients with prostate cancer underwent transrectal MRI before retropubic radical prostatectomy (RP). Patients operated despite a suspicion of extraprostatic extension on MRI had a modified non-nerve-sparing surgical technique. Postoperative histological findings were compared to MRI data. RESULTS: 34/159 patients (21.4%) had suspected extraprostatic extension in MRI. The pT3 rate on the RP specimen was significantly higher for patients with abnormal MRI than for patients with normal MRI (61% versus 39%, p = 0.02). Among pT3 patients, the positive surgical margin rate was significantly lower in the group with abnormal MRI than in the group with normal MRI (24% versus 51%, p = 0.035). CONCLUSIONS: Among patients with stage pT3 on the RP specimen, those in whom extraprostatic extension was suspected on MRI were treated by a modified surgical technique resulting in a lower positive surgical margin rate.

[Sarcomatoid carcinoma with heterologous osteoid differentiation]. / Carcinome sarcomatoïde de vessie à différenciation ostéosarcomateuse.

Sarcomatoid carcinomas of the bladder with heterologous osteoid differentiation are exceptional, aggressive tumors with a poor prognosis. We report a new case, and discuss the clinical and pathological characteristics of this tumor.

Adult papillary renal tumor with oncocytic cells: clinicopathologic, immunohistochemical, and cytogenetic features of 10 cases.

We report a series of 10 oncocytic renal papillary tumors, with the aim of determining their clinicopathologic features. All patients were male (median age, 71 years), treated by radical nephrectomy and free of recurrence or metastasis (median follow-up, 62 months). Tumors (median size, 3.3 cm) were intrarenal and well limited, with no extrarenal extension. They consisted of thin, nonfibrotic papillae lined by a single layer of oncocytic cells, with finely granular eosinophilic cytoplasm and round regular nucleus exhibiting central nucleolus (Fuhrman grade II, except for one grade III). Foci of necrosis were present in most cases. All tumors were immunoreactive for alpha-methylacyl-coenzyme A racemase, vimentin, and CD10; 4 expressed renal cell carcinoma antigen and 3 cytokeratin 7. There were a low number of cytogenetic changes in the 5 analyzed cases (median, 4; range, 1-7), with no trisomy 7 or 17. Papillary architecture, necrosis, and immunohistochemical profiles argued against the diagnosis of oncocytoma and suggested our cases to be part of the papillary renal cell carcinoma group. However, the cases were atypical for type 1 papillary carcinoma (due to oncocytic cells and absence of trisomy 17) and for type 2 (due to a good outcome). These results suggest that adult papillary renal tumors with oncocytic cells might be a distinct variant in the papillary renal cell carcinoma group.