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Lavinia Vija,
Geri Meduri,
Eva Comperat,
Viorel Vasiliu,
Vincent Izard, Sophie Ferlicot,
Kahina Boukari,
Philippe Camparo,
Say Viengchareun,
Elisabeth Constancis,
Constantin Dumitrache,
Marc Lombès,
Jacques Young
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ABSTRACT: Androgen receptor (AR) is essential for testicular physiology and spermatogenesis. SRC-2 and HBO1 are two AR coregulators yet their expression and roles in human testis are unknown. For the first time, we studied by immunohistochemistry and RT-PCR, the expression and distribution of these two coregulators during human testicular ontogenesis, in patients with altered AR signaling (Androgen insensitivity syndrome, AIS) and evaluated the functional impact of SRC-2 and HBO1 on AR signaling in a Sertoli cell context. SRC-2 was present in Sertoli cells at all developmental stages. HBO1 was barely or focally detected in the fetal testis yet its expression, in Sertoli and germ cells, drastically increased postnatally from early infancy to adulthood. In transient co-transfection studies we showed that SRC-2 induced, while HBO1 inhibited AR-mediated transactivation of reporter constructs in murine Sertoli SMAT1 cells. HBO1, but not SRC-2, expression was reduced in testes of patients with AIS compared to normal testes.
Molecular and Cellular Endocrinology 05/2013; · 4.19 Impact Factor
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ABSTRACT: Mucin-producing cystitis glandularis is a rare proliferative and metaplastic change of the bladder mucosa that produces large amounts of mucus, thus taking a pseudotumoral pattern and resulting in urinary tract obstruction. We report a case of florid mucin-producing cystitis glandularis mimicking bladder carcinoma in a 77-year-old man that was documented by computed tomography and magnetic resonance imaging. Computed tomography showed diffuse, circumferential, irregular, and lobulated thickening of the bladder wall suggestive of urinary bladder carcinoma. Magnetic resonance imaging showed findings consistent with mucinous content and suggested the correct diagnosis preoperatively.
Urology 03/2013; · 2.43 Impact Factor
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Morgan Rouprêt,
Sarah J Drouin,
Stéphane Larré,
Yann Neuzillet,
Henry Botto,
Maryam Hitier,
Jerome Rigaud,
Jeremy Crew,
Evanguelos Xylinas,
Laurent Salomon, [......],
Jacques Irani,
Benoit Peyronnet,
Karim Bensalah,
Laura Poissonnier,
Pascale Grès,
Stéphane Droupy,
Julien Casenave,
Hervé Wallerand,
Michel Soulié,
Christian Pfister
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ABSTRACT: To assess the postsurgical survival of patients with urothelial carcinoma of the bladder with pT0 tumor at pathologic examination of cystectomy specimens.
A multi-institutional, retrospective database was analyzed with data from 4758 radical cystectomy (RC) patients who underwent RC without neoadjuvant chemotherapy and who were diagnosed with pT0 on the basis of the pathologic specimen. Survival curves were estimated. A multivariate Cox model was used to evaluate the association between prognosis factors and disease recurrence or survival.
Overall, 258 patients (5.4%) were included in the study. The median age was 64 years. At last resection, 171 tumors were invasive (at least pT2), and 87 were not. Median follow-up was 51 months. At multivariate analysis, initial location of the tumor and absence of lymphadenectomy were associated with tumor recurrence (P = 0.03 and P = 0.005, respectively) and specific mortality (P = 0.005 and 0.001, respectively). The main limitation of the study is its retrospective design, which is due to the rarity of this situation. Cancer-specific and recurrence-free survival rates were 89 and 85%, respectively, at 5 years and 82 and 80%, respectively, at 10 years.
Despite acceptable oncological outcomes, patients with a pT0 tumor at the time of RC are still at risk of recurrence and progression and should not be considered to be entirely cured. In this population, stringent follow-up according to current recommendations should be effective.
Annals of Surgical Oncology 06/2011; 18(13):3833-8. · 4.17 Impact Factor
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Annales de Pathologie 04/2011; 31(2):116-8. · 0.25 Impact Factor
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ABSTRACT: A case of bladder toxoplasmosis in a 57-year-old male Caucasian patient was diagnosed with difficulty due to misleading clinical presentation. The patient presented with pollakiuria and urination burning. Imagery showed pseudotumoral thickening of the vesicle wall. Previously unknown status of HIV infection was found positive through the diagnosis of bladder toxoplasmosis. The patient died rapidly from neurological complications. This is the second published case in which bladder toxoplasmosis reveals an HIV infection.
Annales de Pathologie 02/2011; 31(1):46-9. · 0.25 Impact Factor
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ABSTRACT: Kidneys from haemodynamically unstable donors may suffer from renal ischaemia-reperfusion (RIR) injury. RIR is associated with reactive oxygen species production that induces inflammation and activates the arachidonic acid (AA) pathway which converts AA into prostaglandin E(2). Amifostine was investigated for its renoprotective potential in RIR.
The effect of amifostine (25 mg/kg = 910 mg/m(2)) on the COX pathway, enzymatic antioxidant activity, the lipid peroxidation marker MDA, serum creatinine and apoptosis was determined in rats. Kidneys were subjected to 45 min of ischaemia and 1 or 24 h of reperfusion. Control groups (sham: coeliotomy, no ischaemia; r1: 45 min ischaemia/1 h reperfusion; r2: 45 min ischaemia/24 h reperfusion) were administered physiological saline intraperitoneally, and treated groups (E1: 45 min ischaemia/1 h reperfusion; E2: 45 min ischaemia/24 h reperfusion) received amifostine 30 min before reperfusion.
Serum creatinine increased in non-treated control rats: r1 vs sham (1.6-fold; P <0.007), r2 vs sham (2-fold; P <0.007). Amifostine decreased serum creatinine levels in treated rats: E1 vs r1 (8%; P <0.0025), E2 vs r2 (44%; P <0.0025). Amifostine reduced acute tubular necrosis (25%) 24 h after reperfusion: E1 vs r1 (P <0.004), E2 vs r2 (P <0.03) and reduced COX-2 and microsomal prostaglandin E synthase expression: E1 vs r1 (P <0.03), E2 vs r2 (P <0.02). Amifostine decreased MDA (P <0.04) and reduced caspase-3 expression but did not alter enzymatic antioxidant activity after RIR.
Amifostine decreased the degree and severity of tubular damage after reperfusion, probably by scavenging oxygen free radicals and attenuating the cytotoxic effects of inflammatory infiltrates and apoptosis.
Nephrology Dialysis Transplantation 12/2010; 25(12):3845-51. · 3.40 Impact Factor
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Hugues Michelon,
Jörg König,
Antoine Durrbach,
Lina Quteineh,
Céline Verstuyft,
Valérie Furlan, Sophie Ferlicot,
Alexia Letierce,
Bernard Charpentier,
Martin F Fromm,
Laurent Becquemont
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ABSTRACT: This study aimed to determine the influence of gene candidates on mycophenolic acid (MPA) response during the first year of renal transplantation.
A total of 218 renal transplant recipients who received MPA from the first day of transplantation at a fixed dose of 2 g/day were genotyped for ABCB1, ABCC2, UGT2B7, UGT1A9, SLCO1B1, SLCO1B3 and IMPDH1 polymorphisms. Clinical end points were MPA-related adverse drug reactions (ADRs) and acute rejection episodes during the first year post-transplantation.
After correction for multiple statistical testing, SLCO1B1 (encoding the hepatic uptake transporter OATP1B1) was the only gene associated with MPA-related ADRs, showing a 75% risk reduction in favor of a protective effect of the SLCO1B1*5 allele (p = 0.002). In vitro experiments showed that MPA metabolites MPA-phenyl-glucuronide and MPA-acyl-glucuronide are substrates of OATP1B1. Their transport was decreased in the presence of the variant transporter (OATP1B1*5).
These results suggest for the first time that carriers of the SLCO1B1*5 allele seem to be protected from MPA-related ADRs.
Pharmacogenomics 12/2010; 11(12):1703-13. · 3.97 Impact Factor
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Annales de Pathologie 04/2010; 30(2):156-8. · 0.25 Impact Factor
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Gwenola Maigne, Sophie Ferlicot,
Frederic Galacteros,
Xavier Belenfant,
Tim Ulinski,
Patrick Niaudet,
Pierre Ronco,
Bertrand Godeau,
Antoine Durrbach,
Sabrinel Sahali,
Philippe Lang,
Olivier Lambotte,
Vincent Audard
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ABSTRACT: Sickle cell disease (SCD) is an increasing cause of chronic kidney disease, but the spectrum of glomerular lesions and their underlying mechanisms remain poorly described. We reviewed 18 renal biopsies from patients with SCD and glomerular involvement and studied the expression of hypoxic markers in the biopsy specimens. Four histopathologic variants were distinguished: focal segmental glomerulosclerosis (FSGS) (39%), membranoproliferative glomerulonephritis (28%), thrombotic microangiopathy glomerulopathy (17%), and specific sickle cell disease glomerulopathy (17%). Chronic organ damage and history of acute chest syndrome were associated with the occurrence of SCD glomerulopathy. All patients exhibited macroalbuminuria but only 6 patients displayed impaired renal function. SCD was not associated with a specific FSGS histologic variant. Long-term follow-up analysis revealed that 50% of patients exhibited chronic kidney disease. Regardless of the histologic variants, immunohistochemistry did not reveal a specific induction of hypoxic markers (inducible nitric oxide synthase [iNOS], nitrotyrosine, hypoxia-inducible factor [HIF]-1 alpha) at the time of renal biopsy. This large study shows that a wide spectrum of glomerular lesions is associated with SCD. Whatever lesions are observed, the renal prognosis is poor, and early renoprotective treatment is necessary. Hypoxic state does not seem to play a key role in the progression of glomerular lesions, but its potential role at an early stage of glomerular injury requires further investigation.
Medicine 01/2010; 89(1):18-27. · 4.35 Impact Factor
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ABSTRACT: Recent studies have highlighted the presence of microchimerism in various solid allografts. The biological significance of these chimeric cells is controversial. They may be beneficial, leading to better tolerance of grafts or participating in tissue repair or, in contrast, deleterious if involved in chronic lesions. The aim was to assess the frequency and cellular nature of microchimerism in female renal grafts of male recipients by combined fluorescence in situ hybridization (FISH) for Y chromosome and immunohistochemistry and to investigate associations between intragraft microchimerism and histological lesions or allograft outcome.
We screened 33 renal biopsy specimens, including 11 with acute T-cell-mediated rejection and nine with transplant glomerulopathy, from 22 male recipients transplanted with female kidneys by FISH and immunohistochemistry with antibodies against smooth muscle actin (mesangial cells), CD31 (endothelial cells), KL1 (epithelial cells), CD45 (leucocyte common antigen) and glomerular epithelial protein 1 (podocytes). Tubular microchimerism was detected in 71% of the patients with a mean percentage of chimeric epithelial cells of 1.4%. Glomerular microchimerism involving podocytes, mesangial and endothelial cells was present with a mean number of chimeric cells per glomerular section of, respectively, 0.6, 2.66 and 3.53. There was an association between endothelial microchimerism and a previous episode of acute T-cell-mediated rejection.
In conclusion, microchimerism in renal grafts occurs frequently, but at a low level and affects tubular cells and all glomerular cell compartments in human renal allografts.
Histopathology 01/2010; 56(2):188-97. · 3.08 Impact Factor
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Min-Han Tan,
Chin Fong Wong,
Hwei Ling Tan,
Ximing J Yang,
Jonathon Ditlev,
Daisuke Matsuda,
Sok Kean Khoo,
Jun Sugimura,
Tomoaki Fujioka,
Kyle A Furge, [......],
Thierry Flam,
Nicolas Thiounn,
Marc Zerbib,
Gérard Benoît,
Stéphane Droupy,
Vincent Molinié,
Annick Vieillefond,
Puay Hoon Tan,
Stéphane Richard,
Bin Tean Teh
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ABSTRACT: 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.
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.
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.
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.
BMC Cancer 01/2010; 10:196. · 3.01 Impact Factor
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ABSTRACT: The major cause of non-ischemic high-flow priapism is post-traumatic vascular injury leading to an arterio-lacunar fistula. However, rare causes such as tumors may induce priapism. This is the first report of a malignant glomus tumor localized in the corpora cavernosa.
The aim of this case is to emphasize the importance of the initial management of priapism and to suggest new tracks on the tests to be performed when the usual exams are not sufficient.
We report the case of a hypervascular penile tumor responsible for high-flow priapism as the first clinical symptom of a metastatic glomus tumor. The persistent penile tumescence was initially considered to be a stuttering priapism and treated using an oral α-adrenergic as no provoking event nor fistula was found. After a 2-week reluctance, a penile magnetic resonance imaging (MRI) was performed.
The MRI showed a hypervascular lesion at the proximal part of the right corpora. The lesion was considered as a fistula, and a selective embolization was performed. Two weeks after embolization, the patient came back to the emergency room because of syncopes and dyspnea. Examination by cardiac ultrasound and chest computed tomography revealed the presence of cardiac, pulmonary, and subcutaneous malignant glomus tumors (glomangiosarcoma). Patient received three lines of chemotherapy, and the penile tumor was surgically removed because of persistent erectile dysfunction and perineal pain.
This case supports the use of corporal body blood gas analysis in difficult cases to discriminate high- and low-flow priapism and penile MRI when clinical history, physical examination, and aspiration are not contributory.
Journal of Sexual Medicine 11/2009; 8(12):3518-22. · 3.55 Impact Factor
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ABSTRACT: Renal injury caused by ischemia-reperfusion (IR) can lead to acute renal failure or delayed graft function. Renal ischemia-reperfusion (RIR) induces inflammatory disorders via activation of arachidonic acid metabolism into prostaglandin E(2) (PGE(2)). Two inducible enzymes, COX-2 and microsomal prostaglandin E synthase (mPGES), regulate PGE(2) production. Heme oxygenase-1 (HO-1) is a cytoprotective enzyme activated during cellular stress. Overexpression of HO-1 is beneficial in transplantation models including antigen-independent IR injury, acute and chronic allograft rejection.
We investigated the effect of HO-1 induction on the COX pathway, antioxidant enzyme activities, malondialdehyde (MDA) levels, and apoptosis in rat kidneys subjected to 45 min ischemia and 1 h or 24 h reperfusion. Rats were injected intraperitoneally with either: 50 mg/kg hemin (HO-1 inducer groups: H1, H2); 50 micromol/kg ZnPP (HO-1 inhibitor groups: Hz1, Hz2); or 0.9% saline (control groups: r1, r2). Sham animals (Sh) did not undergo RIR.
Serum creatinine increased significantly after RIR (r vs Sh; p <0.05). Hemin treatment induced a significant decrease in serum creatinine after RIR (H vs r; p <0.05) whereas ZnPP treatment significantly increased serum creatinine levels (Sh vs Hz; p <0.05). Hemin reduced the severity of acute tubular necrosis and significantly reduced COX-2 and mPGES expression (p <0.05). Hemin did not alter depleted antioxidant enzyme activity but did decrease levels of MDA (p <0.05). Hemin also reduced caspase-3 expression.
HO-1 decreased the degree and severity of tubular damage after IR, probably by attenuating the cytotoxic effects of inflammatory infiltrates and apoptosis.
Inflammation & allergy drug targets. 09/2009; 8(4):252-9.
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ABSTRACT: To study the prevalence and the characteristics of renal cell carcinoma (RCC) in patients with autosomal dominant polycystic kidney disease (ADPKD) in our series.
We reviewed retrospectively all the nephrectomies performed in our department between 1982 and 2003 in patients with ADPKD and chronic renal failure.
Seventy-nine patients (42 males and 37 females) with ADPKD and chronic renal failure underwent 89 nephrectomies; in 10 of 79, both kidneys were removed but not simultaneously. Mean age was 50.4 years (range, 32-69 years). Of 79 patients, 50 had end-stage renal disease (ESRD) and were on hemodialysis or had received a transplant for >1 year. On histologic examination, 11 of 89 kidneys were diagnosed with carcinomas. There was 1 patient with bilateral tumor (tubulopapillary Ca) and 3 kidneys (27.3%) with multifocal tumors. Regarding the histologic type, there were 7 of 12 (58.3%) clear cell carcinomas and the remaining 5 (41.7%) were tubulopapillary carcinomas.
The prevalence of RCC was higher in patients with ADPKD and ESRD, with >1 year on dialysis or renal transplantation undergoing nephrectomy according the protocol. It would be 2 to 3 times more frequent than RCC in patients with ESRD alone. The clinician should maintain a high alert of suspicion for RCC in such patients.
Urology 08/2009; 74(3):631-4. · 2.43 Impact Factor
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ABSTRACT: Bladder involvement in metastatic breast carcinoma is a rare situation and accounts for about 3% of secondary bladder neoplasms. Most patients are symptomatic, with evidence of disseminated disease at diagnosis.
Urology 08/2009; 74(4):785-6. · 2.43 Impact Factor
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ABSTRACT: The association between seronegative spondyloarthro- pathies and IgA nephropathy is well documented, mainly in cases of ankylosing spondylitis (AS). However, although these diseases have been associated, the physiopathological links between each other appear unclear. Anti-TNFalpha agents have transformed the outcome of axial forms of AS resistant to conventional anti-inflammatory therapies. Infliximab, a monoclonal anti-TNFalpha antibody, has greatly improved the evolution of AS although several adverse events have been described. On the other hand, infliximab has been demonstrated to reduce renal symptoms associated with chronic inflammatory rheumatological diseases, such as amyloid A (AA) amyloidosis, but few data are available on its efficacy in controlling IgA nephropathy associated with AS [1,2]. We report here a case of IgA nephropathy associated with AS that became symptomatic, whereas infliximab therapy efficiently controlled the rheumatological disease. This suggests that even though infliximab therapy effectively controls rheumatological manifestations, it may not be able to prevent IgA nephropathy associated with AS. Thus, this case report illustrates the complexity of the physiopathology of both diseases.
Nephrology Dialysis Transplantation 07/2009; 24(11):3540-2. · 3.40 Impact Factor
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ABSTRACT: Tacrolimus is a widely used immunosuppressive drug in organ transplantation. Its oral bioavailability varies greatly between individuals, and it is a substrate of cytochrome P450 3A (CYP3A) and P-glycoprotein. Our objective was to determine the influence of CYP3A5 and ABCB1 genetic polymorphisms on tacrolimus daily requirements and on transplantation outcome. One hundred and thirty-six renal graft recipients treated with tacrolimus were genotyped for CYP3A5 (6986A>G), ABCB1 exon26 (3435C>T) and exon21 (2677G>T/A) single nucleotide polymorphisms. Genotypes were correlated to tacrolimus daily dose at 1-week, 1-, 6- and 12-month post-transplantation and with transplantation outcome. At 1-month post-transplantation, tacrolimus daily dose was higher for patients with CYP3A5*1/*1 genotype compared to CYP3A5*3/*3 genotype (0.26 +/- 0.03 versus 0.16 +/- 0.01 mg/kg/day, respectively, P < 0.0001). Similar results were obtained at 6- and 12-month post-transplantation. Furthermore, CYP3A5*1 homozygotes were associated with increased risk of acute rejection episodes compared to patients with CYP3A5*1/*3 and CYP3A5*3/*3 genotypes (38% versus 10% and 9%, respectively, P = 0.01). CYP3A5 genetic polymorphism was not associated with tacrolimus-related nephrotoxicity. ABCB1 polymorphisms were not related with transplantation outcome. CYP3A5 genetic polymorphism appeared in our study to affect tacrolimus daily dose requirements and transplantation outcome. Screening for this single nucleotide polymorphism before the transplantation might be helpful for the selection of adequate initial daily dose and to achieve the desired immunosuppression.
Basic & Clinical Pharmacology & Toxicology 01/2009; 103(6):546-52. · 2.18 Impact Factor
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ABSTRACT: Chronic allograft injury is the major cause of renal allograft loss after the first year of transplantation. Vitamin K epoxide reductase complex subunit 1 (VKORC1) haplotype combinations were found to be associated with the risk of developing vascular diseases. We aimed to study the effect of VKORC1 haplotypes on long-term graft function in a cohort of kidney transplant recipients.
A total of 288 renal allograft recipients participated in the study. Long-term renal graft function was measured by the estimation of the glomerular filtration rate. VKORC1 C+1173T single nucleotide polymorphism (rs9934438) was used as a tagging single nucleotide polymorphism for VKORC1*2 haplotype.
Patients homozygous for VKORC1*2 haplotype showed less deterioration of renal graft function compared with the other patients (hazard ratio: 0.34, 95% confidence interval: 0.26-0.87, P=0.02). The same results were obtained in a multivariate analysis, where VKORC1 haplotypes showed to be an independent predictor of long-term graft function when adjusted to other variables contributing to long-term renal graft outcome.
Our results suggest that VKORC1 haplotypes may play a role in the long-term renal allograft function. These findings need to be replicated in prospective clinical studies.
Transplantation 10/2008; 86(6):779-83. · 4.00 Impact Factor
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Philippe Camparo,
Viorel Vasiliu,
Vincent Molinie,
Jerome Couturier,
Karl J Dykema,
David Petillo,
Kyle A Furge,
Eva M Comperat,
Marick Lae,
Raymonde Bouvier, [......], Sophie Ferlicot,
Eric Forest,
Gaelle Fromont,
Marie C Hintzy,
Myriam Laghouati,
Mathilde Sibony,
Marie L Tucker,
Nina Weber,
Bin T Teh,
Annick Vieillefond
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ABSTRACT: We report clinicopathologic features of a large series of renal translocation carcinomas from a multicentric study. Diagnosis was performed by cytogenetic examination of fresh material and/or by immunochemistry with antibodies directed against the C-terminal part of transcription factor E3 (TFE3) and native transcription factor EB (TFEB) proteins. Clinical data, follow-up, and histologic features were assessed. Antibodies against CK7, CD10, vimentin, epithelial membrane antigen, AE1-AE3, E-cadherin, alpha-methylacyl-coenzyme A racemase, melan A, and HMB45 were tested on tissue microarrays. Whole-genome microarray expression profiling was performed on 4 tumors. Twenty-nine cases were diagnosed as TFE3 and 2 as TFEB renal translocation carcinomas, including 13 males and 18 females, mean age 24.6 years. Two patients had a previous history of chemotherapy and 1 had a history of renal failure. Mean size of the tumor was 6.9 cm. Thirteen cases were > or = pT3 stage. Twelve cases were N+ or M+. Mean follow-up was 29.5 months. Three patients presented metastases and 5 have died. Mixed papillary and nested patterns with clear and/or eosinophilic cells represented the most consistent histologic appearance, with common foci of calcifications regardless of the type of translocation. Using a 30 mn incubation at room temperature, TFE3 immunostainings were positive in only 82% of our TFE3 translocation carcinomas. Both TFE3 and TFEB renal translocation carcinomas expressed CD10 and alpha-methylacyl-coenzyme A racemase in all cases. An expression of E-cadherin was observed in two-third of cases. Cytokeratins were expressed in less than one-third of cases. Melanocytic markers were expressed at least weakly in all cases except two. Unsupervised clustering on the basis of the gene expression profiling indicated a distinct subgroup of tumors. TRIM 63 glutathione S-transferase A1 and alanyl aminopeptidase are the main differentially expressed genes for this group of tumors. Our results suggest that these differentially expressed genes may serve as novel diagnostic or prognostic markers.
The American journal of surgical pathology 06/2008; 32(5):656-70. · 4.06 Impact Factor
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ABSTRACT: Phyllodes tumours of the prostate are very rare tumours, as less than 40 cases have been reported in the literature. The authors report the case of a 28-year-old man managed for a phyllodes tumour of the prostate diagnosed in a context of haemospermia. The diagnosis was established by ultrasound, CT MRI and prostatic biopsies. Radical prostatectomy was performed after multidisciplinary discussion. Thirty six months after the operation, the patient was in complete remission, with spontaneous erections and had fathered a child conceived by medically assisted procreation. The authors stress the importance of nerve-sparing radical surgery and early sexual rehabilitation.
Progrès en Urologie 12/2007; 17(7):1379-81. · 0.58 Impact Factor
