Service danatomopathologie

Casablanca, Morocco

Service danatomopathologie

Casablanca, Morocco

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Lorentz C.,Service ORL et Chirurgie Cervico Faciale | Marie B.,Service dAnatomopathologie | Vignaud J.M.,Service dAnatomopathologie | Jankowski R.,Service ORL et Chirurgie Cervico Faciale
European Archives of Oto-Rhino-Laryngology | Year: 2012

The objective of this study is to report a 5-year experience with Respiratory Epithelial Adenomatoid Hamartoma (REAH) of the olfactory clefts. The study design is retrospective observational study and the setting is in a Tertiary medical center. The charts of all adult patients operated on bilateral nasal polyps between 2003 and 2008 were retrospectively checked up on the diagnosis of REAH. Three periods have been distinguished according to our experience with REAH. REAH can be observed either as bilateral pseudotumours confined to the olfactory clefts (n = 12 between 2003 and 2008) or associated to nasal polyposis of the ethmoid labyrinths. As the diagnosis of associated REAH became more evident, the number of recognized cases increased from 0% in 2003 and 2004 to 1.6% in 2005 (1/64 patients) and 12.5% in 2006 (10/80 patients) (period 1). Systematic endoscopy of the olfactory clefts during ethmoid labyrinth surgery increased the proportion to 27% (27/100 patients) (period 2). Systematic biopsies of abnormal mucosa in the olfactory clefts during ethmoid surgery increased the proportion to 48% (31/65 patients). The histopathological diagnosis of REAH has been described in 1995 and added to the World Health Organization classification of tumours in 2005. Pseudotumoural REAH confined to the olfactory clefts represent a differential diagnosis for bilateral naso-ethmoidal polyposis. The significance of REAH associated to naso-ethmoidal polyposis is unclear. © 2011 Springer-Verlag.


Moreira C.,Unite doncologie Pediatrique | Nachef M.N.,Unite Dhematologie et Doncologie Pediatrique | Ziamati S.,Service Danatomopathologie | Ladjaj Y.,Mustapha University Hospital Center | And 3 more authors.
Pediatric Blood and Cancer | Year: 2012

Background: The multidisciplinary management of nephroblastoma has been defined through multicentric prospective studies and an average 90% of patients cured expected. In Africa, such studies are uncommon and results are fragmentary or unknown in most of the countries. We report the results of the GFAOPNEPHRO 01 study using SIOP 2001 protocol approach. Procedure: From April 1, 2001 to March 31, 2004, 8 African Pilot Units were selected to participate in a nonrandomized prospective study. All patients referred with a clinical and radiological diagnosis of nephroblastoma were registered, those aged over 6 months and less than 18 years with a unilateral tumor not previously treated were included in this study and received preoperative chemotherapy. Patients with unfavorable histology or with a tumor other than Wilms tumor, and those with stage IV tumor and persistent disease after surgery were secondarily excluded. Results: Of the 229 patients initially registered, 166 were included and finally 133 retained in the study, after surgery. Tumor rupture occurred in 7.5% of the patients. Thirty-five percent were stage I, 22% stage II, 23% stage III, and 18% stage IV. Two-year disease-free survival and 5-year survival are, respectively: 77.9% and 76.7% for localized tumors, 72.7% and 71.6% for all study patients. Conclusions: It is possible to conduct African multicentric therapeutic studies within the framework of GFAOP. Results in terms of event-free survival and survival are satisfactory. Improvements with respect to procedure, data collection, and outcome are expected in a new study. © 2011 Wiley Periodicals, Inc.


Thervet E.,University of Paris Descartes | Aouizerate J.,Service de Transplantation | Noel L.H.,Laboratoire dAnatomopathologie | Brocheriou I.,Service dAnatomopathologie | And 3 more authors.
Transplantation | Year: 2011

Background. Henoch-Schonlein Purpura nephropathy (HSPN) recurrence in renal transplant recipients (RTRs) has been reported in 35% of patients, leading in 11% of these patients to graft loss at 5 years. However, its true incidence is unknown. The aim of this study was to investigate this recurrence incidence using routine allograft biopsies (RBs). Methods. All RTRs with biopsy-proven HSP initial nephropathy were included (13 RTRs and 18 renal transplantations). At transplantation, the median age was 34 years, and 85% of RTRs were men. Overall, we analyzed 66 RBs that were routinely performed at 3 and 12 months after RT and when clinically indicated. Histologic recurrence was defined as the presence of IgA deposits within the mesangium and along the glomerular capillary walls. Results. After a median follow-up of 83 months (range, 13-232 months; interquartile range, 26-235 months), histologic recurrence was detected in 69% of patients and in 61% of grafts after a mean period of 24 months (range, 1-156 months). Clinical or biological signs were absent in all but one. Patient survival was 92.8%. Graft loss occurred in five cases, never were related to recurrence. At the last follow-up, the mean glomerular filtration rate was 48±14.2 mL/min/1.73 m; in patients with and without recurrence, the mean rates were 52.1±17.5 and 42.4±5.3 mL/min/1.73 m, respectively (P=0.27). Conclusion. Histologic recurrence of HSPN after RT is frequently observed on routine RBs but is not associated with clinical consequences. The short-term prognosis of recurrence is good, but its long-term prognosis remains to be determined. © 2011 by Lippincott Williams & Wilkins.


Letavernier E.,French Institute of Health and Medical Research | Letavernier E.,University Pierre and Marie Curie | Rodenas A.,Service dAnatomopathologie | Guerrot D.,French Institute of Health and Medical Research | And 3 more authors.
Pediatrics | Year: 2012

Williams-Beuren syndrome (WBS) is a neurodevelopmental disorder associated with hypercalcemia of unknown origin. This syndrome results from the deletion of contiguous genes on chromosome 7, including the general transcription factor IIi gene. The general transcription factor IIi gene encodes TFII-I, which suppresses cell-surface accumulation of transient receptor potential C3 (TRPC3) channels, involved in calcium transport in lymphocytes. We describe the case of a patient with WBS with hypercalcemia associated with abnormal TRPC3 expression. Analysis of peripheral lymphocytes revealed a sharp increase in TRPC3 expression, compared with control patients. To investigate the potential role of TRPC3 in calcium homeostasis, we performed specific immunostaining on the intestine and the kidney,major calcium-regulating tissues. We provide the first demonstration that TRPC3 is expressed in normal digestive epithelium and renal tubules in control patients, and overexpressed in the intestine in the patient with WBS. Taken together, these data suggest that calcium metabolism abnormalities observed in WBS may be attributable to TFII-I haploinsufficiency and subsequent TRPC3 overexpression, thereby increasing both digestive and renal calcium absorption. This original observation prompts further investigation of TRPC3 as a novel actor of calcium homeostasis. Copyright © 2012 by the American Academy of Pediatrics.


Wantz M.,Service de Dermatologie | Spanoudi-Kitrimi I.,Service de Dermatologie | Lasek A.,Service de Dermatologie | Lebas D.,Service de Dermatologie | And 2 more authors.
Annales de Dermatologie et de Venereologie | Year: 2014

Background Herein we report the first case of toxic epidermal necrolysis (TEN) occurring with use of vemurafenib. Patients and methods A 75-year-old female patient was being treated with vemurafenib for stage IV melanoma with BRAF V600E mutation. She suddenly presented fever, diffuse pruriginous maculopapular erythema, palpebral edema, palmar bulla, conjunctivitis, cheilitis and mucosal ulceration. The condition progressed towards detachment affecting 50% of the skin area. Cutaneous biopsy revealed lichenoid dermatosis, chiefly vesicular with numerous eosinophils. Direct immunofluorescence (IFD) was negative. Vemurafenib was the only drug to which the reaction was ascribable and we concluded on vemurafenib-induced TEN. Discussion To our knowledge, this is the first reported case of vemurafenib-induced TEN, but this adverse effect, although already described in the BRIM-3 study, appears rare in clinical practice. Other severe skin reactions have been described in the literature. These include a case of Stevens-Johnson syndrome in a female patient treated with vemurafenib and previously receiving ipilimumab. A more common occurrence is cutaneous reactions involving efflorescence of benign hyperkeratotic lesions, occasionally accompanied by authentic epidermal carcinoma or keratoacanthoma, and requiring regular dermatological monitoring of patients treated with vemurafenib. Conclusion If maculopapular exanthema occurs under vemurafenib, continuation of this treatment should be reassessed since the risk of progression to a more serious condition such as TEN, as seen in the present case, cannot be ruled out. © 2013 Elsevier Masson SAS.


Koukourgianni F.,University of Lyon | Harambat J.,University of Lyon | Ranchin B.,University of Lyon | Euvrard S.,Service de Dermatologie | And 3 more authors.
Nephrology Dialysis Transplantation | Year: 2010

Background. Cancer is a well-recognized complication of organ transplantation. The pattern of malignancies that occur in the paediatric graft population is different from that in the general paediatric population and in the population of adult organ transplant recipients.Methods. We reviewed medical records from 240 consecutive paediatric renal transplantations performed in 219 children, aged less than 19 years, in our centre between April 1987 and March 2007. Data from patients who had been transferred into adult units were extracted from the French registries of dialysis and transplantation.Results. Among the 219 children who underwent renal transplantation during the study period, 16 (7.3) developed malignancy. The cumulative incidence of cancer was 1.9, 4.0, 6.9 and 10.2 at 1, 5, 10 and 15 years post-transplantation, respectively. The 10-year incidence of post-transplantation lymphoproliferative disorder (PTLD) was 4.5. Other identified cancers were Hodgkin lymphoma, Burkitt lymphomas, renal papillary carcinoma, thyroid papillary carcinoma, recurrent ovarian seminoma and skin cancer. The mortality rate was 25 (416).Conclusion. Early detection of cancer in transplant recipients is of great importance. Regular screening for persistent Epstein-Barr virus (EBV) DNA viral load in patients at risk for developing PTLD is recommended. The occurrence of skin cancer in transplanted children is extremely rare during childhood, but cases can develop in early adulthood.


Lessard L.,McGill University | Labbe D.P.,McGill University | Deblois G.,McGill University | Begin L.R.,Service dAnatomopathologie | And 8 more authors.
Cancer Research | Year: 2012

The androgen receptor (AR) signaling axis plays a key role in the pathogenesis of prostate cancer. In this study, we found that the protein tyrosine phosphatase PTP1B, a well-established regulator of metabolic signaling, was induced after androgen stimulation of AR-expressing prostate cancer cells. PTP1B induction by androgen occurred at the mRNA and protein levels to increase PTP1B activity. High-resolution chromosome mapping revealed AR recruitment to two response elements within the first intron of the PTP1B encoding gene PTPN1, correlating with an AR-mediated increase in RNA polymerase II recruitment to the PTPN1 transcriptional start site. We found that PTPN1 and AR genes were coamplified in metastatic tumors and that PTPN1 amplification was associated with a subset of high-risk primary tumors. Functionally, PTP1B depletion delayed the growth of androgen-dependent human prostate tumors and impaired androgen-induced cell migration and invasion in vitro. However, PTP1B was also required for optimal cell migration of androgen-independent cells. Collectively, our results established the AR as a transcriptional regulator of PTPN1 transcription and implicated PTP1B in a tumor-promoting role in prostate cancer. Our findings support the preclinical testing of PTP1B inhibitors for prostate cancer treatment. ©2012 AACR.


Dupouy S.,French Institute of Health and Medical Research | Mourra N.,Service dAnatomopathologie | Doan V.K.,French Institute of Health and Medical Research | Gompel A.,UF de Gynecologie Hotel Dieu | And 2 more authors.
Biochimie | Year: 2011

A growing challenge in medicine today, is the need to improve the suitability of drug treatments for cancer patients. In this field, biomarkers have become the "flags" to provide additional information in tumor biology. They are a relay between the patient and practitioner and consequently, aid in the diagnosis, providing information for prognosis, or in some cases predicting the response to specific therapies. In addition to being markers, these tumor "flags" can also be major participants in the process of carcinogenesis. Neurotensin receptor 1 (NTSR1) was recently identified as a prognosis marker in breast, lung, and head and neck squamous carcinomas. Neurotensin (NTS) was also shown to exert numerous oncogenic effects involved in tumor growth and metastatic spread. These effects were mostly mediated by NTSR1, making the NTS/NTSR1 complex an actor in cancer progression. In this review, we gather information on the oncogenic effects of the NTS/NTSR1 complex and its associated signaling pathways in order to illuminate its significant role in tumor progression and its potential as a biomarker and a therapeutic target in some tumors. © 2011 Elsevier Masson SAS. All rights reserved.


Hardy S.,McGill University | Uetani N.,McGill University | Wong N.,McGill University | Kostantin E.,McGill University | And 5 more authors.
Oncogene | Year: 2015

The three PRL (phosphatases of regenerating liver) protein tyrosine phosphatases (PRL-1, -2 and -3) have been identified as key contributors to metastasis in several human cancers, yet the molecular basis of their pro-oncogenic property is unclear. Among the subfamily of PRL phosphatases, overexpression of PRL-2 in breast cancer cells has been shown to promote tumor growth by a mechanism that remains to be uncovered. Here we show that PRL-2 regulates intracellular magnesium levels by forming a functional heterodimer with the magnesium transporter CNNM3. We further reveal that CNNM3 is not a phosphorylated substrate of PRL-2, and that the interaction occurs through a loop unique to the CBS pair domains of CNNM3 that exists only in organisms having PRL orthologs. Supporting the role of PRL-2 in cellular magnesium transport is the observation that PRL-2 knockdown results in a substantial decrease of cellular magnesium influx. Furthermore, in PRL-2 knockout mice, serum magnesium levels were significantly elevated as compared with control animals, indicating a pivotal role for PRL-2 in regulating cellular magnesium homeostasis. Although the expression levels of CNNM3 remained unchanged after magnesium depletion of various cancer cell lines, the interaction between endogenous PRL-2 and CNNM3 was markedly increased. Importantly, xenograft tumor assays with CNNM3 and a mutant form that does not associate with PRL-2 confirm that CNNM3 is itself pro-oncogenic, and that the PRL-2/CNNM3 association is important for conferring transforming activities. This finding is further confirmed from data in human breast cancer tissues showing that CNNM3 levels correlate positively with both PRL-2 expression and the tumor proliferative index. In summary, we demonstrate that oncogenic PRL-2 controls tumor growth by modulating intracellular magnesium levels through binding with the CNNM3 magnesium transporter.


Abboud I.,Service de Nephrologie et Transplantation Renale | Pillebout E.,Service de Nephrologie et Transplantation Renale | Nochy D.,Service dAnatomopathologie
Nephrologie et Therapeutique | Year: 2014

Hematopoietic stem cell transplantation is a widely used therapeutic modality for many, mainly malignant, diseases. Toxicities of this procedure include acute and chronic renal dysfunction. Acute renal failure, generally reversible is due to acute tubular necrosis (tumor lysis syndrome, marrow-infusion toxicity, sepsis, nephrotoxins), hepatic veno-occlusive disease or acute graft-versus-host disease. Chronic renal failure is often multifactorial, caused by conditioning-associated endothelial cell toxicity (bone marrow transplant nephropathy) and calcineurin inhibitors toxicity. Renal pathologic findings are somewhat similar to thrombotic microangiopathy, with sometimes systemic disease. Rare cases of nephrotic syndrome have been described after hematopoietic stem cell transplantation, mainly membranous nephropathy, associated with graft-versus-host disease. Therapeutic options for renal dysfunction after hematopoietic stem cell transplantation are limited but kidney transplantation is possible in case of end-stage renal disease. © 2013 Association Sociétéde néphrologie. Published by Elsevier Masson SAS. All rights reserved.

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