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Flejou J.-F.,Service dAnatomie et Cytologie Pathologiques
Histopathology | Year: 2015

Although anal cancer remains a relatively uncommon tumour its frequency is rising, especially in high-risk groups. It is now well recognized that anal squamous cell carcinoma, the largely predominant tumour type, shares many similarities with cancer of the uterine cervix, with a major role for oncogenic human papilloma viruses in both tumours. Anal squamous precancerous lesions have now to be classified with the same criteria and terminology as their cervical counterparts, by using the Lower Anogenital Squamous Terminology (LAST) proposal. Only p16 protein is a useful marker in this setting at the present time. As most cases of anal cancer are treated by non-surgical procedures, pathology has a limited role in the staging of the disease, except for early lesions treated by local excision, and when the sentinel lymph node procedure is undertaken that is still under evaluation. A variety of other tumour types can occur more rarely, with difficult diagnostic issues, solved in most cases by immunohistochemistry. © 2015 John Wiley & Sons Ltd. Source


Matsuzaki S.,CHU Clermont Ferrand | Darcha C.,Service dAnatomie et Cytologie Pathologiques | Maleysson E.,CHU Clermont Ferrand | Canis M.,CHU Clermont Ferrand | Mage G.,CHU Clermont Ferrand
Journal of Clinical Endocrinology and Metabolism | Year: 2010

Context: Only a few, small, human studies on E-cadherin and β-catenin expression in normal cycling human endometrium have been reported. It remains unclear whether expression of these molecules might be altered in the endometrium of infertile patients with endometriosis. Objectives: The aim of the present study was to investigate E-cadherin and β-catenin expression in the endometrium of infertile patients with endometriosis, those with uterine fibromas, and patients with unexplained infertility. Design: Expression levels of E-cadherin and β-catenin mRNA and/or protein in the endometrium of infertile patients with endometriosis (n = 151), those with uterine fibromas (n = 41), patients with unexplained infertility (n = 9), as well as healthy fertile controls (n = 57) were measured. This study utilized laser capture microdissection, real-time RT-PCR, and immunohistochemistry. Results: No significant differences in E-cadherin or β-catenin mRNA expression in microdissected epithelial cells were observed among the different groups throughout the menstrualcycle. However, very low or no protein expression of E-cadherin, total β-catenin, or dephosphorylated β-catenin in luminal and glandular epithelial cells was detected in the mid-secretory endometrium of healthy fertile controls. E-cadherin, total β-catenin, and dephosphorylated β-catenin protein expression in the mid-secretory endometrium of infertile patients with endometriosis or unexplained infertility was significantly higher compared to that of healthy fertile controls in both luminalandglandular epithelial cells. Conclusions: These findings suggest that impaired down-regulation of E-cadherin and β-catenin protein expression, along with Wnt/β-catenin signaling pathway activation during the window of implantation, might be one of the potential molecular mechanisms of infertility in patients with endometriosis. Copyright © 2010 by The Endocrine Society. Source


Canaud G.,University of Paris Descartes | Bienaime F.,University of Paris Descartes | Tabarin F.,University of Paris Descartes | Bataillon G.,University Pierre and Marie Curie | And 8 more authors.
New England Journal of Medicine | Year: 2014

Background: Although thrombosis is considered the cardinal feature of the antiphospholipid syndrome, chronic vascular lesions are common, particularly in patients with lifethreatening complications. In patients who require transplantation, vascular lesions often recur. The molecular pathways involved in the vasculopathy of the antiphospholipid syndrome are unknown, and adequate therapies are lacking. Methods: We used double immunostaining to evaluate pathway activation in the mammalian target of rapamycin complex (mTORC) and the nature of cell proliferation in the vessels of patients with primary or secondary antiphospholipid syndrome nephropathy. We also evaluated autopsy specimens from persons who had catastrophic antiphospholipid syndrome. The molecular pathways through which antiphospholipid antibodies modulate the mTORC pathway were evaluated in vitro, and potential pharmacologic inhibitors were also tested in vitro. Finally, we studied the effect of sirolimus in kidney-transplant recipients with the antiphospholipid syndrome. Results: The vascular endothelium of proliferating intrarenal vessels from patients with antiphospholipid syndrome nephropathy showed indications of activation of the mTORC pathway. In cultured vascular endothelial cells, IgG antibodies from patients with the antiphospholipid syndrome stimulated mTORC through the phosphatidyl-inositol 3-kinase (PI3K)-AKT pathway. Patients with antiphospholipid syndrome nephropathy who required transplantation and were receiving sirolimus had no recurrence of vascular lesions and had decreased vascular proliferation on biopsy as compared with patients with antiphospholipid antibodies who were not receiving sirolimus. Among 10 patients treated with sirolimus, 7 (70%) had a functioning renal allograft 144 months after transplantation versus 3 of 27 untreated patients (11%). Activation of mTORC was also found in the vessels of autopsy specimens from patients with catastrophic antiphospholipid syndrome. Conclusions: Our results suggest that the mTORC pathway is involved in the vascular lesions associated with the antiphospholipid syndrome. Copyright © 2014 Massachusetts Medical Society. All rights reserved. Source


Vilasco M.,French Institute of Health and Medical Research | Communal L.,French Institute of Health and Medical Research | Mourra N.,Service dAnatomie et Cytologie Pathologiques | Courtin A.,French Institute of Health and Medical Research | And 3 more authors.
Breast Cancer Research and Treatment | Year: 2011

Stress enhances glucocorticoid (GC) synthesis, which alters inflammation and immune responses, as well as cellular proliferation and apoptosis in a number of tissues. Increasingly, stress has been associated with cancer progression, and in particular in breast cancer. Consequently, an operational glucocorticoid receptor system in breast tissue influences breast cancer development. In this review, we summarize the data on the GC/GR system in normal and tumoral breast tissue. We also review the molecular mechanisms by which GCs control apoptosis and proliferation in breast cancer models and how GCs alter the chemotherapy of breast cancer treatment when used in combination. Finally, we discuss the participation of GR in breast tumorigenesis under hormone replacement therapy. © Springer Science+Business Media, LLC. 2011. Source


Bossard C.,University of Nantes | Dobay M.P.,Swiss Institute of Bioinformatics | Parrens M.,Departement de Pathologie | Lamant L.,Departement de Pathologie | And 12 more authors.
Blood | Year: 2014

The extended use of brentuximab-vedotin was reported for CD30+ nonanaplastic peripheralT-celllymphomas(PTCLs)with promising efficacy. CD30 status assessmentis thus a critical factor for therapeutic decision, but the reliability of immunohistochemistry (IHC) in evaluating its expression remains to be defined. This prompted us to investigate the correlation between semiquantitative CD30 protein assessment by IHC andmessengerRNA(mRNA) assessment by micro arraysinacohortof376 noncutaneous PTCLs representative of the main entities. By IHC, CD30 expression was heterogeneous across and within entities and significantly associated with large tumor cell size. In additionto100% anaplastic large-cell lymphomas, 57%ofother PTCL entities were CD30-positive at a 5% threshold. CD30 protein expression was highly correlated to mRNA levels. mRNA levels were bimodal, separating high from low CD30-expressing PTCL cases. Weconclude that IHC is a valuable tool in clinical practice to assess CD30 expression in PTCLs. © 2014 by The American Society of Hematology. Source

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