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1.  A classification of ductal plate malformations based on distinct pathogenic mechanisms of biliary dysmorphogenesis 
Hepatology (Baltimore, Md.)  2011;53(6):1959-1966.
Ductal plate malformations (DPM) are developmental anomalies considered to result from lack of ductal plate remodeling during bile duct morphogenesis. In mice, bile duct development is initiated by the formation of primitive ductal structures lined by two cell types, namely ductal plate cells and hepatoblasts. During ductal plate remodeling the primitive ductal structures mature to ducts as a result from differentiation of the ductal plate cells and hepatoblasts to cholangiocytes. We here report that this process is conserved in human fetal liver. These findings prompted us to evaluate how DPM develop in three mouse models, namely mice with livers deficient in Hepatocyte Nuclear Factor (HNF)6, HNF1β or cystin-1 (cpk mice). Human liver from a patient with a HNF1B/TCF2 mutation, and from fetuses affected with Autosomal Recessive Polycystic Kidney Disease (ARPKD) were also analysed. Despite the epistatic relationship between HNF6, HNF1β and cystin-1, the three mouse models displayed distinct morphogenic mechanisms of DPM. They all developed biliary cysts lined by cells with abnormal apico-basal polarity. However, the absence of HNF6 led to an early defect in ductal plate cell differentiation. In HNF1β-deficient liver, maturation of the primitive ductal structures was impaired. Cpk mouse livers and human fetal ARPKD showed normal differentiation and maturation but abnormal duct expansion.
DPM is the common end-point of distinct defects initiated at distinct stages of bile duct morphogenesis. Our observations provide a new pathogenic classification of DPM.
PMCID: PMC4271518  PMID: 21391226
liver; development; polycystic disease; polarity; cilium
2.  A Clinical and Pathological Overview of Vulvar Condyloma Acuminatum, Intraepithelial Neoplasia, and Squamous Cell Carcinoma 
BioMed Research International  2014;2014:480573.
Condyloma acuminatum, intraepithelial neoplasia, and squamous cell carcinoma are three relatively frequent vulvar lesions. Condyloma acuminatum is induced by low risk genotypes of human papillomavirus (HPV). Vulvar intraepithelial neoplasia (VIN) and squamous cell carcinoma have different etiopathogenic pathways and are related or not with high risk HPV types. The goal of this paper is to review the main pathological and clinical features of these lesions. A special attention has been paid also to epidemiological data, pathological classification, and clinical implications of these diseases.
PMCID: PMC3956289  PMID: 24719870
3.  Vulvar Skin Disorders throughout Lifetime: About Some Representative Dermatoses 
BioMed Research International  2014;2014:595286.
The objective of this paper is to present general considerations which should be kept in mind by clinicians in charge of women with vulvar diseases. Four representative vulvar dermatoses are described. Lichen simplex chronicus is a pathological condition related to chemical and mechanical irritant agents. Detrimental effects of these irritants, in the presence of other dermatoses, have to be considered when therapeutic responses are unsatisfactory. Lichen sclerosus is the most common vulvar dermatosis in elderly. However, it should be kept in mind that it may be diagnosed at any age. Lichen planus, in spite of sharing a similar range of etiological factors with lichen sclerosus, is a very distinct entity. Finally, Paget's disease, although rare, is also described especially because of the challenge it represents both clinically and therapeutically.
PMCID: PMC3910662  PMID: 24511539
4.  Aberrant Promoter Methylation and Expression of UTF1 during Cervical Carcinogenesis 
PLoS ONE  2012;7(8):e42704.
Promoter methylation profiles are proposed as potential prognosis and/or diagnosis biomarkers in cervical cancer. Up to now, little is known about the promoter methylation profile and expression pattern of stem cell (SC) markers during tumor development. In this study, we were interested to identify SC genes methylation profiles during cervical carcinogenesis. A genome-wide promoter methylation screening revealed a strong hypermethylation of Undifferentiated cell Transcription Factor 1 (UTF1) promoter in cervical cancer in comparison with normal ectocervix. By direct bisulfite pyrosequencing of DNA isolated from liquid-based cytological samples, we showed that UTF1 promoter methylation increases with lesion severity, the highest level of methylation being found in carcinoma. This hypermethylation was associated with increased UTF1 mRNA and protein expression. By using quantitative RT-PCR and Western Blot, we showed that both UTF1 mRNA and protein are present in epithelial cancer cell lines, even in the absence of its two main described regulators Oct4A and Sox2. Moreover, by immunofluorescence, we confirmed the nuclear localisation of UTF1 in cell lines. Surprisingly, direct bisulfite pyrosequencing revealed that the inhibition of DNA methyltransferase by 5-aza-2′-deoxycytidine was associated with decreased UTF1 gene methylation and expression in two cervical cancer cell lines of the four tested. These findings strongly suggest that UTF1 promoter methylation profile might be a useful biomarker for cervical cancer diagnosis and raise the questions of its role during epithelial carcinogenesis and of the mechanisms regulating its expression.
PMCID: PMC3411846  PMID: 22880087

Results 1-4 (4)