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TitleUp-regulation of lipocalin 2 is associated with high-risk human papillomavirus and grade of cervical lesion at baseline but does not predict outcomes of infections or incident cervical intraepithelial neoplasia
Author(s)Syrjänen, Stina
Naud, Paulo
Sarian, Luis
Derchain, Sophie
Roteli-Martins, Cecilia
Tatti, Silvio
Branca, Margerita
Erzen, Mojca
Hammes, Luciano S.
Costa, Silvano
Longatto, Adhemar
Syrjänen, Kari
KeywordsAcute-Phase Proteins
Biomarkers, Tumor
Cervical Intraepithelial Neoplasia
DNA, Viral
Latin America
Mass Screening
Papillomavirus Infections
Predictive Value of Tests
Proto-Oncogene Proteins
Uterine Cervical Neoplasms
Vaginal Smears
High-risk human papillomavirus
Neutrophil gelatinase–associated lipocalin
Viral outcomes
Disease progression
Longitudinal predictive values
Surrogate end points
Issue dateJul-2010
PublisherAmerican Society for Clinical Pathologists (ASCP)
JournalAmerican Journal of Clinical Pathology
Abstract(s)Our objective was to assess whether neutrophil gelatinase-associated lipocalin (NGAL)/lipocalin 2 (LCN2) expression in cervical human papillomavirus (HPV) lesions has implications on the outcome of HPV infections or disease progression. Cervical biopsy specimens from 225 women in the Latin American Screening study were analyzed for NGAL/LCN2 expression using immunohistochemical analysis, to assess associations with cervical intraepithelial neoplasia (CIN) grade, high-risk HPV, and in predicting outcomes of high-risk (HR)-HPV infections. Expression of NGAL/LCN2 increased with lesion grade (odds ratio [OR], 3.86; 95% confidence interval [CI], 1.53-9.71; P = .001). Up-regulation was also related to HR-HPV detection (OR, 2.21; 95% CI, 1.15-4.24; P = .016) and showed a linear relationship to HR-HPV load (P = .002). NGAL/LCN2 expression was of no value in predicting the outcomes of HR-HPV infections or the surrogate end points (incident CIN 1+ and CIN 2+) of progressive disease. Because the SV40 large T antigen is a powerful up-regulator of this lipocalin, up-regulation of NGAL/LCN2 in CIN is probably induced by HR-HPV E6 oncoprotein, most likely by eliminating its normal transcription repression exerted by wild-type p53.
AccessRestricted access (UMinho)
Appears in Collections:ICVS - Artigos em revistas internacionais / Papers in international journals

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