Our study showed that p16 INK4A expressions correlate well with the increasing grade of CIN. Although survivin does not correlate well to the increasing grade of CIN, it could be useful in differentiating CIN 3 from SCC.

Aim: The aim of our study was to determine the endocan-1 expression in placenta of hypertensive women, and its association with maternal and fetal outcomes. Methods: This was a cross-sectional study consisted of 21 pregnant women with hypertension and 23 without hypertension. The gestational age ranged from 28 to 39 weeks (hypertensive) and 32 to 40 weeks (normotensive). The paraffin embedded formalin fixed placenta tissue blocks were retrieved from the pathology archives. Endocan immunohistochemistry was performed on tissue sections of full thickness and maternal surface of the placenta. The endocan expression was determined in fetal endothelial cells, maternal endothelial cells, cytotrophoblasts, syncytiotrophoblasts and decidual cells. The differences in endocan expression in placenta between hypertensive and normotensive subjects were evaluated by Pearson chi-square test and ttest were used in the statistical analysis. Results: The endocan expression was significantly higher in fetal endothelial cells (P < 0.001), maternal endothelial cells (P = 0.003) and decidual cells (P < 0.001) in the placenta of women with hypertension. When comparing positive and negative endocan expression in maternal outcomes, endocan was associated with the development of pre-eclampsia (P = 0.03). Also, a positive endocan expression was associated with low birthweight (P = 0.001) and prematurity (P = 0.005) in the fetal outcomes. Conclusion: This study showed endocan is highly expressed in fetal endothelial cells, maternal endothelial cells and decidual cells in placenta of hypertensive women. In addition, its expression was associated with poorer maternal and fetal outcomes. These findings suggest endocan may play an important role in the progression of hypertension in pregnancy.

Nonepithelial ovarian cancer (NEOC) is a rare cancer that is often misdiagnosed as other malignant tumors. Research on this cancer using fresh tissues is nearly impossible because of its limited number of samples within a limited time provided. The study is to identify potential genes and their molecular pathways related to NEOC using formalin-fixed paraffin embedded samples. Total RNA was extracted from eight archived NEOCs and seven normal ovaries. The RNA samples with RNA integrity number >2.0, purity >1.7 and cycle count value <28 cycles were hybridized to the Illumina Whole-Genome DASL assay (cDNA-mediated annealing, selection, extension, and ligation). We analyzed the results using the GeneSpring GX11.0 and FlexArray software to determine the differentially expressed genes. Microarray results were validated using an immunohistochemistry method. Statistical analysis identified 804 differentially expressed genes with 443 and 361 genes as overexpressed and underexpressed in cancer, respectively. Consistent findings were documented for the overexpression of eukaryotic translation elongation factor 1 alpha 1, E2F transcription factor 2, and fibroblast growth factor receptor 3, except for the down-regulated gene, early growth response 1 (EGR1). The immunopositivity staining for EGR1 was found in the majority of cancer tissues. This finding suggested that the mRNA level of a transcript did not always match with the protein expression in tissues. The current gene profile can be the platform for further exploration of the molecular mechanism of NEOC.

Objectives Gestational trophoblastic disease comprises of a spectrum of pregnancy-related tumours which includes complete (CHM) and partial hydatidiform moles (PHM). Accurate diagnosis and subclassification of HM subtypes are crucial as prognosis differs. Histopathological examination using haemotoxylin and eosin (H&E) staining remains the basis for diagnosing HM, with only 80% accuracy. p57kip2 is a cyclin-dependent kinase inhibitor (CDKI) protein and is strongly paternally imprinted, being expressed from maternal allele. Therefore, complete mole (CHM) with only paternal genome has nearly absent expression of p57kip2 compared to partial mole (PHM) having both paternal and maternal genomes. This study is aimed to determine usefulness of p57kip2 immunohistochemistry (IHC) analysis in the diagnosis of HM subtypes. Methods A total of 82 archived paraffin embedded HM tissues with subtypes classified based on H&E staining – 39 (47.5%) CHM, 41 (50.0%) PHM and two (2.43%) unclassified molar pregnancy were retrieved. All tissue samples were subjected for p57kip2 IHC analysis and HM subtypes were then reclassified. Results A total of 66 cases (80.5%) were re-classified as CHM, 14 cases (17.1%) as PHM and two cases (2.4%) were decidual and cystic tissues. Analysis using p57kip2 immunostaining showed a diagnostic discrepancy of 33.0% from routine H&E staining and helps to improve the characterisation of the HM subtypes specifically at early gestations which have less distinctive morphologies. Conclusions IHC using p57kip2 monoclonal antibody should be considered as a routine ancillary test to H&E in improving the diagnosis of HM subtypes particularly in developing countries with limited resources.