Anna Semczuk-Sikora

Expression of genes coding for proangiogenic factors and their receptors in human placenta complicated by preeclampsia and intrauterine growth restriction.

The aim of the study was to investigate the expression of genes coding for vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF) as well as their receptors, fms-like tyrosine kinase receptor 1 (VEGFR-1/Flt-1) and VEGF receptor 2 (VEGFR-2/KDR) in the placentae of patients with pregnancies complicated by preeclampsia (PE) and intrauterine growth restriction (IUGR). Tissue samples were collected from placentae of women with PE (n=31) and IUGR syndrome (n=25) as well as of healthy control women (n=31). Total RNA was extracted and purified, mRNA reversely transcribed, and amplified using real-time PCR. Expression of the examined genes was normalized to β-actin. Higher levels of PlGF (p<0.001) and Flt-1 (p<0.05) transcription were found in PE placentae compared to normal ones. A positive correlation between PlGF and Flt-1 expression was revealed in the PE patients. In conclusion, the presented data indicate the upregulation of both PlGF and Flt-1 in placentae of women with PE, which could be induced by a pathological process possibly due to endothelial dysfunction.

TGFβ-pathway is down-regulated in a uterine carcinosarcoma: A case study

Data assessing the role of various genetic alterations in uterine carcinosarcoma (CS), particularly the transforming growth factors-β (TGFβ) that play a crucial role in many cellular processes, including proliferation, differentiation, adhesion and migration, are scarce. TGFβ exert their effects through specific receptors and associated auxiliary receptors. In the current study, we investigated the expression of TGFβ isoforms and their receptors, as well as selected genes in a case of CS. We applied the real-time fluorescence detection PCR method with FAM dye-labeled TaqMan specific probes. In a comparison to the normal counterpart, TGFB1, TGFB2, TGFBRII, TGFBR3, ENG and CD109 were all down-regulated in uterine CS samples at different extents. BIRC5 and hTERT, markers of tumor survival, were up-regulated in CS as compared with normal counterparts. A concomitant increase of the hypoxia marker HIF1A expression pattern was noted, whereas the expression of GPR120, responsible for free fatty acids sensing, was not different in both counterparts evaluated. In conclusion, deregulation of various cellular mechanisms in uterine CS is associated with alterations at many levels - cell growth and proliferation, apoptosis, and impaired response to stimuli from extracellular environment.

The Putative Role of TP53 Alterations and p53 Expression in Borderline Ovarian Tumors - Correlation with Clinicopathological Features and Prognosis: A Mini-Review

Borderline ovarian tumors (BOTs) represent an independent group among ovarian malignancies, being diagnosed at clinical stage earlier than invasive ovarian carcinomas (OCs) and characterized by a rather favorable outcome after careful surgical management. Data published worldwide showed a substantial discordance of p53 expression in BOTs. The purpose of this work was to present the current status of knowledge on the significance of TP53 gene and p53 protein product alterations in BOTs. In general, higher p53 expression patterns were reported for ovarian malignancies compared to BOTs. Serous, mucinous, and endometrioid BOTs differ substantially in relation to p53 immunostaining, but data concerning the relationship between the proteins immunoreactivity and other clinico-pathological variables are scarce. Finally, reports published to date support the view that TP53 alterations may not be commonly associated with the borderline phenotype of ovarian tumors but they probably occur during the development of invasive OCs. In light of these uncertainties, the impact of TP53 alterations and p53 expression on overall survival in women affected by BOTs requires further multi-institutional studies in large cohorts of patients.

Multiple recurrences of early-stage, endometrioid-type G2 endometrial cancer with a long-time follow-up: A case study

The recurrence after a long-time free period of time, in women primarily operated on for early-stage of endometrial cancer (EC), is a unique phenomenon. Currently, we present the case of a 59-year-old woman with multiple recurrences from the moderately-differentiated, stage Ib, endometrioid-type, uterine cancer. All recurrences were pathologically proven to originate from the primary tumor, and the patient expired 12 years after the primary surgery for disseminated neoplasm. We summarize the current data to give a short overview of the role of late recurrences in women operated on for early-stage EC.

p53 is not related to Ki-67 immunostaining in the epithelial and mesenchymal components of female genital tract carcinosarcomas

Carcinosarcomas (CSs) are composed of two separate histological components and are rare neoplasms of the female genital tract. Therefore, CS pathogenesis has not yet been fully elucidated. In the present study, immunohistochemical techniques were used to determine the role of p53 and Ki-67 overexpression in female genital tract CSs. The study group was comprised of 36 patients with CSs originating from the uterus (n=31), cervix (n=3) and ovary (n=2), as well as 3 metastatic tissues. p53 was overexpressed in the epithelial component of 23 out of 36 (64%) tumors, and in the mesenchymal component of 20 out of 36 (56%) tumors. In both CS components, there was a significant correlation between p53 overexpression and patient age and ovarian metastases. Ki-67 overexpression was detected in the epithelial component in 15 out of 36 (42%) cases, and in the mesenchymal component in 13 out of 36 (36%) neoplasms. There was a significant correlation of p53 overexpression between the carcinomatous and sarcomatous components (R=0.884, P<0.001). A significant correlation was also found in Ki-67 immunoreactivity between the two CS components (R=0.676, P<0.001). However, p53 overexpression was not correlated with Ki-67 immunostaining in both tumor components. In conclusion, based on immunohistochemical results, p53 was overexpressed in more than half of the female genital tract CSs included in the present study, either at the epithelial or mesenchymal component. The correlation between p53 or Ki-67 overexpression in both tumor components supports the combination theory of histogenesis in the majority of these tumors.