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05). Furthermore, western blotting analyses also confirmed that the protein expression levels of HIF-1α and VEGF were increased after miR-200a overexpression.

MiR-200a facilitates the proliferation of CC cells and activates the HIF-1α/VEGF signaling pathway by targeting EGLN1.

MiR-200a facilitates the proliferation of CC cells and activates the HIF-1α/VEGF signaling pathway by targeting EGLN1.

Ovarian cancer is the fifth leading cause of cancer related death in women. Platin-based doublet regimens plus bevacizumab is standard treatment in relapse. Due to formal regulation of Turkish Ministry of Health, adjuvant bevacizumab has not been reimbursed and clinicians can use bevacizumab at a dose of 7.5 mg/kg/3wk in platin-resistant and sensitive relapse settings. The primary aim of this study was to evaluate 7.5 mg/kg/3wk bevacizumab dosing in platin-resistant and sensitive relapse ovarian cancer and compare these findings with the current literature.

A total of 106 patients with relapsed ovarian cancer and treated with bevacizumab (bevacizumab is not reimbursed as a part of adjuvant treatment in Turkey) on their first relapse were included.

At a median follow-up of 32.1 months (5.3-110.8), 56 (52.8%) patients died. Progression-free survival (PFS) and overall survival (OS) were estimated at 18.8 months (14.4-23.3) vs 29.7 months (24.3-35.1) of the whole group overall survival. We observed that 78.owed that 7.5 mg/kg/3week dosing of bevacizumab in relapsed ovarian cancer could have similar effectiveness compared to standard 15 mg/kg/3week dosing. Increase of OS and PFS in patients treated with primary and secondary debulking surgery with no-visible disease was more pronounced. No new safety information was observed but lower rate of grade 3 or above hypertension with similar rate of severe vascular and intestinal complications were detected.

In conclusion, our findings showed that 7.5 mg/kg/3week dosing of bevacizumab in relapsed ovarian cancer could have similar effectiveness compared to standard 15 mg/kg/3week dosing. Increase of OS and PFS in patients treated with primary and secondary debulking surgery with no-visible disease was more pronounced. No new safety information was observed but lower rate of grade 3 or above hypertension with similar rate of severe vascular and intestinal complications were detected.

This study was designed to explore the value of carbohydrate antigen 72-4 (CA72-4) combined with carbohydrate antigen 15-3 (CA153) in diagnosing gynecologic malignancies.

64 patients with ovarian cancer admitted to our hospital from February 2014 to February 2016 comprised the group A; 52 cases of cervical cancer were regarded as group B; 46 cases of endometrial cancer comprised the group C; and 150 cases of healthy women were considered as a control group. The CA72-4 and CA15.3 levels in serum of each group were detected, and receiver operating characteristics (ROC) curve was used to analyze the diagnostic value of CA72-4 and CA15.3 in ovarian, cervical, as well as in endometrial cancer.

CA72-4 and CA15.3 increased dramatically in cancer patients (p<0.001). CA15.3 in group C was higher than in groups A and B (p<0.05). Joint diagnosis of the two had good sensitivity, specificity and area under the curve (AUC) for ovarian, cervical as well as for endometrial cancer (p<0.001). CA72-4 and CA15.3 were closely related to the occurrence of gynecologic malignancies (p<0.001). The results of follow-up revealed that CA72-4 had a higher value in predicting the death of ovarian cancer patients within 3 years, while CA15.3 had a better effect in predicting the death of ovarian and cervical cancer (p<0.05).

CA72-4 and CA15.3 were dramatically higher in ovarian, cervical and endometrial cancer among gynecologic malignancies. Joint detection of the two had better diagnostic value for ovarian and cervical cancer.

CA72-4 and CA15.3 were dramatically higher in ovarian, cervical and endometrial cancer among gynecologic malignancies. Joint detection of the two had better diagnostic value for ovarian and cervical cancer.

Changes in the expression levels of genes involved in cancer cell adhesion and motility have been reported to have an important role in tumor progression. In this study, we aimed to investigate the clinical significance of ITGAV and CALD1 gene expression in epithelial ovarian cancer (EOC), the most lethal gynecological malignancy.

Reverse transcription quantitative polymerase chain reaction was used to evaluate ITGAV and CALD1 expression levels in 47 EOC and 19 benign formalin-fixed paraffin-embedded samples. We used Spearman's test to determine the association between ITGAV and CALD1 expression and Wilcoxon test to compare expression levels between malignant and benign ovarian tumor specimens as well as to determine their association with clinicopathological characteristics of EOC. Survival analysis was done by the Kaplan-Meier method and the log-rank test. P ≤ 0.05 was considered statistically significant.

CALD1 and ITGAV showed significantly lower expression in EOC than in benign ovarian samples (p<0.001). Furthermore, CALD1 was significantly lower expressed in high-grade tumors (p=0.037) while there was a trend for a lower expression of ITGAV in tumors with high histological grade (p=0.043), in tumors with ascites (p=0.055), and in tumors of patients who relapsed (p=0.083). We also found a significant positive association between ITGAV and CALD1 expression (ρ=0.640, p<0.001) in EOC samples. Tasquinimod manufacturer Kaplan-Meier analysis showed no significant impact of ITGAV and CALD1 expression levels on overall survival of EOC patients (p=0.149 and p=0.430, respectively).

Our findings indicate that CALD1 and ITGAV gene expression levels correlate with poor clinicopathological features of the EOC.

Our findings indicate that CALD1 and ITGAV gene expression levels correlate with poor clinicopathological features of the EOC.

Liver cancer or hepatocellular carcinoma (HCC) is considered as one of the most frequent malignancies with significantly high morbidity and mortality across the globe. MicroRNAs (miRs) are regarded as important regulators of liver cancer formation and its development. However, the full biochemical mechanism of their role is still very less understood. The main objective of the current research work was to examine the role of miR-16/cyclin-B1 axis in liver cancer regulation and how this pathway along with liver cancer migration and invasion are targeted by zingiberene molecule.

Quantitative reverse transcriptase polymerase chain reaction was used to evaluate miR-16 expression in HCC cell lines. Western blotting was performed to evaluate the expression of the miR-16 target genes. Effects on cell migration and invasion were evaluated by in vitro wound healing assay and transwell Matrigel assay, respectively. Effects of zingiberene on HCC cell viability were evaluated by MTT assay.

Zingiberene treatment led to downregulation of miR-16 in HepG2 human hepatocellular carcinoma cells, accompanied by induction of G0/G1 cell cycle arrest targeting cyclin B1 as direct target.