To investigate the relationship between aberrant promoter CpG islands methylation status of secreted frizzled related protein 1 (SFRP1) and long intersper sed nuclear element 1 (LINE1) gene and clinicopathologic parameters to determine their prognosis value for hepatocellular carcinoma (HCC).

To construct a cDNA phage expression library for human esophageal cancer cells.

To investigate the expression and clinical significance of microRNA-218(miR-218)in human cervical cancer and the effects ofmiR-218 on proliferation, cell apoptosis and invasion of HeLa cells.

To investigate the expressions of Livin and phosphate and tension homology deleted on chromsome ten (PTEN) protein in the cancerous tissues of ovary endometriosis.

To analyze the correlation between the expression of PTEN and LKB1 in non-small cell lung cancer (NSCLC).

To analyze the cellular function of the newly discovered DNA damage repair factor WDR70, and investigate the mutation in ovarian cancer to verify if function loss of the WDR70gene was associated with ovarian cancer.

To investigate the influence of interferon-alpha-2b (IFN-α2b) with JAK2 kinase, COX-2 and microvessel density in patients of MPN and the relation of JAK2V617F and COX-2 in human erythroleukemia cell line (HEL) cells.

To study the expression levels of tumor suppressor gene RIKP and miRNA224 in esophageal squamous cell carcinoma (ESCC) tissues. To determine whether miRNA224 targets RKIP and the methylation status of miRNA224 gene promoter region in esophageal carcinoma.

To study the regulation to colon cancer cellular biological properties through miR-18a targeting ataxia-telangiectasia mutated gene (ATM).

Objectives: The present study aims to investigate the interest of young adults in predictive oncological genetic testing and their willingness to pay for such a test. Furthermore, major determinants of the 2 variables of interest were identified. Methods: 348 students of economics from the Leibniz University of Hanover were queried in July 2013 using an extensive questionnaire. Among other things, the participants were asked if they are interested in information about the probability to develop cancer in the future and their willingness to pay for such information. Data were analysed using descriptive statistics and ordinal probit regressions. Additionally marginal effects were calculated. Results: About 50% of the students were interested in predictive oncological genetic testing and were willing to pay for the test. Moreover, the participants who were willing to pay for the test partly attach high monetary values to the information that could so be obtained. The study shows that the interest of the students and their willingness to pay were primarily influenced by individual attitudes and perceptions. Conclusions: The study proves that young adults were interested in predictive genetic testing and appreciate information about their probability of develop cancer someday.

Immunoglobulin G (IgG) has been implicated in the progression of various cancers. This study explored the role of IgG in the proliferation, apoptosis, cell cycle and in vitro invasive properties of LNCaP prostate cancer cells. We used IGHG1 small interfering RNA to silence IgG1 expression in LNCaP cells. The efficacy of IgG1 gene knockdown was confirmed using qPCR and western blotting. The colony formation, proliferation, migration and invasion abilities of LNCaP cells after transfection were assessed using colony-forming, flow cytometry and transwell assays. The expressions of PCNA and caspase-3 proteins in LNCaP cells after transfection were detected with immunofluorescence staining and western blotting. IgG1 silencing significantly decreased the colony formation, survival, cell cycle progression, migration and invasion of LNCaP cells (p < 0.05). IgG1 silencing also reduced the amount of the proliferation marker PCNA and induced formation of the apoptotic marker caspase-3 (p < 0.05). Our results show that IgG1 produced by LNCaP cells confers advantages for tumor cell survival, proliferation, migration and invasion, suggesting that IgG1 is a potential target for prostate cancer treatment.

Long non-coding RNAs (lncRNAs) play critical and complicated roles in the regulation of various biological processes, including chromatin modification, transcription and post-transcriptional processing. Interestingly, some lncRNAs serve as miRNA "sponges" that inhibit interaction with miRNA targets in post-transcriptional regulation. We constructed a putative competing endogenous RNA (ceRNA) network by integrating lncRNA, miRNA and mRNA expression based on high-throughput RNA sequencing and microarray data to enable a comparison of the SHEE and SHEEC cell lines. Using Targetscan and miRanda bioinformatics algorithms and miRTarbase microRNA-target interactions database, we established that 51 miRNAs sharing 13,623 MREs with 2260 genes and 82 lncRNAs were involved in this ceRNA network. Through a biological function analysis, the ceRNA network appeared to be primarily involved in cell proliferation, apoptosis, the cell cycle, invasion and metastasis. Functional pathway analyses demonstrated that the ceRNA network potentially modulated multiple signaling pathways, such as the MAPK, Ras, HIF-1, Rap1, and PI3K/Akt signaling pathways. These results might provide new clues to better understand the regulation of the ceRNA network in cancer.

Determination of the role of insulin-like growth factor (IGF) family components in carcinogenesis of several human tumors is based on numerous epidemiological and pre-clinical studies, experiments in vivo and in vitro and on attempts at application of drugs affecting the IGF axis. Investigative hypotheses in original studies were based on biological functions manifested by the entire family of IGF (ligands, receptors, linking proteins, adaptor molecules). In the context of carcinogenesis the most important functions of IGF family involve intensification of proliferation and inhibition of cell apoptosis and effect on cell transformation through synthesis of several regulatory proteins. IGF axis controls survival and influences on metastases of cells. Interactions of IGF axis components may be of a direct or indirect nature. The direct effects are linked to activation of PI3K/Akt signaling pathway, in which the initiating role is first of all played by IGF-1 and IGF-1R. Activity of this signaling pathway leads to an increased mitogenesis, cell cycle progression, and protection against different apoptotic stresses. Indirect effects of the axis depend on interactions between IGF and other molecules important for cancer etiology (e.g. sex hormones, products of suppressor genes, viruses, and other GFs) and the style of life (nutrition, physical activity). From the clinical point of view, components of IGF system are first of all considered as diagnostic serous and/or tissue biomarkers of a given cancer, prognostic factors and attractive target of modern anti-tumor therapies. Several mechanisms in which IGF system components act in the process of carcinogenesis need to be clarified, mainly due to multifactorial etiology of the neoplasms. Pin-pointing of the role played in carcinogenesis by any single signaling pathway remains particularly difficult. The aim of this review is to summarize the current data of several epidemiological studies, experiments in vitro and on animal models, to increase our understanding of the complex role of IGF family components in the most common human cancers.

Human papillomaviruses (HPVs) are the causative agents of 5% of all human cancers, with cervical cancer being the most important. Two viral oncoproteins, E6 and E7, are essential for the development and maintenance of malignancy. Both proteins function by targeting critical pathways that are essential for maintaining cellular homeostasis. As a consequence of these activities, this produces an environment that is favourable for the normal viral life cycle, but when perturbed, can result in the initiation of changes to the host cell, which ultimately results in the development of a malignancy. In this review we discuss the role of these different functions of the viral oncoproteins during the viral life cycle and carcinogenesis, with an emphasis on how induction of DNA damage by the viral oncoproteins, in conjunction with the stem like nature of the target cells, can ultimately result in the development of cancer.

Laron syndrome (LS) is a unique model of congenital IGF-I deficiency. It is characterized by dwarfism and obesity, and is caused by deletion or mutations of the growth hormone receptor (GH-R) gene. It is hypothesized that LS is an old disease originating in Indonesia and that the mutated gene spread to South Asia, the Middle East, the Mediterranean region and South America.

The insulin-like growth factors (IGFs) system regulates cell growth, differentiation and energy metabolism and plays crucial role in the regulation of key aspects of tumor biology, such as cancer cell growth, survival, transformation and invasion. The current focus for cancer therapeutic approaches have shifted from the conventional treatments towards the targeted therapies and the IGF system has gained a great interest as anti-cancer therapy. The proliferative, anti-apoptotic and transformation effects of IGFs are mainly triggered by the ligation of the type I IGF receptor (IGF-IR). Thus, aiming at developing novel and effective cancer therapies, different strategies have been employed to target IGF system in human malignancies, including but not limited to ligand or receptor neutralizing antibodies and IGF-IR signaling inhibitors. In this review, we have focused on the clinical studies that have been conducted targeting the various components of the IGF system for the treatment of different types of cancer, providing a description and the challenges of each targeting strategy and the degree of success.

The most common inactivation mechanism of tumor suppressor genes, RASSF1A and p16INK4a, in lung cancer is hypermethylation. We detected the methylation status of RASSF1A and p16INK4a in serum of lung cancer patients using methylation-specific PCR and analyzed their clinicopathological significance. Each of RASSF1A and p16INK4a hypermethylation was detected in 31.1% cancer patients but not in benign lung lesion patients. Hypermethylation was preferentially observed in small cell lung cancer (SCLC) for RASSF1A (50%), but not for p16INK4a. In non-small cell lung cancer (NSCLC), RASSF1A and p16INK4a hypermethylation were found in 27% and 37.8% respectively. Hypermethylation of RASSF1A was not correlated with clinicopathological character. While, p16INK4a hypermethylation was associated with age >60 years, smoking and squamous cell carcinoma (SCC) (P = 0.033), but not with gender and pathological stages of NSCLC. Sensitivity and specificity of each gene were 31.1% and 100% respectively and the sensitivity improved with evaluation of a combination of the two genes (55.6%). These findings suggest that serum RASSF1A and p16INK4a hypermethylation are promising diagnostic method for detection of lung cancer. As regard the clinicopathological characteristics, p16INK4a hypermethylation may provide a more specific approach than RASSF1A hypermethylation.

Cbp/P300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2) is a pleiotropic protein associated with numerous cell functions, including transcription and differentiation. The role of CITED2 has been investigated in a number of malignancies; however, the roles of this protein in gastric cancers remain unclear. Therefore, we determined the role of CITED2 in gastric cancers.

Recent years have witnessed the discovery of similar gene variations between breast cancer and ovarian cancer, inherited breast and ovarian cancer in particular. A large number of case-control studies have been conducted to explore the association of Methylenetetrahydrofolate Reductase (MTHFR) A1298C polymorphism with breast cancer and/or ovarian cancer risk. However, the results are still inconsistent and inconclusive. Consequently, we performed a meta-analysis to evaluate the association between MTHFR A1298C polymorphism and breast, ovarian cancer risk.