Blocking the functional domain of TIP1 by antibodies sensitizes cancer to radiation therapy.

Non-small-cell lung cancer (NSCLC) and glioblastoma (GB) have poor prognoses. Discovery of new molecular targets is needed to improve therapy. Tax interacting protein 1 (TIP1), which plays a role in cancer progression, is overexpressed and radiation-inducible in NSCLC and GB.

Organochlorine pesticides induce epithelial as well as inflammatory mediators following exposure to human ovarian surface epithelial cells: An in vitro study.

Although studies have suggested organochlorine pesticides (OCPs) exposure increased the risk of epithelial ovarian cancer, the mechanisms underlying its potential tumorigenic effects in the human ovary are not well understood. In this study, we investigated the impact of dichlorodiphenyldichloroethylene (DDE), endosulfan, and heptachlor exposure on epithelial cadherin (E-cadherin) and proinflammatory mediators in human ovary surface epithelial (HOSE) cells. We found that DDE, endosulfan, and heptachlor exposure resulted in epithelial differentiation accompanied by upregulation of E-cadherin expression and overexpression of proinflammatory cytokines (TNFα, IL-1β, and IL-6) in HOSE cells.

Organochlorine pesticides induce inflammation, ROS production, and DNA damage in human epithelial ovary cells: An in vitro study.

Although the etiology of ovarian cancer is not clear, certain factors are implicated in this disease, such as ovulation, gonadotropic and steroid hormones, growth factors, cytokines, environmental agents, etc. Epidemiological studies have proven environmental exposure to pesticides with an increased risk of Epithelial Ovarian Cancer (EOC); however, the molecular mechanism underlying the carcinogenic effects of pesticides in human ovary remains poorly understood. The present study aimed to study the pro-inflammatory response of organochlorine pesticides (OCPs) namely β-hexachlorocyclohexane (β-HCH), dichlorodiphenyldichloroethylene (DDE) and Dieldrin following exposure to human ovary surface epithelial cells (HOSE) for risk prediction of epithelial ovarian cancer.

High Resolution Based Quantitative Determination of Methylation Status of CDH1 and VIM Gene in Epithelial Ovarian Cancer.

Background: DNA promoter methylation is widely explored epigenetic phenomena, known to effect gene expression and further perturbation in cellular homeostasis. Myriad of studies have leveraged promoter methylation and its potential as biomarker for various types of cancer. Aim of present study is to investigate promoter methylation of CDH1 and VIM gene and etiology of epithelial ovarian cancer (EOC).

Delineating Potential Transcriptomic Association with Organochlorine Pesticides in the Etiology of Epithelial Ovarian Cancer.

Background: Recent studies have shown that there is an increased risk of Epithelial Ovarian Cancer (EOC) with Organochlorine Pesticides (OCPs). However, the alteration in the gene expression profile has not been explored so far. The goal of the present study is to understand the probable molecular mechanism of OCPs toxicity towards discovery of dysregulation of signaling pathway associated with differential gene expression and candidate transcriptomic set of markers in the pathophysiology of EOC in OCPs exposed population.