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Showing 3 results for Esophageal Neoplasms
Comparison of Serum Strontium and Antimony Levels in Patients with Esophageal Cancer and Healthy People
Shima Akbari Rad , Hamid Reza Joshaghani, Masoud Khoshnia , S.mehran Hosseini ,
Volume 10, Issue 4 (7-2016)
Abstract

ABSTRACT

       Background and Objective: Esophageal cancer is the third most common type of cancer in Iran. Studies on water, soil, grains, waste and sediments in Golestan Province have shown that the environmental concentrations of antimony and strontium are increased in areas with high incidence rate for cancer. The carcinogenic effects of strontium have been reported, but carcinogenicity of antimony is still unclear. Since there is not enough information regarding the relationship between the concentration of strontium and antimony and prevalence of esophageal cancer in the province, this study aimed to evaluate serum levels of these elements in patients with esophageal cancer using atomic absorption spectroscopy.

       Methods: This study was performed on 30 patients with esophageal squamous cell carcinoma and 30 healthy matched controls. After sampling, concentrations of strontium and antimony were measured using atomic absorption spectroscopy.

       Results: Half of the esophageal cancer patients and control participants were male. The mean age of patients and controls was 66 ± 13 and 64 ± 8 years, respectively. The mean serum concentration of strontium in patients and controls was 24.18 ± 1.62 and 24.08 ± 1.46 μg/L, respectively. The mean serum concentration of antimony in patients and controls was 18.61 ± 1.48 and 18.98 ± 1.93 μg/L, respectively. No statistically significant difference was observed between the serum concentrations of the two elements in patients and controls.

        Conclusion: There is no difference between serum levels of strontium and antimony in cancer patients and healthy controls, which could be due to tissue accumulation.

          Keywords: Antimony, Strontium, Esophageal Neoplasms.


Docetaxel Toxicity Optimization in Esophageal Squamous Cell Carcinoma Cell Line YM-1: A Study of Cell Cycle and Doubling Time Effect
Boshra Haghi, Marie Saghaeian Jazi, Mahdi Zarie, Ayyoob Khosravi, Mahboubeh Tajaldini, Jahanbakhsh Asadi,
Volume 15, Issue 2 (3-2021)
Abstract
Background and objectives: Docetaxel is a chemotherapeutic agent commonly used for treatment of many cancers, including esophageal squamous cell carcinoma. Docetaxel induces G2/M phase cell cycle arrest and ultimately cell death. In this study, we aimed to assess the effects of docetaxel on YM1 cells considering exposure time and dose.
Methods: After calculating the doubling time of YM1 cells, the anti-proliferative effect of different concentrations of docetaxel () [A1]  after 24, 48 and 72 hours was assessed by the standard colorimetric assay. In addition, the effect of docetaxel on cell cycle was evaluated by flow cytometry.
Results: The results showed that docetaxel toxicity was not significant until 24 hours at the tested concentrations (P>0.05). In addition, the effect of docetaxel on the cells was time-dependent at all tested concentrations. Overall, the duration of exposure to docetaxel had more significant role in docetaxel toxicity in YM1 cells compared to concentration.
Conclusion: Our findings suggest that the cytotoxicity of docetaxel on YM1 cells is time-dependent.
 [A1]Please write the concentrations

High Dose of 3, 7-Dimethyl-1-Propargylxanthine Induces Cell Death in YM-1 and KYSE30 Cancer Cell Lines
Parisa Zeinali, Marie Saghaeian, Jahanbakhsh Asadi, Seyyed Mehdi Jafari,
Volume 16, Issue 5 (9-2022)
Abstract
Background and objectives: Activation of adenosine A2a receptor has been shown to induce the growth and metastasis of cancer cells. The role of this receptor in esophageal cancer has not yet been determined. The present study aimed to investigate effects of an adenosine A2a receptor antagonist (3, 7-dimethyl-1-propargylxanthine) on growth of esophageal cancer cells.
Methods: Real-time polymerase chain reaction was performed to evaluate mRNA expression of the A2a adenosine receptor in KYSE-30 and YM-1 esophageal cancer cell lines. Effects of the antagonist on viability of the cells were evaluated by MTT assay.
Results: At low concentrations, the antagonist had no effect on cell viability. However, at concentrations ≥200 μM, the antagonist significantly reduced viability of both cell lines (p<0.05).
Conclusion: The results of this study indicate that the adenosine A2a receptor antagonist exerts inhibitory effects on KYSE30 and YM-1 cancer cells in a dose-dependent manner. Therefore, the use of this antagonist can be exploited as a therapeutic target for the treatment of esophageal cancer.
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