Abstract
Gastric cancer is one of the most common lethal malignancy in global and survival mainly depends on prognosis. Sister Chromatid Exchanges (SCEs) assay is a very sensitive method of detecting chromosome fragility. The aim of our study was to determine the chromosomal fragility of gastric cancer patients in vitro. Samples from 32 gastric cancer patients and 12 healthy donors were controlled. Cancer patients lymphocytes’ genome is highly fragile as treatment of the cell cultures with MMC caused a statistically significant increase of the mean SCEs frequency (p<0.01). Also, so simultaneous as MMC-induced SCEs frequency of gastric cancer patients was statistically significant (p<0.01) higher compared to the healthy donors. PRI and MI of treated with MMC and untreated lymphocytes of gastric cancer patients were significantly (p<0.01) lower than that of healthy donors. These results suggest that peripheral lymphocyte chromosomes of cancer patients are highly fragile and alkyliotic agents increase their fragility.
Highlights
Gastric cancer is the third most common malignancy worldwide and the second most common cause of cancer related mortality (Parkin et al, 2001)
Values in baseline of each column are the mean values for each in vitro treatment of chromosome preparations derived from the two groups examined, the gastric cancer patients and the healthy donors
After MMC treatment the PRI value of lymphocyte cultures derived from gastric cancer patients significantly (p
Summary
Gastric cancer is the third most common malignancy worldwide and the second most common cause of cancer related mortality (Parkin et al, 2001). Gastric cancer as all other types of cancer is the result of multiple genetic abnormalities accumulated during the process of carcinogenesis. The molecular mechanism of multi-step carcinogenesis is poorly understood (Vogelstein and Kinzler, 2004; Yasui et al, 2001). It has been shown that the development of gastric cancer is a multi-step process starting from chronic gastritis passing to atrophy, intestinal mataplasia, dysplasia and to invasive cancer (Pasechnikov et al, 2004; Testino, 2004). Many genes polymorphisms have been proposed to be implicated in gastric cancer, such as TLR gene cluster of Toll-like receptor, Igk gene and p53 (Hu et al, 2008; Etokebe et al, 2009; Ke-Xiang et al, 2012)
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