PANC-1 Cell Treatment - Essay Example

PANC cells Pancreatic cancer is one common gastrointestinal tumor having a poor prognosis. The illness has a survival rate of about five years. A phenomena referred to as the Warburg effect shows that the cells of cancer display enhanced glucose that is converted to lactate and preferentially ensure the metabolisation of glucose to satisfy their demand of energy. This is true even for cases where there exist some adequate oxygen level. This effect shows that the cancer cells have minimum depended on oxygen and their own satisfaction using adequate energy. In patients who go through the resection and have the free margins of tumor, the reported 5-year rate of survival can only be between ten to twenty five percent (Ke, Wang, Xu, and Abassi, 2011). Whenever the pancreatic cancer turns to be metastatic, it becomes uniformly fatal having an overall survival of approximately six months from the time of diagnosis (Blackburn, Vay Liang, and Milner, 2011). For the past thirty years a combined method of radiotherapy, surgery, and chemotherapy have been applied in treating pancreatic cancer (Mani, Guo, & Liao, 2008). However, there has been no huge improvement in the rate of survival. This means that a powerful therapeutic method is required. In attempts of obtaining an appropriate therapeutic strategy for pancreatic cancer, this paper investigates the effect of caffeine on the PANC-1 cells. Pancreatic Cancer is one of the leading causes of deaths in world. Even with recent efforts to come up with modalities, the rate of mortality remains being high. Caffeine can be used in treating this illness, even though the molecular mechanisms of the agents are not understood fully. This is, to some extent, responsible for the failing of these agents in treating pancreatic cancer. In a study conducted in this field, PANC –1 mutant p53 was used in investigating the influence of caffeine on the growth of cells and the effect on cell modulation cycle and the gene apoptosis relation (Rückert, Werner, & Aust, 2012). The extraction of proteins from these cells was treated 4 mM of Caffeine was put to a western blot analysis. The cells of drug treating were analyzed for the calculation of the number of those cells that experience apoptosis. In the observation, the study found out the time and dose dependent inhibition of growth was seen in the PANC cells after the treatment with caffeine (Mani, Guo, & Liao, 2008). The analysis by the western blot displayed an up regulation of the p21WAF1 in the cell lines that were treated with caffeine. In addition, the treatment y caffeine led to the cyclin B down regulation without any detection of the cdk1 protein (Kim, and Gallick, 2008). The analysis of the apoptotic cell displayed an increasing quantity of cells that goes through the apoptosis in the 24th and 48th hour of treatment with caffeine. As reported in earlier studies, the p21WAF1 and the cyclin down regulation suggested a possibility of G2/M cycle arrest resulting from the caffeine. This study concluded that differential molecular changes seen in such a study could establish the cellular influence of the agents on the PANC-1 cells. This means that the chemotherapeutic agents may be influenced by the endogenous p53 mutation status determining the therapeutic effects of the agents in treating pancreatic cancer. Other studies conducted in this field have reported that a the caffeine drinkers take in over three cups of coffee each day having a more risk of pancreatic cancer of about 2.7 than with the other non coffee drinkers (Blackburn, Vay Liang, and Milner, 2011; Arumugam, Ramachandran, & Fournier, 2009 ). This has, for decades stimulated a link between the consumption of coffee and pancreatic cancer. Another cohort study involving one hundred and ten thousand Japanese participants showed that a heavy consumption of caffeine could increase the pancreatic cancer risk. Other studies have concluded that there is no association between these two (Wang, Li, & Kong, 2009; Rückert, Werner, & Aust, 2012). A clear reported confounder in the conducted studies could be the smoking of cigarette, since not all the studies had this factor as a control and the self reporting of the participants is not accurate (Arumugam, Ramachandran, & Fournier, 2009). A case control study involving the Spanish participants showed a link between the consumption of coffee and the mutations of K-ras (Arumugam, Ramachandran, & Fournier, 2009). In about 121 cases, the mutations of K-ras were extremely common in those tumors affecting the regular drinkers of coffee in comparison to the coffee drinkers who are non regular (Wang, Li, & Kong, 2009). The mutated tumor odds were increased in a linear form with high levels of the consumption of coffee. However, this study did not show whether caffeine, different components of coffee, or the different factors for which the drinkers of coffee are associated could activate the K-ras modulus. In many cases, the components of coffee can inhibit or induce pathways of relevant metabolism, which take part in the inactivation or activation of the molecules of carcinogen (Kim, and Gallick, 2008). On the other hand, such components could inhibit the repair mechanism of DNA. A different study done in Califonia failed to display a significant link between K-ras pattern of mutation or the staining of p53 and the drinking of coffee. The key limitation of this study was the idea that the used questionnaire made an average of the coffee consumption habits a year before the diagnosis. This means that the study failed to capture the required etiology for the period exposed. Even these studies display inconsistent results, and the underlying mechanism of association between diet and K-ras cannot be understood, the studies display the ability to identify the relevant nutrient of gene interaction within the pancreatic cancer (Wang, Li, & Kong, 2009; Rückert, Werner, & Aust, 2012). Inhibiting the tumorigenesis in animals that are modeled by black, or green preparation of tea, has been shown in many organ targets like lung, skin, esophagus, oral cavity, pancreas and mammary glands. The epidemiology studies fail to be clear concerning the protective effects of consuming tea and formation of cancer in humans (Blackburn, Vay Liang, and Milner, 2011). Few studies have reported an inverse link between the consumption of tea and the pancreatic cancer for the humans. A study done in Shanghai showed a reduced risk of pancreatic cancer in women and men having a consistence consumption of tea (Arumugam, Ramachandran, & Fournier, 2009). This was similar to a study conducted in Lowa, which showed no link between the intake of tea and pancreatic cancer cases (Blackburn, Vay Liang, and Milner, 2011). Another study conducted in this field reported that EGCG (major component of polyphenol found in green tea) stops the growth of about three cells lines of pancreatic carcinoma in a manner that is dose depended (Arumugam, Ramachandran, & Fournier, 2009). Further, the study added that green and black tea extracts and the extracts components to establish their link to the cells of tumor. Other similar studies of a polyphenol mixture and of thenaflavins obtained out of black tea, and components of purification of EGCG and ECG ( Epicate chin-3-gallate ) (Ke, N., Wang, Xu, and Abassi, 2011; Arumugam, Ramachandran, & Fournier, 2009). The results of this stud displayed the cell growth inhibition in the pancreatic cost. MF and GTP significantly influence the growth of the PANC-1 cells (Blackburn, Vay Liang, and Milner, 2011). The promotion of tumor and pancreatic carcinogenesis was inhibited in two models of hamster with the green tea feeding extracts displaying a vivo effect. Combining the green tea with polyphenols and palm carotene, the similar effect was observed in the diminishing preneoplastic lesions of the pancreas and the epithelial duct hyperplasia (Blackburn, Vay Liang, and Milner, 2011). References Blackburn, G., Vay Liang, W., and Milner, J., 2011. Nutritional Oncology. New York: Oxford publishers. Arumugam, T., Ramachandran, V., & Fournier, K., 2009. Mesenchymal epithelial transition contributes to resistance of drug in pancreatic cancer. Cancer Res. 69:5820–5828. Wang, Z., Li, Y., & Kong, D., 2009. Epithelial-mesenchymal acquisition of transition phenotype of gemcitabine-resistant pancreatic cells of cancer linked with activation of the notch signaling pathway. Cancer Res. 69:2400–2407. Kim, M., and Gallick, G., 2008. The Gemcitabine resistance of the pancreatic cancer: picking the key players. Clin Cancer Res. 14:1284–1285. Mani, S., Guo, W., & Liao, M., 2008. The transition of epithelial-mesenchymal generates cells with properties of stem cells. Cell. 133:704–715. Rückert, F., Werner, K., & Aust, D., 2012. Analysis of Immunohistological six new primary pancreatic adenocarcinoma cell lines. Global J Biochem. 3:11 Ke, N., Wang, X., Xu, X and Abassi,Y., 2011. The xCELLigence system for labelfree and realtime - monitoring of cell viability. Methods Mol Biol. 740:33–43. Read More