Gastric cancer as one of the most common cancers worldwide has various genetic and environmental riskfactors including Helicobacter pylori (H.pylori) infection. Recently, loss of a tumor suppressor gene namedpromyelocytic leukemia (PML) has been identified in gastric cancer. However, no mutation has been found in thisgene in gastric cancer samples. Cag A H.pylori protein has been shown to exert post transcriptional regulationof some tumor suppressor genes. In order to assess such a mechanism for PML degradation, we performed insilico analyses to establish any interaction between PML and Cag A proteins. In silico interaction and dockingstudies showed that these two proteins may have stable interactions. In addition, we showed that imatinib kinaseinhibitor can restore PML function by inhibition of casein kinase 2.
(2015). In Silico Interaction and Docking Studies Indicate a New Mechanism for PML Dysfunction in Gastric Cancer and Suggest Imatinib as a Drug to Restore Function. Asian Pacific Journal of Cancer Prevention, 16(12), 5005-5006.
MLA
. "In Silico Interaction and Docking Studies Indicate a New Mechanism for PML Dysfunction in Gastric Cancer and Suggest Imatinib as a Drug to Restore Function". Asian Pacific Journal of Cancer Prevention, 16, 12, 2015, 5005-5006.
HARVARD
(2015). 'In Silico Interaction and Docking Studies Indicate a New Mechanism for PML Dysfunction in Gastric Cancer and Suggest Imatinib as a Drug to Restore Function', Asian Pacific Journal of Cancer Prevention, 16(12), pp. 5005-5006.
VANCOUVER
In Silico Interaction and Docking Studies Indicate a New Mechanism for PML Dysfunction in Gastric Cancer and Suggest Imatinib as a Drug to Restore Function. Asian Pacific Journal of Cancer Prevention, 2015; 16(12): 5005-5006.
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