Gastric cancer is the fourth most common form of incident cancer and the second most common cause of cancer death in the world. This malignancy is considered to be poorly treatable, and the surgery that is the mainstay of current treatment carries significant morbidity and mortality. To better treat and prevent this disease, it is important to understand factors that affect its development. p53 tumor suppressor is among the cellular factors that play an important role in the prevention of gastric tumors. Although the p53 protein has been relatively well characterized, less is known about other members of the p53 family, p73 and p63. Accumulating evidence suggest that p73 and p63 significantly affect the p53 activity and function in concert with p53 in regulation of tumorigenesis. Our data suggest that p73 plays an important role in the interaction of gastric epithelial cells with H. pylori, a Gram-negative bacterial pathogen that is a prominent risk factor for the development of gastric cancer.
We aim to delineate the role of the p53 protein family in the development of gastric tumor using mouse models and other in vitro and in vivo approaches. These comprehensive studies may provide new avenues for the development of novel prognostic and therapeutic targets.
Gastric cancer is the second most common cause of cancer death in the world. Despite recent advances in treatment of this disease, gastric cancer remains to be a serious health problem. Our research analysis may provide valuable information on the mechanisms of development of this disease and its potential treatment.
|Horvat, Andela; Zaika, Alexander I (2017) How does bacterial pathogen Helicobacter pylori control responses to cellular stress? Future Microbiol 12:105-108|
|Zaika, Alexander I (2015) Bacterial Pathogen Helicobacter pylori: A Bad AKTor Inhibits p53 Protein Activity [corrected]. Dig Dis Sci 60:822-3|
|Bhardwaj, Vikas; Noto, Jennifer M; Wei, Jinxiong et al. (2015) Helicobacter pylori bacteria alter the p53 stress response via ERK-HDM2 pathway. Oncotarget 6:1531-43|
|Zaika, Alexander I; Wei, Jinxiong; Noto, Jennifer M et al. (2015) Microbial Regulation of p53 Tumor Suppressor. PLoS Pathog 11:e1005099|
|Wei, Jinxiong; Noto, Jennifer M; Zaika, Elena et al. (2015) Bacterial CagA protein induces degradation of p53 protein in a p14ARF-dependent manner. Gut 64:1040-8|
|Peng, DunFa; Hu, TianLing; Soutto, Mohammed et al. (2014) Glutathione peroxidase 7 has potential tumour suppressor functions that are silenced by location-specific methylation in oesophageal adenocarcinoma. Gut 63:540-51|
|Sehdev, Vikas; Katsha, Ahmed; Ecsedy, Jeffrey et al. (2013) The combination of alisertib, an investigational Aurora kinase A inhibitor, and docetaxel promotes cell death and reduces tumor growth in preclinical cell models of upper gastrointestinal adenocarcinomas. Cancer 119:904-14|
|Zaika, Elena; Bhardwaj, Vikas; Wei, Jinxiong et al. (2013) Proinflammatory cytokines and bile acids upregulate ?Np73 protein, an inhibitor of p53 and p73 tumor suppressors. PLoS One 8:e64306|
|Peng, Dunfa; Belkhiri, Abbes; Hu, Tianling et al. (2012) Glutathione peroxidase 7 protects against oxidative DNA damage in oesophageal cells. Gut 61:1250-60|
|Sehdev, Vikas; Peng, DunFa; Soutto, Mohammed et al. (2012) The aurora kinase A inhibitor MLN8237 enhances cisplatin-induced cell death in esophageal adenocarcinoma cells. Mol Cancer Ther 11:763-74|
Showing the most recent 10 out of 19 publications