• ATDC gene as a novel prognostic marker for the treatment of pancreatic ductal adenocarcinoma: A review Study
  • Ali Karimzadeh,1,*
    1. Student Research Committee, Urmia University of Medical Sciences, Urmia, Iran


  • Introduction: Introduction: Pancreatic cancer is the 7th leading cause of cancer in developed countries. The Mortality/Incidence ratio is 98% and because it’s generally diagnosed in the advanced state the overall five-year survival rate is 6%. Pancreatic ductal adenocarcinoma (PDAC) is the prevalent form of pancreatic cancer which develops by acinar-ductal metaplasia and neoplastic precursor lesions. So there is a necessity to find novel targets to enhance treatment of PDAC. Ataxia-telangiectasia group D complementing gene (ATDC), also called TRIM29 is a cancer associated gene which is overexpressed in numerous cancer types such as bladder, lung, ovarian and gastric cancer. According to the research, ATDC regulates the proliferation, metastasis and radioresistance of pancreatic cancer cells. This review study discusses recent research regarding on the significance and prognostic value of ATDC in PDAC.
  • Methods: Methods: In the present review, we conducted a comprehensive review of the published literatures by searching International valid databases such as PubMed, Scopus, Science Direct and Google scholar. For all relevant papers published until 2018 according to the following terms: ATDC, TRIM29 and Pancreatic Ductal Adenocarcinoma.
  • Results: Results: Research showed that ATDC is expressed 4.7 fold higher in pancreatic cancer stem cells (CSCs) compared to differentiated cancer cells and causes resistance to radiation and chemotherapy. Patients with positive ATDH expression showed shorter overall survival rate and shorter recurrence-free survival rate than those with negative ATDH expression. The relationship between protein expression with lymph node metastasis (p=0.019) was significant whereas It was not statistically significant with other factors, such as age, gender, histologic differentiation and local invasion. ATDC increased cancer cell proliferation in vitro and improved tumor growth and metastasis in vivo. It functions by activating beta–catenin signaling and up-regulation of CD44, resulting in EMT and an invasive phenotype throughout cancer progression.
  • Conclusion: Conclusion: Cancer is one of the most common causes of death. Prevention in the early stages is effective in reducing mortality, which requires research into related biomarkers. Our findings indicated that ATDC is overexpressed in malignant pancreatic ducts and such expression is an independent prognostic marker in patients with PDAC. Knockdown of ATDC notably suppresses pancreatic cancer cell growth and motility in vitro. These data suggest that ATDC promotes tumor progression and can be a potential target of curative intervention in PDAC.
  • Keywords: Pancreatic Ductal Adenocarcinoma , ATDC , TRIM29