Abstract
Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer mortality. Although advances have been made in understanding the pathogenesis of PDAC, the outcome still remains poor. The aim of this study is to conduct a meta-analysis to evaluate the precise association between SMAD4 loss and clinicopathological significance in PDAC. A literature search was made in PubMed, Web of Science, Google scholar, and EMBASE for related publications. The data were extracted and assessed by two reviewers independently. Analysis of pooled data was performed, Odds Ratio or Hazard Ratio with corresponding confidence intervals was calculated and summarized. 12 relevant articles were included for full review in detail and meta-analysis. The frequency of SMAD4 protein loss was significantly increased in PDAC than in nonmalignant pancreatic tissue, Odd Ratio was 0.05 with 95% confidence interval 0.01-0.23, p<0.0001. SMAD4 loss was significantly associated with poor overall survival in patients with PDAC, Hazard Ratio was 0.61 with 95% confidence interval 0.38-0.99, p=0.05. SMAD4 loss was not correlated with the size, grades, and lymph node metastasis of PDAC. In conclusion, SMAD4 is a biomarker for the diagnosis of PDAC. SMAD4 loss is significantly related to poor prognosis in patients with PDAC.
Highlights
Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer mortality
SMAD4 was known as the deleted in pancreatic carcinoma 4 (DPC4), is located on chromosome 18q21 [4,5]
The rate of SMAD4 protein loss was significantly higher in PDCA than in nonmalignant pancreatic tissue, Odds ratios (OR) was 0.05 with 95% CI 0.01-0.23, z=3.97, p
Summary
Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer mortality. Because of a lack of specific symptoms and appropriate markers for early stages, most PDAC patients are diagnosed at advanced stages, when radical pancreatic resection is not possible. SMAD4 is a co-factor that facilitates gene transcription and tumor suppression through the TGF-beta signaling pathway. TGF-beta/SMAD4 signaling pathway regulates tumor development through mediating growth arrest and inducing apoptosis [5,6,7,8,9,10,11]. Previous studies have attempted to correlate the alteration of SMAD4 with clinical features and prognosis in patients with PDAC [12,13,14,15]. We conducted a meta-analysis to investigate the association of SMAD4 status with clinicopathlogical significance and prognosis in patients with PDAC
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