Thus, the potential benefits of DFO to the treatment of head and neck tumor remains to be tested in human. In conclusion, our study provided the evidence that DFO administration could protect salivary glands from radiation damage in a mice model. The improvement in function of salivary glands is accompanied with reduced apoptotic acinar cells, enhanced angiogenesis and more survived Sca-1+ salivary stem cells. The potential of our finding as an alternative therapeutic approach to WZ8040 side effects prevent radiation-induced dysfunction of salivary glands in clinical application deserves more investigation in future. Globally, gastric cancer is currently the fourth most common malignancy and the second leading cause of cancer mortality. More new cases of GC are diagnosed in China each year than in any other country. The incidence of GC has declined over time, due to improving living standards, improvements in early diagnosis, advanced surgical techniques and combined therapy. However, distant metastasis and local recurrence cannot be avoided easily in most cases, and the prognosis of GC patients remains far from satisfactory. Tumorigenesis of GC has been considered a multifactorial and multistep process that involves the activation of oncogenes and the inactivation of tumor suppressor genes at different stages. Further understanding of these alterations and the molecular mechanisms involved in gastric carcinogenesis will be critical for improved diagnosis, therapy and prognosis of GC. Protein tyrosine phosphatases are signaling molecules that regulate a variety of cellular processes, including cell growth, differentiation, cell cycle and oncogenic transformation. The constitutive activation of PTPs signaling pathways is a biochemical hallmark of cancer. This is mostly occurs via activation of tyrosine kinase receptors, such as amplification of HER2/Neu and mutations of the epidermal growth factor receptor. The protein encoded by the PTPRD gene is one of 38 known human receptor-type PTPs, a group of proteins that are increasingly thought to be important in human neoplasia and cancer progression. The PTPRD gene is located at chromosome 9p23–24.1, a locus frequently lost in neuroblastoma, gliomas, lung cancer and other malignancies. Weir et al. detected homozygous deletions and missense mutations of PTPRD in adenocarcinoma of the colon and lung. David et al. identified frequent deletion and mutation of PTPRD in glioblastoma multiforme and malignant melanoma, and showed that these mutations were inactivating. A recent study showed reduced PTPRD expression in the majority of cell lines and surgical specimens of lung cancer, indicating that PTPRD is a candidate tumor suppressor. These researches suggested that PTPRD might be one of a select group of tumor suppressor genes that are inactivated in a wide range of common human tumor types. However, the role of PTPRD in human gastric adenocarcinoma has not yet been investigated. In the present study, we detected PTPRD expression level in gastric adenocarcinoma using quantitative real-time reverse transcription PCR, western blotting and immunohistochemistry. Meanwhile, prognostic and clinicopathological features of PTPRD were investigated in 513 gastric adenocarcinoma tissue samples.