title: Comprehensive analysis of the percentage of surface receptors and cytotoxic granules positive natural killer cells in patients with pancreatic cancer, gastric cancer, and colorectal cancer.
abstract: BACKGROUND
  Digestive malignancies, especially pancreatic cancer (PC), gastric cancer (GC), and colorectal cancer (CRC), still occur at persistently high rates, and disease progression in these cancers has been associated with tumor immunosurveillance escape. Natural killer (NK) cell dysfunction may be responsible for this phenomenon, however, the exact relationship between tumor immunosurveillance escape in digestive malignancies and NK cell dysfunction remains unclear.
  
  
  METHODS
  Percentage of the surface receptors NKG2A, KIR3DL1, NKG2D, NKp30, NKp44, NKp46, and DNAM-1, as well as the cytotoxic granules perforin and granzyme B positive NK cells were determined in patients with pancreatic cancer (n=31), gastric cancer (n=31), and CRC (n=32) prior to surgery and healthy controls (n=31) by multicolor flow cytometry. Independent t-tests or Mann-Whitney U-tests were used to compare the differences between the patient and healthy control groups, as well as the differences between patients with different pathologic features of cancer.
  
  
  RESULTS
  Percentage of NKG2D, NKp30, NKp46, and perforin positive NK cells was significantly down-regulated in patients with PC compared to healthy controls, as well as GC and CRC; reduced levels of these molecules was associated with indicators of disease progression in each malignancy (such as histological grade, depth of invasion, lymph node metastasis). On the contrary, percentage of KIR3DL1 positive NK cells was significantly increased in patients with PC, as well as GC and CRC, but was not associated with any indicators of disease progression.
  
  
  CONCLUSIONS
  Altered percentage of surface receptors and cytotoxic granules positive NK cells may play a vital role in tumor immunosurveillance escape by inducing NK cell dysfunction in patients with PC, GC, and CRC.
authors.forename: Yun-Peng
authors.initials: YP
authors.lastname: Peng
authors.forename: Yi
authors.initials: Y
authors.lastname: Zhu
authors.forename: Jing-Jing
authors.initials: JJ
authors.lastname: Zhang
authors.forename: Ze-Kuan
authors.initials: ZK
authors.lastname: Xu
authors.forename: Zhu-Yin
authors.initials: ZY
authors.lastname: Qian
authors.forename: Cun-Cai
authors.initials: CC
authors.lastname: Dai
authors.forename: Kui-Rong
authors.initials: KR
authors.lastname: Jiang
authors.forename: Jun-Li
authors.initials: JL
authors.lastname: Wu
authors.forename: Wen-Tao
authors.initials: WT
authors.lastname: Gao
authors.forename: Qiang
authors.initials: Q
authors.lastname: Li
authors.forename: Qing
authors.initials: Q
authors.lastname: Du
authors.affiliation: Department of General Surgery, The first Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, People's Republic of China. miaoyi@njmu.edu.cn.
authors.forename: Yi
authors.initials: Y
authors.lastname: Miao
mesh_terms: D015179:Colorectal Neoplasms / Q000378:metabolism*; D003594:Cytoplasmic Granules / Q000378:metabolism*; D005260:Female; D006801:Humans; D007694:Killer Cells, Natural / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D010190:Pancreatic Neoplasms / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism*; D013274:Stomach Neoplasms / Q000378:metabolism*
chemical_list: D011956:Receptors, Cell Surface