To the Editor: Although the causes and mechanisms of lung cancer (LC) are still not clear, with the advances in science and technology and the progress in research methods, it has been shown that tumor cells aggregate with platelets (PLTs) and escape being recognized by the immune system. They adhere to distant vascular endothelial cells and continue to metastasize, invade and grow through the blood circulation.[1] Therefore, the hypercoagulable state and enhancement of PLT functions promote tumor growth, invasion, and metastasis.[2,3] Therefore, the effective reduction in PLT counts and their activities can help reduce the progression and prognosis of LC. We conducted this research to explore the effect of the tumor on circulating platelets in patients with LC. Forty patients with LC (LC group) hospitalized in the 96th Hospital of the People's Liberation Army of China were selected for the study. This study follows relevant ethical regulations and is approved by the Ethics Committee of the 96th Hospital of the People's Liberation Army of China (2016 Number 40, the Jinan Military Region General Hospital). All the patients provided written informed consent. The group included 28 men and 12 women (mean age: 58.08 ± 10.22 years). Among these patients, 12, 26 and 2 had squamous cell carcinoma, adenocarcinoma, and small cell carcinoma, respectively. During the same period, 50 healthy individuals formed the control group and included 32 men and 18 women (mean age: 58.52 ± 11.93 years). Fasting venous blood samples were collected in the morning from both the LC and control group subjects who were not given hemostasis and anticoagulant medication for up to two weeks prior to the blood sampling. Thromboelastograms were drawn using a thromboelastograph, and PLT counts were determined using an automatic blood analyzer. From the initial study sample, 30 NSCLC patients (17 men and 13 women, mean age: 61.27 ± 7.90 years) and 20 control individuals (11 men and nine women, mean age: 57.00 ± 10.08 years) were selected for determination of CD62P positivity. Peripheral blood samples (2 mL) were centrifuged at 2000 r/min for 10 min. Using a straw-type pipette 100 μL of the intermediate gray cloudy interfacial layer, containing PLT-rich plasma was removed (making sure not to recover other layers) and transferred into a flow tube. PLT-rich plasma (5 μL each) was taken into test tube A (negative control tube) and test tube B (study tube). While CD61-FITC + IgG1-PE antibody (5 μL) was added to tube A, CD61-FITC + CD62P-PE antibody (5 μL) was added to tube B and incubated in the dark at room temperature for 20 min. Cells were washed once with 5 volumes of phosphate-buffered saline (PBS) solution, centrifuged at 2000 r/min for 5 min, and discarded the supernatant. CD62P positive rate = (CD61 + CD62P + count/CD61 + count) × 100%. Compared with the control group, the LC group showed lower values of reaction time (R), K time (K), and PLT distribution width (PDW). However, values of angle, maximum amplitude (MA), coagulation composite index (CI), PLT, mean PLT volume (MPV) and FIB were higher in the LC group compared to the control group. Based on the 2017 version of clinical TNM staging, patients were divided into two groups: early stage (I/II) and late stage (III/IV). The differences in MA values were statistically significant between the two groups [Table 1]. The PLT counts in the LC group was (250.60 ± 57.09) × 109/L, which was significantly higher than that in the control group (192.35 ± 43.37) ×109/L. At the same time, patients with LC also had a significantly higher rate (%) of CD62P positive expression (50.42 ± 15.42), compared to the control group (27.31 ± 18.16).