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Y. Sen



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    P1.01 - Advanced NSCLC (ID 757)

    • Event: WCLC 2017
    • Type: Poster Session with Presenters Present
    • Track: Advanced NSCLC
    • Presentations: 2
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      P1.01-017 - ALK-Rearranged May Promote VTE by Increasing the Expression of TF in Advanced Lung Adenocarcinoma (ID 9778)

      09:30 - 16:00  |  Author(s): Y. Sen

      • Abstract
      • Slides

      Background:
      Patients with lung cancer are at increased risk for venous thromboembolism (VTE).About 8% to 15% of patients with advanced none small-cell lung cancer(NSCLC) experience a VTE in the course of their disease. However, the incidences of VTE in different molecular subtypes of NSCLC are rarely reported though they have big differentiation in clinical feature and therapeutic effect.Tissue Factor (TF) expressed in many solid tumors could bind and activate coagulation factor FVII and trigger the downstream coagulation cascade leading to thrombin generation and clot formation.

      Method:
      Here we extracted retrospective data from electronic medical records at Henan Cancer Hospital in China between January 2015 and January 2016. Lung adenocarcinomas with ALK-rearranged, EGFR mutation and both negative were classified. The incidence rate of VTE after diagnosed with lung adenocarcinoma was calculated and analyzed. Then we randomly selected ALK-rearranged and ALK-rearranged negative lung adenocarcinoma tissues and detected TF expression in them with imunohistochemistry.

      Result:
      At a median follow-up of 19 months, 5.85% (30 in 513) patients with advanced lung adenocarcinoma experienced VTE. Patients with different molecular subtypes put up different rate of VTE (P=0.0021). Among them ALK-rearranged were more likely to experience VTE (6 in 29, 20.69%). EGFR and both negative had lower rate of VTE and had no big difference between them (11 in 218, 5.05%; 13 in 266, 4.89% respectively).The expression of TF performed similar feature. TF high expression in ALK-rearranged tissues is 41.67% (10 in 24) dramatically higher than that in ALK-rearranged negative tissues (11.54%, 3 in 26, P=0.0152).

      Conclusion:
      The rate of VTE in ALK-rearranged advanced lung adenocarcinoma cohorts was about 4 fold higher than that in EGFR mutation and both negative patients. ALK-rearranged may promote that by increasing TF expression. The mechanism warrants further research.

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      P1.01-047 - Analysis of EGFR Mutation Status in CSF and Blood in Lung Adenocarcinoma Patients with EGFR Mutation and CNS Metastasis (ID 9717)

      09:30 - 16:00  |  Author(s): Y. Sen

      • Abstract
      • Slides

      Background:
      Patients with non-small cell lung cancer(NSCLC)harboring epidermal growth factor receptor (EGFR) mutations benefit a great deal from EGFR tyrosine kinase inhibitors(TKIs). However, most patients get recrudesced within one or two years, and many of them progressed in central nerve system(CNS).Owing to the blood– brain barrier, detecting tumor-derived cell-free DNA (cfDNA) in the blood of brain metastasis tumor patients is challenging. Detecting tumor-specific mutations in cerebral spinal fluid (CSF) became an alternative method.

      Method:
      41 initial or progressed lung adenocarcinoma patients with EGFR mutation and CNS metastasis from Henan Cancer Hospital were included in this study. 41 patients were all detected EGFR mutation status in CSF with dropplet digital PCR (ddPCR) and 37 in 41 patients were detected EGFR mutation status in blood with the same method. Their clinical informations were also collected at the same time.

      Result:
      The rate of EGFR mutations in CSF (15/41,36.6%)were obviously lower than that in blood(24/37,64.9%)(P=0.013), especially in those with EGFR exon 19del mutation patients (7/18 vs 13/16, P = 0.017), without TKIs treated patients (3/13 vs 8/11,P = 0.038) and less than 60 years patients (10/25 vs 17/22, P = 0.010). In patients with CNS symptoms positive, the rate of EGFR mutations in CSF was higher than those negative (13/27 vs 2/14 , P=0.033). In patients with MRI indicating leptomeningeal metastasis, the rate of EGFR mutations in CSF was higher than those not indicating(8/11 vs 7/30 , P=0.003).

      Clinical characteristics, EGFR mutation status in CSF and plasma (n = 41)
      Characteristic n(%)
      Gender
      Male 23 (56.1)
      Female 18 (43.9)
      Age
      ≥ 60 16 (39)
      < 60 25 (61)
      Smoking status
      Yes 12 (29.3)
      No 29 (70.7)
      Brain metastases (MRI)
      Only metastatic tumors 30 (73.2)
      With meningeal lesions 11 (26.8)
      Brain metastatic tumor number
      Single 10 (24.4)
      Multiple 31 (75.6)
      Neurological symptoms
      Positive 15 (36.6)
      Negtive 26 (63.4)
      Prior TKIs treat
      Yes 28 (68.3)
      No 13 (31.7)
      CSF EGFR mution
      19 7 (17.1)
      21 6 (14.6)
      Both 2 (4.9)
      Negtive 26 (63.4)
      Blood EGFR mution
      19 13 (31.7)
      21 10 (24.4)
      Both 1 (2.4)
      Negtive 13 (31.7)


      Conclusion:
      The EGFR mutations status in CSF is different from that in blood in patients with EGFR mutation and CNS metastasis. This warrants confirmation in larger cohorts and further more studies are needed to find out the internal mechanism. Detecting EGFR mutations status in both blood and CSF will be helpful to make individualized treatment.

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