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, 94 (30), e951

D-Dimer Can Serve as a Prognostic and Predictive Biomarker for Metastatic Gastric Cancer Treated by Chemotherapy

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D-Dimer Can Serve as a Prognostic and Predictive Biomarker for Metastatic Gastric Cancer Treated by Chemotherapy

Se-Il Go et al. Medicine (Baltimore).

Abstract

Systemic activation of hemostasis and thrombosis has been implicated in tumor progression and metastasis. D-dimer has been used as an indicator for the thrombosis. Here, we investigated the role of the activation of coagulation in patients with metastatic gastric cancer by measuring D-dimer level.We conducted an observation study of 46 metastatic gastric cancer patients who received palliative chemotherapy (CTx). D-dimer levels were assessed before CTx and at the first response evaluation after CTx.The overall survival (OS) of patients with pretreatment D-dimer levels <1.5 μg/mL was significantly longer than that of patients with D-dimer levels ≥1.5 μg/mL (22.0 vs 7.9 months, P = 0.019). At the first response evaluation, the mean level of D-dimer was significantly decreased by 2.11 μg/mL in patients either with partial response or stable disease (P = 0.011) whereas the mean level of D-dimer, although the difference did not reach statistical significance, was increased by 2.46 μg/mL in patients with progressive disease. In addition, the OS of patients with D-dimer levels <1.0 μg/mL at the first response evaluation was significantly longer than that of patients with D-dimer levels ≥1.0 μg/mL (22.0 vs 7.0 months, P = 0.009). The lower D-dimer levels (<1.0 μg/mL) at the first response evaluation after CTx was independent predictive factor for better survival in multivariate analysis (P = 0.037).This study suggests that D-dimer levels may serve as a biomarker for response to CTx and OS in patients with metastatic gastric cancer.

Conflict of interest statement

The authors have no conflicts of interest to disclose.

Figures

FIGURE 1
FIGURE 1
Mechanisms for cancer-induced hypercoagulation and consequential D-dimer formation. Cancer cells promote a hypercoagulable status and activate the hemostatic system. The cancer cells induce the hypercoagulable status by cell-to-cell interaction with endothelial cells, direct release of TF and CP, production of cytokines such as IL-1and TNF, and activation of monocyte, macrophage, and platelet. CP = cancer procoagulants, IL-1 = interleukin-1, PAI = plasminogen activator inhibitor, TF = tissue factor, TNF = tumor necrosis factor.
FIGURE 2
FIGURE 2
Dot plot with the raw data for the relationship between D-dimer levels at pretreatment and at the first response evaluation.
FIGURE 3
FIGURE 3
OS curve by D-dimer levels. (A) Patients with D-dimer levels <1.5 μg/mL at the pretreatment showed a significantly longer OS than those with D-dimer levels ≥1.5 μg/mL (median OS, 22.0 vs 7.9 mo, respectively). (B) Patients with D-dimer levels <1.0 μg/mL at the first response evaluation showed a significantly longer OS than those with D-dimer levels ≥1.0 μg/mL (median OS, 22.0 vs 7.0 mo, respectively). OS = overall survival.
FIGURE 4
FIGURE 4
OS curve by CEA levels. There was no significant difference in OS between low and high CEA groups (A) at the pretreatment (median OS, 10.7 vs 7.0 mo, respectively) and (B) at the first response evaluation (median OS, 16.1 vs 10.5 mo, respectively). CEA = carcinoembryonic antigen, OS = overall survival.

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