Shucai Zhang

Jialin Lv3
Jingying Nong3
3Jialin Lv
3Jingying Nong
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EML4-ALK is a new driver gene of non-small cell lung cancer and a target of crizotinib. The objectives of this study were to determine the frequency of ALK rearrangements in a large cohort of patients with primary lung adenocarcinoma and to analyze the association of ALK rearrangements with clinicopathological characteristics and clinical outcomes. The(More)
BACKGROUND To explore the efficacy and safety of crizotinib versus platinum-based double agent chemotherapy as the first-line treatment in patients with advanced anaplastic lymphoma kinase (ALK)-positive lung adenocarcinoma. METHOD We retrospectively analyzed data from 19 patients with advanced ALK-positive lung adenocarcinoma who had received no previous(More)
Data processing is required to extract meaningful results from huge and complicated data. Existing work normally use complicated equations to compute huge data, and use math software to analysis them. However, these methods are not intuitive to design operations, and hard to understand the analysis results, which is also not simple to manage the operation.(More)
BACKGROUND Matrix metalloproteinase 9 (MMP-9) plays an important role in tumor invasion and metastasis, including lung cancer. However, whether variations in serum MMP-9 levels can serve as a biomarker for monitoring chemotherapy curative effect remains unclear. This study was designed to investigate the association between variations in serum MMP-9 levels(More)
BACKGROUND c-ros oncogene 1 (ROS1) rearrangement presents one of the newest molecular targets in non-small cell lung cancer (NSCLC). ROS1 rearrangement is predominantly found in adenocarcinoma cases and is exclusive to other oncogenes, such as epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene homolog (KRAS), and anaplastic lymphoma(More)
BACKGROUND Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) effectively treat advanced non-small cell lung cancer with EGFR-mutation. However, most patients develop acquired resistance without effective therapy subsequent to EGFR-TKI failure. We evaluated the efficacy of subsequent treatment strategies for EGFR-TKI resistance. (More)
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