Bevacizumab for the treatment of non-small cell lung cancer patients with synchronous brain metastases

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作者
Mustafa S. Ascha
Jacqueline Fang Wang
Priya Kumthekar
Andrew E. Sloan
Carol Kruchko
Jill S. Barnholtz-Sloan
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[1] Case Western Reserve University School of Medicine,Center for Clinical Investigation, Department of Population and Quantitative Health Sciences
[2] Case Western Reserve University School of Medicine,Northwestern University Feinberg School of Medicine
[3] Department of Neurology,Department of Neurosurgery
[4] University Hospitals Cleveland Medical Center,Department of Population and Quantitative Health Sciences
[5] Seidman Cancer Center,undefined
[6] and the Case Comprehensive Cancer Center,undefined
[7] Central Brain Tumor Registry of the United States,undefined
[8] Case Western Reserve University School of Medicine,undefined
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Bevacizumab is FDA-approved in the treatment of primary brain tumors, but its efficacy in patients with brain metastases could be better-studied. This study examines a population of non-small cell lung cancer (NSCLC) patients with synchronous brain metastases to identify predictors of the decision to use bevacizumab and survival following bevacizumab treatment. Primary cancer registry data were used to determine which NSCLC patients diagnosed in the years 2010 through 2012 had synchronous brain metastases at the time of diagnosis, and Medicare claims used to identify a population of patients treated with bevacizumab. Record of bevacizumab treatment was found for 81 and 666 patients with and without brain metastases, respectively. After adjusting for clinical and demographic characteristics, bevacizumab was associated with 0.88 times the hazard of mortality in the elderly NSCLC population (95% CI: 0.81–0.96, p: 0.003) and a corresponding hazard ratio of 0.75 in the population of elderly NSCLC patients with synchronous brain metastases (95% CI: 0.59–0.96, p: 0.020). Bevacizumab may benefit NSCLC patients with synchronous brain metastases more than it does patients without intracranial disease, possibly as a result of its multiple potential mechanisms of action simultaneously inhibiting angiogenesis and minimizing vasogenic edema.
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