4.7 Article

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

Journal

SCIENTIFIC REPORTS
Volume 9, Issue -, Pages -

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-019-54513-3

Keywords

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Funding

  1. Central Brain Tumor Registry of the United States (CBTRUS)
  2. Centers for Disease Control and Prevention (CDC) [2016M-9030]
  3. American Brain Tumor Association
  4. Sontag Foundation
  5. Novocure
  6. AbbVie
  7. Musella Foundation
  8. National Brain Tumor Society
  9. Zelda Dorin Tetenbaum Memorial Fund
  10. Uncle Kory Foundation
  11. NIH [CA217956]
  12. Peter D Cristal Chair
  13. Center of Excellence for Translational Neuro-Oncology
  14. Kimble Family Foundation
  15. Gerald Kaufman Fund for Glioma Research
  16. Ferry Family Foundation at University Hospitals of Cleveland
  17. [P50CA221747 SPORE]
  18. [CA221747]

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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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