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An 18-Gene Signature for Vascular Invasion Is Associated with Aggressive Features and Reduced Survival in Breast Cancer

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  • Monica Mannelqvist
  • Elisabeth Wik
  • Ingunn M Stefansson
  • Lars A Akslen

Abstract

Aims: Vascular invasion by tumor cells is known to be important for cancer progression. By microarray and qPCR analyses, we earlier identified an 18-gene signature associated with vascular involvement in endometrial cancer. Here, we explored the significance of this vascular invasion signature in multiple series of breast cancer patients. Methods and Results: The study includes 11 open access gene expression data sets which collectively provide information on 2423 breast cancer patients. The 18-gene signature showed consistent associations with aggressive features of breast cancer, like high tumor grade, hormone receptor negativity, HER2 positivity, a basal-like phenotype, reduced patient survival, and response to neoadjuvant chemotherapy. Also, the vascular invasion signature was associated with several other gene expression profiles related to vascular biology and tumor progression, including the Oncotype DX breast cancer recurrence signature. Conclusions: The 18-gene vascular invasion signature showed strong and consistent associations with aggressive features of breast cancer and reduced survival.

Suggested Citation

  • Monica Mannelqvist & Elisabeth Wik & Ingunn M Stefansson & Lars A Akslen, 2014. "An 18-Gene Signature for Vascular Invasion Is Associated with Aggressive Features and Reduced Survival in Breast Cancer," PLOS ONE, Public Library of Science, vol. 9(6), pages 1-10, June.
  • Handle: RePEc:plo:pone00:0098787
    DOI: 10.1371/journal.pone.0098787
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    1. Carey K Anders & Chaitanya R Acharya & David S Hsu & Gloria Broadwater & Katherine Garman & John A Foekens & Yi Zhang & Yixin Wang & Kelly Marcom & Jeffrey R Marks & Sayan Mukherjee & Joseph R Nevins , 2008. "Age-Specific Differences in Oncogenic Pathway Deregulation Seen in Human Breast Tumors," PLOS ONE, Public Library of Science, vol. 3(1), pages 1-8, January.
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