4.6 Article

The CD47 don't eat me signal is highly expressed in human ovarian cancer

期刊

GYNECOLOGIC ONCOLOGY
卷 143, 期 2, 页码 393-397

出版社

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ygyno.2016.08.325

关键词

CD47; SIRP alpha; Ovarian cancer; CD4(+) T cells; NY-ESO-1; IFN-gamma; CD8(+) T-cell activation anti-tumor effect

资金

  1. Cancer Research Institute/Ludwig Institute for Cancer Research Cancer Vaccine Collaborative Grant
  2. Anna-Maria Kellen Clinical Investigator Award of the Cancer Research Institute
  3. Ovarian Cancer Research Fund
  4. Roswell Park Alliance Foundation
  5. NCI Cancer Center Support Grant [P30 CA016056]
  6. NIH [T32CA108456, NIH1R01CA158318-01A1]
  7. RPCI-UPCI Ovarian Cancer SPORE [P50CA159981-01A1]
  8. Empire State Stem Cell Board from the New York State Health Department (NYSTEM) [N14C-002]

向作者/读者索取更多资源

Objectives. The CD47 don't eat me signal allows tumor immune evasion. We tested the association of CD47 expression with outcomes in EOC. Methods. CD47 expression was examined within the TCGA database for ovarian carcinoma. For validation, IHC was performed on a TMA consisting of specimens from 265 patients with EOC. The medical records of the patients were also retrospectively reviewed to correlate demographic and survival data. Results. CD47 was amplified in 15/316 (5%) ovarian serous cancers in TCGA. In the validation cohort, the majority of patients had stage III/IV disease (208/265, 78.4%). CD47 expression was seen in 210/265 (79.2%). Patients were categorized into CD47hi (129/265; 48.7%) versus CD47lo (136/265; 513%). Patients with CD4710 tumors were more likely to have a complete response to adjuvant therapy than CD47hi (65% vs 50%, p = 0.026). Although there was a trend towards an increase in median OS (37.64 vs 45.26 months, p = 0.92) in the CD4710 group compared with CD47hi, the difference was not significant. Conclusions. CD47 is expressed at high frequency in EOC. Patients with CD47lo EOC had a better treatment response to standard therapy, and trended towards improved OS. This demonstrates that while CD47 may be an immunologic shield that may be considered for targeted therapies, it is likely that it operates in concert with other mechanisms of immune evasion. Future studies to evaluate CD47 expression with other known mechanisms of immune escape in the tumor microenvironment may help further define its role. (C) 2016 Elsevier Inc. All rights reserved.

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