B7-H1 expression in Wilms tumor: correlation with tumor biology and disease recurrence.


Journal Article

PURPOSE: Despite tremendous gains in improving prognosis, 10% of patients with Wilms tumor will ultimately experience disease recurrence. The identification of novel prognostic markers and tumor associated targets for patients at risk could enable clinicians to treat recurrences more aggressively and, thus, optimize outcomes. We have previously shown that tumor expression of the T cell coregulatory ligand B7-H1 portends a poor prognosis for adults with renal cell carcinoma and represents a promising target to improve therapy. We hypothesize that this finding may be true for Wilms tumor. MATERIALS AND METHODS: We identified 81 patients with Wilms tumor treated at 1 institution between 1968 and 2004. Histopathological features, including Wilms tumor B7-H1 expression, were correlated with clinical observations and outcome. RESULTS: Tumor recurrences were noted in 22% of patients with Wilms tumor and 14% died. B7-H1 was expressed in 11 tumors (14%) and was more likely to occur in anaplastic Wilms tumor (p = 0.03). Tumor B7-H1 expression was associated with a 2.7-fold increased risk of recurrence, although this difference did not achieve statistical significance (p = 0.06). However, in favorable histology tumors B7-H1 expression was associated with a 3.7-fold increased risk of recurrence (p = 0.03). CONCLUSIONS: B7-H1 is expressed by Wilms tumor, correlates with tumor biology and is associated with an increased risk of recurrence in patients with favorable histology tumors. B7-H1 may prove useful in identifying high risk patients who could benefit from more aggressive initial treatment regimens, and may represent a promising therapeutic target. Multi-institutional studies to elucidate the role of B7-H1 in the treatment of Wilms tumor are warranted.

Full Text

Duke Authors

Cited Authors

  • Routh, JC; Ashley, RA; Sebo, TJ; Lohse, CM; Husmann, DA; Kramer, SA; Kwon, ED

Published Date

  • May 2008

Published In

Volume / Issue

  • 179 / 5

Start / End Page

  • 1954 - 1959

PubMed ID

  • 18355839

Pubmed Central ID

  • 18355839

Electronic International Standard Serial Number (EISSN)

  • 1527-3792

Digital Object Identifier (DOI)

  • 10.1016/j.juro.2008.01.056


  • eng

Conference Location

  • United States