Abstract
Axillary lymph node-negative breast cancer patients have a low risk for disease recurrence, and the majority of these patients are cured by surgery alone. However, accurate identification of that 30% of node-negative patients who are at high-risk for relapse and who might therefore benefit from adjuvant systemic therapy has not been possible using traditional histomorphological and clinical prognostic factors alone. Identification of novel tumor-associated molecules may therefore provide a basis for a better understanding of and eventually for an interference with disease progression. We have recently reported on tumor-associated RNA up-regulation of the secreted, soluble T1-S receptor in node-negative breast cancer. In the present study we analyzed the tumor-associated level of the T1-S receptor using semiquantitative immunohistochemistry in a collective of 102 node-negative breast carcinomas to study its clinical relevance. A high T1-S immunoreactivity score indicating T1-S overexpression was observed in 58 of 102 (57%) cases. The T1-S score was independent of the tumor size, type, grade, steroid hormone receptor status, and the proliferation rate determined by monoclonal antibody against KI-67 protein (MIB1) immunohistochemistry. In univariate and multivariate analysis of disease-free survival, a high T1-S score (p = 0.003) and a low MIB1 score (p = 0.001) were the only parameters that were highly significantly associated with an improved disease-free survival period. We conclude that T1-S receptor overexpression is a novel and independent tumor biological factor that may be associated with reduced progression of lymph node-negative breast cancer.
| Original language | English |
|---|---|
| Pages (from-to) | 159-165 |
| Number of pages | 7 |
| Journal | Laboratory Investigation |
| Volume | 81 |
| Issue number | 2 |
| DOIs | |
| State | Published - 2001 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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