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Poster display session

4722 - B7-H3 (CD276) on circulating epithelial tumor cells (CETCs) correlates with proliferation marker Ki-67 and may be associated with aggressiveness of tumor in breast cancer patients

Date

11 Sep 2017

Session

Poster display session

Presenters

Monika Pizon

Citation

Annals of Oncology (2017) 28 (suppl_5): v573-v594. 10.1093/annonc/mdx390

Authors

M. Pizon, D. Schott, U. Pachmann, K. Pachmann

Author affiliations

  • Tzb Bayreuth, TZB Bayreuth, 95448 - Bayreuth/DE
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Resources

Abstract 4722

Background

CETCs in the peripheral blood are a prerequisite for the development of metastases. B7-H3 is an important immune checkpoint member of the B7 family and inhibits T-cell mediated anti-tumor immunity. It is highly overexpressed on a wide range of solid cancers and often correlates with both negative prognosis and poor clinical outcome in patients. Based on the clinical success of the inhibitory immune checkpoint blockade, mAbs against B7-H3 appear to be promising therapeutic strategy. In order to better understand the role of B7-H3 in cancer development we used a non-invasive, real-time biopsy for determining B7-H3 on CETCs in breast cancer patients.

Methods

Blood from 50 patients suffering from breast cancer were analyzed for CETCs. The number of vital CETCs and the expression of B7-H3 and Ki-67 were evaluated using the maintrac® method.

Results

CETCs were detected in all examined patients (ranged from 2-676 CETCs in 100 µl of blood). B7-H3 expression on the surface of CETCs was found in 82% of patients. Triple negative breast cancer patients had statistically significantly more B7-H3 positive CETCs than patients with hormone receptor positive tumor tissue (median 50 vs. 26.3; p 

Conclusions

Breast cancer patients have detectable CETCs with high frequency of B7-H3 expression regardless of stage of disease. B7-H3 seems to be an important factor in immune evasion and may be a promising target of anticancer therapies. Furthermore, radiation leads to an up-regulation of B7-H3 expression on CETCs, which could be a possible mechanism of acquired radio-resistance.

Clinical trial identification

Legal entity responsible for the study

N/A

Funding

None

Disclosure

U. Pachmann, K. Pachmann: Holder of patent. All other authors have declared no conflicts of interest.

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