High Receptor-interacting Serine/Threonine-protein Kinase 3 (RIP3) Expression Serves as an Independent Poor Prognostic Factor for Triple-negative Breast Carcinoma
- Authors
- Chung, Y.[Chung, Y.]; Kim, S.[Kim, S.]; Kim, H.-S.[Kim, H.-S.]; DO, S.-I.[DO, S.-I.]
- Issue Date
- May-2022
- Publisher
- International Institute of Anticancer Research
- Keywords
- Breast; immunohistochemistry; prognosis; receptor-interacting serine/threonine-protein kinase 3; triple-negative breast carcinoma
- Citation
- Anticancer Research, v.42, no.5, pp.2753 - 2761
- Indexed
- SCIE
SCOPUS
- Journal Title
- Anticancer Research
- Volume
- 42
- Number
- 5
- Start Page
- 2753
- End Page
- 2761
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/98927
- DOI
- 10.21873/anticanres.15754
- ISSN
- 0250-7005
- Abstract
- Background/Aim: Receptor-interacting serine/ threonine-protein kinase 3 (RIP3) is a key component related to tumor necrosis factor-dependent necroptosis. RIP3 has been known to be a predictive biomarker in many types of carcinomas. We aimed to investigate whether RIP3 expression is correlated with clinicopathological characteristics and the outcomes of patients with breast carcinoma. Patients and Methods: We performed immunostaining for RIP3 and analyzed the association of RIP3 expression status with the clinicopathological characteristics and survival of 203 patients with invasive ductal carcinoma of the breast. Results: High RIP3 expression was significantly correlated with lymph node metastasis and human epidermal growth factor receptor 2 positivity. In patients with triple-negative breast carcinoma (TNBC), high RIP3 expression was an independent prognostic factor for disease-free survival (DFS). RIP3-high TNBC showed the lowest DFS rate. Conclusion: High RIP3 expression is associated with aggressive clinical behavior of breast carcinoma. Our data suggest that RIP3 serves as an independent prognostic factor in TNBC. © 2022 International Institute of Anticancer Research. All rights reserved.
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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