ArticleJournal of thrombosis and thrombolysis2022
Modelling the procoagulatory effect of Anastrozole relative to ERα and ERβ expression in breast cancer cells.
Article in Journal of thrombosis and thrombolysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Secretomics reveals hormone-therapy of breast cancer may induce survival by facilitating hypercoagulation and immunomodulation in vitro.Scientific reports · 2024Article
- Targeting Platelet Activation Pathways to Limit Tumour Progression: Current State of Affairs.Pharmaceuticals (Basel, Switzerland) · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAnastrozole is commonly used for the treatment of oestrogen receptor (ER)-positive breast cancer but can increase thromboembolic risk. It is unclear if ER presentation is associated with platelet-mediated hypercoagulation. We investigated the relationship between hypercoagulation and ERα and ERβ expression in breast cancer cell lines under Anastrozole treatment.
methodsIn Model 1, MCF-7 or T47D cancer cells were treated with Anastrozole, then exposed to whole blood and platelet-rich plasma, modelling platelet engagement in the tumour bed. In Model 2, blood components were treated with Anastrozole, then exposed to cancer cells, modelling circulatory effects in the vasculature. Hypercoagulation was assessed as a combined function of thrombin activity, platelet CD62P and CD63 expression, and corresponding platelet ultrastructure. Tumour ERα and ERβ were immunolocalised and following quantification assessed for correlation with hypercoagulatory parameters.
resultsAnastrozole enhanced hypercoagulation in both Models and cell lines. T47D cells induced more distinct features of hypercoagulation and responded by heightening ERβ expression and sustaining expression of ERα, indicative of a more aggressive phenotype. Post-exposure to cell lines, CD62P and CD63 expression correlated, but this was not maintained following Anastrozole treatment. Substantive correlations could not be found explaining the changes in ER expression and hypercoagulatory parameters, indicating unknown causative factors.
conclusionThese results provide basic science evidence showing that the hypercoagulatory effects induced by Anastrozole treatment may be related to the tumour subphenotype. Clinical studies are required to determine whether tracking of hypercoagulatory parameters may hold value in describing subphenotypic alterations or metastatic potential during tumour progression.
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