Key result
Active breast cancer is linked to greater agonist-induced VEGF release versus healthy controls.
Why the study?
Does active breast cancer alter platelet phenotype and response to P2Y12 inhibition compared to healthy controls?
Population
24 women with active breast cancer and 10 healthy controls not receiving antiplatelet therapy
Comparison
Ex vivo platelet activation and P2Y12 receptor… vs Healthy controls
Design
Case-control
Authors
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May reflect altered platelet angiogenic potential in breast cancer; leaves open effects on P2Y12 response and clinical translation.
Case-Control (n=34)
Does active breast cancer alter platelet phenotype and response to P2Y12 inhibition compared to healthy controls?
p-value: p=0.02 for ADP, <0.001 for PAR1AP, PAR4AP, and convulxin
Breast cancer and its treatment increase the secretion of pro-angiogenic proteins following platelet activation and enhance the response to P2Y12 inhibition.
Holmes et al. (2016) conducted a case-control in Breast cancer (n=34). Active breast cancer vs. Healthy controls was evaluated on Agonist-induced release of VEGF (p=0.02 for ADP, <0.001 for PAR1AP, PAR4AP, and convulxin). Active breast cancer was associated with greater agonist-induced release of VEGF compared to healthy controls (p=0.02 for ADP, p<0.001 for PAR1AP, PAR4AP, and convulxin).
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