Key result
Reduced EGFR activity caused by the Egfr wa2 mutation led to severe calcific aortic stenosis, left ventricular hypertrophy, and >50% mortality by 1 year in C57BL/6J mice, but not in 129S1/SvImJ mice.
Why the study?
Does reduced EGFR signaling cause abnormal valvular differentiation and calcific aortic stenosis in susceptible mouse strains?
Does reduced EGFR signaling cause abnormal valvular differentiation and calcific aortic stenosis in susceptible mouse strains?
Absolute Event Rate: 50% vs 10%
p-value: p=<0.001
Reduced EGFR signaling leads to calcific aortic stenosis and left ventricular hypertrophy in a strain-dependent manner in mice, suggesting potential valvular consequences of long-term EGFR inhibition.
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Alerts clinicians to possible valvular risks with EGFR inhibitors; leaves open genetic modifiers of susceptibility in humans.
Barrick et al. (2009) studied Calcific aortic stenosis and left ventricular hypertrophy. Egfr wa2 mutation (reduced EGFR activity) vs. Heterozygous controls (Egfr wa2/+) was evaluated on Mortality at 1 year (C57BL/6J background) (p=<0.001). Reduced EGFR activity caused by the Egfr wa2 mutation led to severe calcific aortic stenosis, left ventricular hypertrophy, and >50% mortality by 1 year in C57BL/6J mice, but not in 129S1/SvImJ mice.
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