Why the study?
Does S100A1 expression change in response to cardiotoxicity induced by trastuzumab or lapatinib in normal rat hearts?
Does S100A1 expression change in response to cardiotoxicity induced by trastuzumab or lapatinib in normal rat hearts?
S100A1 expression is significantly down-regulated in chemotherapy-induced cardiotoxicity in rats, suggesting its potential as a diagnostic blood biomarker.
S100A1 may flag chemotherapy cardiotoxicity in rat models; leaves open clinical biomarker validation in patients.
This study examined the value of blood marker S100A1 in detecting cardiotoxicity induced by chemotherapy agents; trastuzumab and lapatinib, in normal rat heart. The rats were divided into three groups: control (n = 8, no treatment), T (n = 8, one time ip treatment with 10 mg/kg trastuzumab) and L (n = 8, oral treatment with 100 mg/kg/day lapatinib for 7 days). The activities of oxidative stress parameters Malondialdehyde (MDA), Superoxide dismutase (SOD), Catalase (CAT) and Glutathione (GSH) were measured from the extracted cardiac tissues. The levels of troponinI and S100A1 expressions were measured from blood samples. All biomarkers responded to the treatments as they exhibited alterations from their normative values, validating the chemically induced cardiotoxicity. S100A1 expression attenuated significantly (75%), which made the sensitive detection of cardiotoxicity feasible. Assessment of cardiotoxicity with S100A1 may be a valuable alternative in clinical oncology of cancers in some organs such as breast and prostate, as they do not overexpress it to compete against.
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Eryılmaz et al. (2015) studied this question.
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