Introduction. Patients receiving chemotherapy for breast cancer may be at risk of developing cardiac dysfunction and electrophysiological abnormalities. The aim of this study is to evaluate alterations in electrocardiographic (ECG) parameters in breast cancer patients receiving chemotherapy. Materials and Methods. This was a prospective single-center cohort study conducted in the Fourth Hospital of Hebei Medical University, China. Participants with breast cancer referred for chemotherapy from May 1, 2019, to October 1, 2019, were invited to participate in the study. Standard 12-lead ECG and echocardiography were performed at baseline or before chemotherapy (prechemotherapy) (T0), after 1 cycle (T1), after 3 cycles (T2), and at the end of chemotherapy (T3). Results. A total of 64 patients with diagnosed breast cancer undergoing chemotherapy were included. Echocardiographic parameters showed no significant variation during the entire procedure (all P > 0.05 ). The incidence of abnormal ECG increased from 43.75% at baseline to 65.63% at the end of chemotherapy, of which only the prevalence of fragmented QRS (fQRS) was significantly increased after the drug regimen (26.56% to 53.13%). At the end of the treatment, heart rate, P-wave dispersion, corrected QT interval, T-peak to T-end, RR, SV1, RV5, Sokolow–Lyon index (SLI), and index of cardioelectrophysiological balance deteriorated markedly (all P < 0.05 ). The area under the curve for SLI and QT dispersion (QTd) derived by ECG was 0.710 and 0.606, respectively. The cutoff value with 2.12 of SLI by ECG had a sensitivity of 67.2% and specificity of 71.9% for differentiating patients after therapy from baselines. The cutoff value with 0.55 of QTd had a sensitivity of 60.9% and specificity of 60.9%. Conclusions. The current study demonstrated that ECGs can be used to detect electrophysiological abnormalities in breast cancer patients receiving chemotherapy. ECG changes can reflect subclinical cardiac dysfunction before the echocardiographic abnormalities.

Let-7 was one of the earliest discovered miRNAs and while it reportedly acts as a tumor suppressor in various solid tumors, its function in breast cancer has not been fully studied. Therefore, we examined let-7a and MAGE-A1 expression in breast tissues by qRT-PCR and found that let-7a expression significantly correlates with larger tumor size, higher histological grade (p<0.05) and is significantly lower in patients with Her-2-positive cancers and Ki-67 >14% (p=0.028 and p=0.023). MAGE-A1 expression incidence is 50.8% (33/65) and it inversely correlates with let-7a expression (p=0.008). let-7a inhibition of breast cancer cell proliferation, migration and invasion was also observed in in vitro cell culture experiments, and dual-luciferase reporter assays showed that melanoma-associated antigen A1 (MAGE-A1) was its target gene; the target comprised bases 451-457 of the 3'UTR region of the MAGE-A1 mRNA. RT-qPCR and Western blot analyses showed that let-7a inhibited MAGE-A1 expression at both the nucleic acid and protein levels. In our final co-transfection experiment, we targeted MAGE-A1 in a breast cancer cell line and observed that let-7a inhibited cell proliferation, migration and invasion. These combined results confirm that let-7a functions as a tumor suppressor by targeting MAGE-A1 in breast cancer and it therefore provides a novel target in breast cancer clinical treatment.

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Rationale: Wellens syndrome is a comprehensive electrocardiographic (ECG) diagnosis that combines medical history with characteristic ECG changes. These changes, characterized by biphasic T-wave inversions or symmetric and deep T-wave inversions in the anterior precordial leads, often indicate that the left anterior descending coronary artery is at a high risk of severe stenosis. Chemotherapy-related cardiovascular toxicity refers to damage to the cardiovascular system caused by chemotherapeutic drugs, which is unpredictable and may occur during or after chemotherapy. Patient concerns: In this case report, a 41-year-old male patient with cholangiocarcinoma received sequential adjuvant chemotherapy with gemcitabine/nanoparticle albumin–bound paclitaxel and gemcitabine/cisplatin. This patient presented with recurrent brief chest pain episodes after the third dose of gemcitabine/cisplatin, and the characteristic T-wave morphological changes were captured in routine ECG monitoring prior to the 6th dose. Diagnoses: Acute coronary syndrome due to chemotherapy-related cardiovascular toxicity was diagnosed on the basis of characteristic ECG changes. Interventions: The patient underwent coronary angiography, which revealed diffuse stenosis of up to 95% in the middle segment of the left anterior descending coronary artery. Stents were implanted in the stenotic segment for vascular reconstruction. Outcomes: The patient’s chest pain was completely resolved, and electrocardiography returned to normal. Lessons: Cardiovascular toxicity during chemotherapy in patients with cancer may be life threatening. This rare case highlights the importance of identifying the characteristic ECG pattern of the Wellens syndrome by monitoring electrocardiography during chemotherapy. Immediate and accurate identification of the morphological ECG features of Wellens syndrome with a slight elevation of the ST-segment is related to patient prognosis.