Revealing symptom profiles: A pre-post analysis of docetaxel therapy in individuals with breast cancer.

PURPOSE: This study aimed to explore the symptom profiles and predominant symptoms in newly diagnosed breast cancer women before and after receiving docetaxel chemotherapy. METHODS: A pre-post study recruited adult women with stage I-III breast cancer undergoing docetaxel chemotherapy using convenience sampling. The 13-item symptom severity subscale of the M. D. Anderson Symptom Inventory-Taiwan Form was used to measure symptoms. The study employed latent profile analysis to identify subgroups based on symptom severity before and after docetaxel chemotherapy. Descriptive statistics, including mean and frequency, were used to compare and contrast the most prevalent and severe symptoms within each subgroup to confirm the predominant symptoms. RESULTS: The study identified four and two symptom profiles before and after docetaxel treatment, respectively. Disturbed sleep was identified as a prevalent symptom for all participants, regardless of their chemotherapy status. The predominant symptoms before treatment were disturbed sleep, dry mouth, difficulty remembering, and fatigue, while disturbed sleep and numbness were the predominant symptoms after treatment. CONCLUSION: The findings of this study are significant, as they contribute to the current understanding of the symptom experience of breast cancer individuals undergoing docetaxel chemotherapy. Healthcare professionals should prioritize assessing and managing these symptoms, including identifying contributing factors to poor sleep. Addressing symptom profiles related to sleep can improve the quality of life of breast cancer individuals undergoing docetaxel chemotherapy.

The tyrosine kinase inhibitor nintedanib activates SHP-1 and induces apoptosis in triple-negative breast cancer cells

Triple-negative breast cancer (TNBC) remains difficult to treat and urgently needs new therapeutic options. Nintedanib, a multikinase inhibitor, has exhibited efficacy in early clinical trials for HER2-negative breast cancer. In this study, we examined a new molecular mechanism of nintedanib in TNBC. The results demonstrated that nintedanib enhanced TNBC cell apoptosis, which was accompanied by a reduction of p-STAT3 and its downstream proteins. STAT3 overexpression suppressed nintedanib-mediated apoptosis and further increased the activity of purified SHP-1 protein. Moreover, treatment with either a specific inhibitor of SHP-1 or SHP-1-targeted siRNA reduced the apoptotic effects of nintedanib, which validates the role of SHP-1 in nintedanib-mediated apoptosis. Furthermore, nintedanib-induced apoptosis was attenuated in TNBC cells expressing SHP-1 mutants with constantly open conformations, suggesting that the autoinhibitory mechanism of SHP-1 attenuated the effects of nintedanib. Importantly, nintedanib significantly inhibited tumor growth via the SHP-1/p-STAT3 pathway. Clinically, SHP-1 levels were downregulated, whereas p-STAT3 was upregulated in tumor tissues, and SHP-1 transcripts were associated with improved disease-free survival in TNBC patients. Our findings revealed that nintedanib induces TNBC apoptosis by acting as a SHP-1 agonist, suggesting that targeting STAT3 by enhancing SHP-1 expression could be a viable therapeutic strategy against TNBC.