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BackgroundEarly identification of response to neoadjuvant chemotherapy (NAC) is instrumental in predicting patients prognosis. However, since a fixed criterion with high accuracy cannot be generalized to molecular subtypes, our study first aimed to redefine grades of clinical response to NAC in invasive breast cancer patients (IBC). And then developed a prognostic model based on clinical features and ultrasound semantics.MethodsA total of 480 IBC patients were enrolled who underwent anthracycline and taxane-based NAC between 2018 and 2020. The decrease rate of the largest diameter was calculated by ultrasound after NAC and their cut-off points were determined among subtypes. Thereafter, a nomogram was constructed based on clinicopathological and ultrasound-related data, and validated using the calibration curve, receiver operating characteristic (ROC) curve, decision curve analysis (DCA), and clinical impact curve (CIC).ResultsThe optimal cut-off points for predicting pCR were 53.23%, 51.56%, 41.89%, and 53.52% in luminal B-like (HER2 negative), luminal B-like (HER2 positive), HER2 positive, and triple-negative, respectively. In addition, time interval, tumor size, molecular subtypes, largest diameter decrease rate, and change of blood perfusion were significantly associated with pCR (all p < 0.05). The prediction model based on the above variables has great predictive power and clinical value.ConclusionTaken together, our data demonstrated that calculated cut-off points of tumor reduction rates could be reliable in predicting pathological response to NAC and developed nomogram predicting prognosis would help tailor systematic regimens with high precision.

Breast cancer is the most common cancer among women worldwide. Chemoresistance remains to be a considerable obstacle in breast cancer therapy and it is often involves dysregulation of a variety of microRNAs (miRNAs). miR-485-5p functions as a tumor suppressor in several types of human cancers. However, its role in breast cancer chemosensitivity have not been determined. In the present study, we demonstrated that overexpression of miR-485-5p suppresses breast cancer progression and enhances chemosensitivity both in vitro and in vivo. Further study demonstrated that miR-485-5p directly targeted the 3'-untranslated region of survivin and overexpression of survivin overcomes the miR-485-5p induced effects on breast cancer. In conclusion, our study identified that miR-485-5p suppresses cancer progression and enhances the chemosensitivity by targeting survivin. Targeting survivin by miR-485-5p may provide a potential approach to reverse chemosensitivity in breast cancer cells.