Background: Triple-negative breast cancer (TNBC) is a malignant subtype of breast cancer, the main treatments for which are chemotherapy and surgery. PIK3CA is an oncogene that encodes the p110α subunit of class IA PI3K to regulate cell proliferation and apoptosis. Some reports have observed neoadjuvant chemotherapy (NAC) to have poor pathological complete response (pCR) rates in TNBC with PIK3CA mutation. This study aimed to explore the mechanism of how mutant PIK3CA alters chemotherapeutic susceptibility in TNBC. Methods: TNBC cell lines (MDA-MB-231 and MDA-MB-468) with PIK3CA gene mutations (E545K and H1047R regions) and overexpression were established by transfection. NOD/SCID mice were used for in vivo experiments. Epirubicin was used as the chemotherapeutic agent. Cell viability, cell cycle, apoptosis, and Transwell assays were conducted for phenotype analysis. Western blot, quantitative reverse transcriptionpolymerase chain reaction, and immunohistochemistry were used to detect gene and protein expression levels. A clinical analysis of 50 patients with TNBC was also performed.Results: Cell viability and Transwell assays showed that PIK3CA mutation promoted TNBC cell growth and conferred an enhanced migratory phenotype. Cell cycle and apoptosis assays showed that PIK3CA mutation moderately improved the proliferation ability of TNBC cells and remarkably inhibited their apoptosis. After epirubicin therapy, the proportion of early apoptotic cells decreased among cells with PIK3CA mutation. Further, xenograft tumors grew faster in NOD/SCID mice injected with mutated cell lines than in control group, suggesting that PIK3CA mutation caused chemotherapy resistance. Importantly, western blot and immunohistochemical analysis showed that cells and mouse tumors in the PIK3CA mutation groups exhibited different expression levels of apoptosis-related markers (Xiap, Bcl-2, and Caspase 3) and proteins associated with the PI3K/AKT/mTOR pathway (p110α, AKT, p-AKT, mTOR, p-mTOR, p-4E-BP1, p-p70S6K, and Pten). Moreover, prognostic analysis of 50 patients with TNBC indicated that PIK3CA mutation might be linked with relapse and death.Conclusions: PIK3CA mutation confers resistance to chemotherapy in TNBC by inhibiting apoptosis and activating the PI3K/AKT/mTOR signaling pathway.

Background: Sexual dysfunction is common in postoperative breast cancer patients, which seriously affects the quality of life of the patients, especially young patients. The aim of the present study was to investigate the incidence and risk factors of sexual dysfunction in young breast cancer survivors, so as to provide evidence for further intervention. Methods: A total of 201 young breast cancer patients who were hospitalized in our department from October 2017 to October 2018 were retrospectively enrolled. The general information questionnaire and the female sexual function index (FSFI) questionnaire were used to evaluate the patients. Results: Of these patients, 83.08% (167/201) of young breast cancer patients had sexual dysfunction. Total mastectomy (OR value single factor =7.843, OR value multiple factor =6.815), chemotherapy (OR value single factor =11.876, OR value multiple factor =38.711), and endocrine therapy (OR value single factor =19.688, OR value multiple factor =46.251) were independent risk factors of sexual dysfunction in young breast cancer survivors (P<0.05).Conclusions: Our study suggests that the incidence of sexual dysfunction in young breast cancer survivors is at a high level. Increasing the rate of breast conserving surgery and targeted intervention in patients with risk factors may help to reduce the incidence of sexual dysfunction and improve the quality of life in young breast cancer survivors.

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Background: Recent studies have shown that chemotherapy can cause abnormal glucose and lipid metabolism in breast cancer patients; however, the effects of different chemotherapy regimens on the glucose and lipid profiles in this population remain unclear. Methods:The clinical data of 141 invasive breast cancer patients who were treated in our center from January 2019 to December 2020 were retrospectively collected. All patients received surgical treatment and postoperative chemotherapy in our center. According to the postoperative chemotherapy regimens, these patients were divided into an observation group (n=100, treated with anthracycline-based regimens) and a control group (n=41, treated with non-anthracycline-based regimens). Blood glucose and lipid profiles were compared between the 2 groups.Results: Compared with the control group, the observation group had a significantly higher radiotherapy rate (74.00% vs. 43.90%, P=0.001) and a significantly higher proportion of patients receiving >6 cycles of chemotherapy (85.00% vs. 4.88%, P=0.000). There were no significant significances in the levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) before and after treatment (P>0.05) in both groups. TC and high-density lipoprotein (HDL) were not significantly different between the observation group and control group before chemotherapy (P>0.05). After chemotherapy, fasting blood glucose significantly increased in the observation group (5.31±0.98 vs. 4.96±0.53, P=0.031), while HDL significantly decreased (1.08±0.28 vs. 1.19±0.31, P=0.042). Multivariate logistic regression analysis showed that anthracycline-based chemotherapy was a protective factor for increased fasting blood glucose after chemotherapy in invasive cancer breast patients [P=0.022, odds ratio (OR) =0.227, 95% confidence interval (CI): 0.064-0.808], whereas receiving >6 cycles of chemotherapy was a risk factor for increased fasting blood glucose (P=0.014, OR =4.216, 95% CI: 1.337-13.296). Conclusions:Anthracyclines have little effect on fasting blood glucose in breast cancer patients; however, the incidence of abnormal blood glucose metabolism is gradually increasing after prolonged anthracycline use. Compared with other chemotherapy drugs, anthracycline-based chemotherapy has no significant impact on blood lipid metabolism.