SPARC/osteonectin expression is reportedly altered in various malignancies. However, little is known regarding to the prognostic value of SPARC in triple-negative breast cancer (TNBC) patients. In this study, immunohistochemistry and immunoreactive scores (IRSs) were used to evaluate SPARC protein expression in primary tumors from 211 TNBC patients with up to 10 years of clinical follow-up data. High SPARC expression (IRS ≥3) was detected in 52.1% of primary tumors. Patients expressing high SPARC levels had worse disease-free survival (DFS) (HR=1.58, 95% CI: 1.01-2.47, P=0.044) and overall survival (OS) (HR=1.74, 95% CI: 1.06-2.85, P=0.029) than patients with lower SPARC levels. Furthermore, high SPARC expression was an independent prognostic factor for both DFS (HR=1.73, 95% CI: 1.10-2.73, P=0.018) and OS (HR=1.90, 95% CI: 1.14-3.16, P=0.014) in TNBC patients. These results suggest that increased SPARC expression may be an indicator of greater aggressiveness, and may serve as a prognostic factor for triple-negative breast cancer.
Breast cancer is a multistep, multifactorial, and heterogeneous disease. Significant transformations have occurred in the systemic management of breast cancer in the past decade. Due to the further understanding of pathogenesis, scientists have found plenty of signaling pathways and correspondingly therapeutic targets in breast cancer, such as hormone receptor, human epidermal growth factor receptor 2 (HER2), epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF), phosphoinositide-3-kinase (PI3K), v-akt murine thymoma viral oncogene homolog (AKT), mechanistic target of rapamycin (mTOR), cyclin-dependent kinase 4/6 (CDK4/6), poly (adenosine diphosphate-ribose) polymerase (PARP), and programmed death-1 (PD-1). Targeted therapy, which optimizes the accuracy of antitumor activity and minimizes toxicity to normal tissues, plays a crucial role in breast cancer treatment in the era of precision medicine. In this review, we aimed to summarize the latest developments in targeted therapy for breast cancer and discuss the existing problems.
Locally advanced or metastatic disease accounts for the majority of breast cancer-associated cases of mortality. Treatment options for patients with locally advanced or metastatic disease are limited. The current study aimed to explore the efficacy and safety of apatinib combined with chemotherapy in patients with previously treated advanced breast cancer in real-world clinical practice. A total of 85 patients with advanced breast cancer, who had previously been exposed to anthracyclines or taxanes, received combined treatment. Tumor response was evaluated by a computed tomography scan based on the Response Evaluation Criteria in Solid Tumors. Adverse events were graded based on the Common Terminology Criteria for Adverse Events. The Kaplan-Meier method and a log-rank test were used to analyze the univariate discrimination of progression-free survival (PFS) and overall survival (OS) by demographic data, baseline clinical information and toxicities. The combined effects of these variables were analyzed by a Cox proportional hazards regression model. At a median follow-up time of 9.7 months, 73 patients exhibited disease progression and 48 had succumbed to the disease. During the follow-up, 19 patients demonstrated a partial response (PR) and 53 patients achieved stable disease (SD), with an objective response rate of 23.2%. Additionally, 39 patients demonstrated a PR or SD for ≥24 weeks, with a clinical benefit rate of 47.6%. The median PFS was 4.4 months [95% confidence interval (CI)=2.8–6.0] and the median OS was 11.3 months (95% CI=8.9–13.8). No treatment-associated mortalities occurred. The most common adverse events of all grades included myelosuppression (49.4%), gastrointestinal reaction (45.9%) and fatigue (43.5%). Proteinuria was an independent predictive factor for PFS and OS. Apatinib combined with chemotherapy appeared to be efficacious for pretreated advanced breast cancer, with acceptable toxicity for real-world clinical practice.
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