Prognostic role of derived neutrophil-to-lymphocyte ratio in surgical triple-negative breast cancer.

INTRODUCTION: The role of derived neutrophil-to-lymphocyte ratio (dNLR) in predicting the prognosis of patients with triple-negative breast cancer (TNBC) has not been well studied. Here, we attempted to investigate the significance of dNLR in predicting the prognosis of patients with surgical (nonmetastatic) TNBC. METHODS: A total of 281 patients diagnosed with surgical TNBC in The First Affiliated Hospital of University of Science and Technology of China from February 2005 to March 2015 were retrospectively included in this study. Kaplan-Meier curve analysis was used to assess the disease-free survival (DFS) and overall survival (OS). We used Cox regression model to assess the prognostic significance of pretreatment dNLR and other clinicopathological parameters in TNBC patients. RESULTS: The median DFS in TNBC patients who had low dNLR and high dNLR was 28.9 and 15.1 months (P<0.001), respectively, whereas the median OS in patients who had low dNLR and high dNLR was 71.2 and 42.3 months (P<0.001), respectively. In patients aged ≤50 years and with invasive ductal carcinoma, a low dNLR predicted better DFS and OS compared with a high dNLR. Multivariate analysis demonstrated that the increased dNLR was a risk factor of poor DFS (HR=1.90, 95% CI: 1.52-2.46, P=0.007) and OS (HR=2.56, 95% CI: 1.69-3.58, P=0.001). CONCLUSION: Pretreatment dNLR is an independent factor of prognosis for TNBC patients, which potentially allows clinical doctors to improve outcomes of patients with high dNLR by treating with aggressive therapy, such as high-dose adjuvant chemotherapy and radiotherapy.

Downregulation of cell division cycle 25 homolog C reduces the radiosensitivity and proliferation activity of esophageal squamous cell carcinoma.

Radiation therapy is one of the most important methods of contemporary cancer treatment. Cells in the G2 and M phases are more sensitive to radiation therapy, and cell division cycle 25 homolog C (CDC25C) is essential in shifting the cell cycle between these two phases. In this study, the knockdown of CDC25C in human esophageal squamous carcinoma EC9706 cells was mediated by transfecting shRNA against human CDC25C-subcloning into pGV248. The levels of CDC25C mRNA and protein expression were assessed by reverse transcription-polymerase chain reaction (RT-PCR) and western blotting, respectively. Moreover, cell proliferation and radiosensitivity were measured. Stable CDC25C-knockdown EC9706 cell lines were successfully established. Furthermore, the proliferation of both control and CDC25C-shRNA-EC9706 cells was inhibited after the cells were treated with increasing X-ray doses, and the proliferation of the control cells was affected more significantly (p<0.05). Moreover, cell colony formation assays allowed us to reach the same conclusion. Taken together, our experiments demonstrated that the knockdown of CDC25C can reduce both the radiotherapy sensitivity and the proliferation activity of EC9706 cells. Thus, CDC25C might be a potential biomarker for radiotherapy treatment.