Jia Ying Chen

Comparison of molecular analysis and touch imprint cytology for the intraoperative evaluation of sentinel lymph nodes in primary breast cancer: Results of the China Breast Cancer Clinical Study Group (CBCSG) 001c trial

BACKGROUND To validate the clinical value of the One-Step Nucleic Acid Amplification (OSNA) Breast Cancer System for the intraoperative detection of sentinel lymph node (SLN) metastases in early-stage breast cancer patients in a Chinese population, a prospective, multicenter trial, the China Breast Cancer Clinical Study Group (CBCSG)-001c trial, was conducted. The present study focused on the prospective comparison of the performance between OSNA and touch imprint cytology (TIC). METHODS The retrieved SLNs were divided into sections. Alternate slices from the tissue blocks were subjected either to OSNA analysis or to postoperative histopathology evaluation through serial sectioning. TIC was performed on every sample surface of each tissue block and was used by the surgeon to determine whether to perform an immediate ALND. RESULTS A total of 552 patients qualified for the analysis. The sensitivity, specificity, and overall accuracy of OSNA were 87.8%, 89.6%, and 88.4%, respectively, on a per-patient basis compared with those of TIC, which were 81.3%, 96.9%, and 92.0%, respectively. OSNA detected more micrometastasis-involved nodes than TIC (52.8% vs. 25.0%; p = 0.029) on a per-node basis. Tissue allocation bias (TAB) was the main cause of discordant results. The performance of TIC varied significantly among the institutes, while the performance of OSNA was steady. CONCLUSIONS Both OSNA and TIC can serve as qualified intraoperative assessments of SLNs. For institutes lacking the support of experienced cytopathologists, OSNA can be the first choice for the intraoperative assessment. In addition, OSNA can be applied as a complement to histopathology assessment. However, the results of the present study do not support the routine application of OSNA in the entire SLNs in place of pathology with serial sectioning.

The Usefulness of Preoperative Thyroid-Stimulating Hormone for Predicting Differentiated Thyroid Microcarcinoma

Objective Thyroid-stimulating hormone (TSH) is a known thyroid growth factor, but the pathogenic role of TSH in thyroid tumorigenesis is controversial. The aim of this study is to examine the relationship between preoperative TSH and differentiated thyroid microcarcinoma (DTMC). Data Sources We searched PubMed, EMBASE, Ovid, Web of Science, and the Cochrane Library from their inception to March 2015 and performed a systematic literature review of original studies. Review Methods Published studies that explored the relationship between preoperative TSH and DTMC were included for the review. We calculated odds ratio referring to different TSH concentrations between DTMC and control groups and used random effects model for the meta-analysis. Results Nine eligible studies that included 6523 patients were identified. Meta-analysis revealed that DTMC was associated with high TSH concentration (odds ratio = 1.23, 95% confidence interval = 1.03-1.46, P = .001). Metaregression analysis indicated that the disparity of control groups was the possible factor resulting in heterogeneity among the studies. Conclusions The risk of DTMC increases significantly in parallel with TSH concentration. These results support the hypothesis that TSH is involved in tumorgenesis of differentiated thyroid cancer.

Verteporfin inhibits papillary thyroid cancer cells proliferation and cell cycle through ERK1/2 signaling pathway

Verteporfin, a FDA approved second-generation photosensitizer, has been demonstrated to have anticancer activity in various tumors, but not including papillary thyroid cancer (PTC). In current pre-clinical pilot study, we investigate the effect of verteporfin on proliferation, apoptosis, cell cycle and tumor growth of PTC. Our results indicate verteporfin attenuates cell proliferation, arrests cell cycle in G2/S phase and induces apoptosis of PTC cells. Moreover, treatment of verteporfin dramatically suppresses tumor growth from PTC cells in xenograft mouse model. We further illustrate that exposure to MEK inhibitor U0126 inactivates phosphorylation of ERK1/2 and MEK in verteporfin-treated PTC cells. These data suggest verteporfin exhibits inhibitory effect on PTC cells proliferation and cell cycle partially via ERK1/2 signalling pathway, which strongly encourages the further application of verteporfin in the treatment against PTC.