ABSTRACT
BACKGROUND@#Gastric cancer (GC) is one of the most globally prevalent cancers in the world. The pathogenesis of GC has not been fully elucidated, and there still lacks effective targeted therapeutics. The influence of altered kinesin superfamily protein 22 (KIF22) expression in GC progression is still unclearly. The aim of this study was to investigate the KIF22 effects on GC and related mechanisms.@*METHODS@#Gastric carcinoma tissues and matching non-cancerous tissues were collected from patients with GC who have accepted a radical gastrectomy in Lanzhou University Second Hospital from May 2013 to December 2014. The expression of KIF22 was examined in GC of 67 patients and 20 para-carcinoma tissues by immunochemical staining. The relationship between the expression of KIF22 and clinicopathologic characteristics was next investigated in the remaining 52 patients except for 15 patients who did not complete follow-up for 5 years. Cell viability was performed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) test and colony formation assay in the MGC-803 and BGC-823 GC cells. Cell scratch and trans-well invasion assay was performed to assess migration ability in the MGC-803 and BGC-823 GC cells. Gene set enrichment analysis (GSEA) pathway enrichment analysis was performed to explore the potential functions. Cell cycle was detected by flow cytometry. In addition, the two GC cell lines were used to elucidate the underlying mechanism of KIF22 in GC in vitro via assessing the effects on mitogen-activated protein kinase and extracellular regulated protein kinases (MAPK/ERK) signal transduction pathway-related expressions by Western blotting assays. The differences were compared by t tests, one-way analysis of variance, and Chi-squared tests.@*RESULTS@#The study showed that KIF22 was up-regulated in GC, and KIF22 high expression was significantly related to differentiation degree (χ = 12.842, P = 0.002) and poorly overall survivals. GSEA pathway enrichment analysis showed that KIF22 was correlated with the cell cycle. Silence of KIF22 decreased the ability of the proliferation and migration in gastric cells, induced G1/S phase cell cycle arrest via regulating the MAPK-ERK pathways.@*CONCLUSIONS@#KIF22 protein level was negatively correlated with prognosis. KIF22 knockdown might inhibit proliferation and metastasis of GC cells via the MAPK-ERK signaling pathway.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of different injection techniques of radiotracer on the visualization rate of internal mammary sentinel lymph nodes (IMSLN) in breast cancer patients.</p><p><b>METHODS</b>A series of 137 consecutive breast cancer patients was included in this prospective study. Fifty-eight patients (group A) received the radiotracer (99)Tc(m)-sulphur colloid injected only into 1-2 points in the breast parenchyma in one quadrant, and seventy-nine patients (group B) received the radiotracer injection into the breast parenchyma in two quadrants of the breast. The differences of IMSLN visualization rates of the two groups were compared and the relevant affecting factors were analyzed.</p><p><b>RESULTS</b>The IMSLN visualization rate of the group B (70.9%, 56/79) was significantly higher than that of the group A (13.8%, 8/58) (P < 0.001). Both techniques seemed to be reliable to identify sentinel lymph node in the axilla (98.7% vs. 98.3%, P = 0.825). In addition, the visualization rate of internal mammary hotspots (82.2%) was more commonly seen in patients receiving injection of a larger volume of radiotracer ( ≥ 0.5 ml/point) than those receiving a smaller volume of radiotracer (<0.5 ml/point, 55.9%, P = 0.011).</p><p><b>CONCLUSIONS</b>The modified injection technique (two quadrants, large volume radiotraver, and ultrasound guidance) can significantly improve the visualization rate of IMSLN. Our findings should make the biopsy of IMSLN widely implemented and provide an effective and minimally invasive technique to evaluate the internal mammary lymph node status.</p>