The treatment of recurrent head and neck cancers has improved from single modality interventions of surgery and radiation therapy alone to include combined modality therapy with surgery, chemotherapy and radiation. Combined therapy has led to improved local control and disease-free survival. New developments in radiation oncology such as intensity-modulated radiotherapy, brachytherapy, stereotactic radiosurgery, fractionated stereotactic radiotherapy, have helped to improve this outlook even further. These recent advances allow for a higher dose to be delivered to the tumor while minimizing the dose delivered to the surrounding normal tissue. This article provides an update of the new developments in radiotherapy in the management of previously-irradiated recurrent head and neck carcinoma.

Objective To study multiple-drug resistance expression of CNE1 and CNE2 cell lines induced by radiation and its reversal by cyclosporine A and interferon. Methods Drug-resistant CNE1 and CNE2 cell lines were induced by radiation, and expression of P-gp, MRP, TOPⅡ and GST-? on protein and mRNA level were analyzed by flow cytometry and reverse transcription-polymerase chain reaction methods before and after radiation. At the same time, effect of cyclosporine A and interferon on multiple-drug resistance expression induced by radiation was studied. Results The results showed that expression of P-gp, MRP and GST-? proteins on CNE1 and CNE2 cell lines were up-regulated by radiation, and cyclosporine A and interferon could reverse the up-regulation of P-gp and MRP proteins induced by radiation. Conclusion Radiation can induce multiple-drug resistance in CNE1 and CNE2 cell lines, and it can be reversed by cyclosporine A and interferon.

To elucidate the mechanism of mitochondrial damage induced by rotenone and the possible biological function of NADH in repairing mitochondrial damage of PC12 cells, cytotoxicity test, immunocytofluorescence and flow cytometric analysis were used to investigate the changes of cell proliferation genes (c myc, c erbB 2), apoptosis inhibition genes bcl 2, p53 tumor suppressor protein, cell immediate early gene (c fos) and proliferating cell nuclear antigen (PCNA) in PC12 cells before and after exposure to rotenone. The results showed that rotenone could significantly inhibit the proliferation rate of PC12 cells and expression of c erbB 2, c myc, p53, and bcl 2 in PC12 cells, NADH could restore the proliferation activity of PC12 cell damaged by rotenone by gene regulation. It is suggested that rotenone could induce PC12 cells apoptosis not only by regulating mitochondria phosphorylation process, but also by down regulating the expression of oncogene proteins (C erbB 2, c myc), anti apoptotic gene protein (bcl 2), p53 tumor suppressor gene protein, and upregulating the expression of the immediate early gene c fos. Regulation of bcl 2, c myc, c erbB 2 and p53 might be involved in the repair of mitochondrial damage of PC12 cells.

Objective To study the effect of hypoxia on EMT molecule E-cadherin, Vimentin and invasion of human breast cancer MCF-7 cells, reveal the mechanism of breast cancer invasion and metastasis and provide experimental and theoretical basis. Methods Western blot was used to observe the change of HIF-1α, E-cadherin and Vimeutin during hypoxia on MCF-7. MTT was used to study the effects of viability.Transwell chamber was used to detect the ability of invasion and metastasis. Results The expression of E-cadherin was significantly lower (0.09±0.02)(t=30.98,P=0.0007) and the expression of Vimentin was significantly higher (0.69±0.04) (t=915,P=0.0000) with the extension of hypoxia.The capability of adhesion (81.23±0.74) (t=82.05,P=0.000),invasion(120±6) (t=22.78,P=0.0009) and migration(190±6) (t=23.49,P=0.000)was significantly increased after 72 h hypoxia(P＜0.05).Conclusion Hypoxia can downregulate E-cadherin and upregulate Vimentin and enhance the adhesion,invasion and migration of MCF-7.

Objective To collect the hot spots, development trends, high yield authors and their affiliated institutions by analyzing the papers on pancreatic cancer chemotherapy in recent 5 years. Methods The papers on pancreatic cancer chemotherapy were downloaded from PubMed. Their high frequency subject headings extracted by BICOMB were analyzed by bibliometric double clustering analysis and strategic coordinate analysis. The high yield authors were analyzed by co-authorship group analysis. Results The current studies on pancreatic cancer chemotherapy in foreign countries were focused on the pathological features of pancreatic duct adenocarcinoma before and after chemotherapy, drug therapy of pancreatic cancer according to its genetics, metabolism and pharmacology of antitumor drugs, surgical treatment combined with radiotherapy and chemotherapy for pancreatic cancer. The high yield authors could be divided into two large groups from Japan and USA and a number of small groups. Conclusion New breakthrough points should be found from the matured topics, the topics with a further developmental space should be greatly concerned, and cooperation should be strengthened between study groups or teams.

Objective: To compare the difference of Response Evaluation Criteria in Solid Tumors 1.1 (RECIST 1.1) and modified Re-sponse Evaluation Criteria in Solid Tumors (mRECIST) in the treatment of hepatocellular carcinoma (HCC) after stereotactic body radio-therapy (SBRT). Methods:From Janurary 2014 to August 2015, thirty-five patients with HCC treated with SBRT were included in De-partment of Radiation Oncology and Integrative Oncology of Navy General Hospital of PLA, and SBRT efficacy was evaluated based on RECIST 1.1 and mRECIST criteria. Results:Under RECIST 1.1, one patient had complete response (CR), 20 had partial response (PR), and 11 achieved stable disease (SD) at three months. Three patients had progressive disease (PD). The overall best response rate (CR+PR) was 60%. In comparison, under mRECIST, 10 patients had CR, 16 had PR, and 6 achieved SD at three months. Three patients had PD. The overall best response rate was 74.28%. The statistical analysis showed that Kappa=0.402 (χ2=43.3, P<0. 001) was less than 0.75 but greater than 0.4, indicating that it had not reached the two diagnostic criteria of consistency degree of satisfaction. According to the mRECIST criteria, the objective remission group (CR+PR) was superior to the nonobjective remission group (SD+PD) in progression-free survival (P<0.001). Conclusion:For unresectable HCC, mRECIST may be more useful than RECIST 1.1 in evaluating HCC response to SBRT.

BACKGROUND: Flubendazole is an anthelmintic and categorized in benzimidazole. Previous evidence indicates its suppression on proliferation of colon cancer and breast cancer cells. Our study aims to explore the effects of flubendazole on non-small cell lung cancer A549 and H460 cell lines and the underlying mechanism. METHODS: CCK-8 assay was used to detect the effect of flubendazole at different concentrations on viability of both cell lines A549 and H460. We used western blot to detect the expression levels of autophagy-related proteins p62 and LC3 after flubendazole treatment. Cells were transfected with tandem fluorescent adenovirus (mRFP-GFP-LC3), and the impact of flubendazole treatment on autophagic flux were analyzed. RESULTS: Cell viability analysis showed a dose-dependent inhibitory effect on proliferation of both A549 and H460, comparing to cells without flubendazole treating (P<0.001). Level of p62 decreased and LC3 II/I ratio increased in cells treated with 2 μmol/L flubendazole for 24 h and 48 h, compared to control groups (P<0.005). Red fluorescence signals increased in mRFP-GFP-LC3 transfected cells after flubendazole treating, suggesting an elevation in autophagic flux. CONCLUSIONS Flubendazole may inhibit the proliferation of A549 and H460 cells and promote autophagy.

Objective To investigate the effect of long non-coding RNA (lncRNA) LNC01309 on the proliferation and migration abilities of human hepatocellular carcinoma (HCC) cells and its mechanism of action. Methods HCC samples and corresponding adjacent tissue samples were collected from 12 patients with HCC who underwent surgical treatment in The Sixth Medical Center of PLA General Hospital from February 2018 to June 2019, and quantitative real-time PCR was used to measure the relative expression level of LNC01309. Quantitative real-time PCR was also used to measure the expression level of LNC01309 in human hepatoma cell lines (HepG2, SNU-398, and Hep3B) and the human immortalized normal liver cell line THLE-2. After LNC01309 was overexpressed in HepG2 cells, the cells were divided into plasmid control group (pEXP-control) and overexpression group (pEXP-LNC01309). CCK-8 assay was used to observe the change in cell proliferation, and wound healing assay and Transwell assay were used to observe migration ability. RNA co-immunoprecipitation was used to detect the interaction between LNC01309 with RBM38, with cells divided into IgG group and RBM38 antibody group, and cycloheximide chase assay was used to analyze the effect of LNC01309 on the stability of RBM38 protein. RBM38 was overexpressed in HepG2 cells to conduct the recovery experiment, and CCK-8 assay, wound healing assay, and Transwell assay were used to observe the changes in cell proliferation and migration abilities. The t -test was used for comparison of continuous data between two groups. Results The mean expression level of LNC01309 in HCC tissue was significantly higher than that in adjacent tissue (4.225±2.285 vs 1.541±0.530, t =3.618, P =0.004), and the relative expression level of LNC01309 in hepatoma cells (HepG2, SNU-398, and Hep3B) was also significantly higher than that in normal hepatocytes (THLE-2) ( t =4.231、6.489、14.480, all P < 0.05). Compared with the control group, HepG2 cells with the overexpression of LNC01309 had significant increases in growth rate (OD 450 value at 96 hours: 1.885±0.107 vs 2.527±0.234, t =4.330, P =0.012) and migration ability (11.65%±2.40% vs 35.66%±4.90%, t =9.837, P < 0.001; 100.00%±3.11% vs 161.00%±35.93%, t =4.399, P =0.005); however, the upregulated proliferation and migration abilities of hepatoma cells induced by LNC01309 overexpression were partially inhibited by RBM38 (OD 450 value at 96 hours: 2.500±0.227 vs 1.913±0.282, t =2.812, P =0.048; 168.00%±9.43% vs 117.20%±18.03%, t =6.622, P < 0.001). Compared with the IgG control group, RBM38 antibody significantly enriched the precipitation of LNC01309 ( t =3.846, P =0.031). The results of cycloheximide chase assay showed that the LNC01309 overexpression group had a significant reduction in the stability of RBM38 protein ( t =8.038, P =0.001). Conclusion The newly identified LNC01309 reduces the stability of RBM38 protein through interaction with RBM38 and promotes the proliferation and migration of HCC cells.