Laryngeal cancer is one of the most common malignant tumors in the respiratory tumors, and its incidence ranks second highest in the respiratory tumors. Resveratrol (Res) is a kind of polyphenols, which can inhibit nucleotides can inhibit the growth of liver cancer cells, gastric cancer cells, pancreatic cells and other tumor cells by inhibiting ribonucleotide reductase in the cells. Taxol (Tax) is a kind of secondary metabolites of Taxus chinensis, which has anti-tumor activity for breast cancer, cervical cancer, ovarian cancer and other tumors by inhibiting cellular microtubule depolymerization. But at present the effects of resveratrol combined with taxol on human laryngeal carcinoma cell strain Hep-2 and their underlying molecular mechanisms are rarely reported. After human laryngeal cancer cell Hep-2 cells were processed with resveratrol (Res) and taxol (Tax), CCK-8 assay was used to evaluate the effect of these two herbs on the proliferation of cancer cells; AO/PI staining and JC-1 were used to detect Hep-1 cells apoptosis; the expression of Bax, Bcl-2, PARP, TRIB3, and XIAP genes was detected by real time quantitative PCR; the activity of caspase-3 and caspase-8 was determined with quantitative fluorescence method. The experimental results showed that compared with Tax, Res medication alone, joint group significantly enhanced inhibition of Hep-2 cells activity, decreased the dosage of Tax, increased the expression of Bax and PARP, TRIB3, reduced the expression of the Bcl-2 and XIAP, and promoted the activity of caspase-3 and caspase-8. The test results showed that compared with the single medication, combined group could significantly increase the inhibitory effect on Hep-2 cells, significantly reduce Tax dosage, increase expressions of Bax, PARP, TRIB3, reduce expressions of Bcl-2, XIAP, and promote activity of caspase-3, caspase-8. This indicated apoptosis of human laryngeal carcinoma cell strain Hep-2 may be induced with Res, Tax, and the combination of these two herbs by mitochondria pathway. It provides valuable clue for further research on combination of Res and Tax for the treatment of laryngeal cancer, and expanding the combined application of Res and Tax.

To assess the efficacy of vinorelbine (NVB)-based regimens in patients with metastatic triple negative breast cancer (mTNBC) pretreated with anthracyclines and taxanes.

This study aims to evaluate the efficacy and safety of crizotinib for advanced ALK-positive non-small cell lung cancer (NSCLC) patients.

To investigate whether SIS3, a specific inhibitor of Smad3 phosphorylation, can reverse the stemness of multidrug-resistant(MDR) hepatocellular carcinoma cells.

One of the most often distance metastasis site of non-small cell lung cancer (NSCLC) is brain and the standard treatment of brain metastasis was radiotheraphy including whole brain irradiation (WBI) and stereotactic radiotherapy (SRT). It has been reported that epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) had the active response in brain metastasis of lung cancer. In the present study, we reported one case of EGFR 19el in cerebrospinal fluid tested by ARMS got partial response given erlotinib.

Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) resistance significantly limits its use in clinical practice. Study found that TRIM24 was overexpressed in non-small cell lung cancer (NSCLC) tissues and regulate cell growth, cell cycle and apoptosis in lung cell lines. The aim of this study is to explore the mechanism of TRIM24 to regulate resistance of Gefitinib in NSCLC cells.

The DNA damage of the irradiated tumor cells is mainly single strand breaks (SSBs) and double strand breaks (DSBs), in which the frequency of occurrence of SSBs is dozens of times than DSBs. However, most of the SSBs could be repaired by the Poly (ADP-Ribose) Polymerase (PARP) and other related factors. Recently listed drug-Olaparib (PARP1/PARP2/PARP3 inhibitor) could target the repair pathways of single strand breaks, and recent clinical trials of PARP inhibitors combined with chemotherapy obtained encouraging results. The aim of this study is to investigate the effect and potential mechanism of radiosensitization of Poly (ADP-Ribose) polymerase inhibitor-Olaparib on lewis cells and xenografts.

To analyze the duration of preventive filgrastim administration as support for chemotherapy and its affecting factors.

To observe the efficacy and safety of chemotherapy regimens oxaliplatin combined with capecitabine (CAPOX) or oxaliplatin combined with tegafur, gimeracil and oteracil potassium capsules (S-1)(SOX), and to investigate the value of expression of thymidine phosphorylase (TP) and dihydropyrimidine dehydrogenase (DPD) proteins in tumor tissue for predicting the efficacy of CAPOX and SOX regimens in advanced gastric cancer patients.

To explore the safety and efficacy of pegylated recombinant human granulocyte colony-stimulating factor (PEG-rhG-CSF) in preventing chemotherapy-induced neutropenia in patients with breast cancer and non-small cell lung cancer (NSCLC), and to provide the basis for clinical application.

To explore the effect of a Chinese medicine, Xiaoaiping, in combination with cisplatin on the proliferation, invasion and apoptosis in human ovarian cancer HO-8910PM cells in vitro and vivo.

To investigate the changes of ID1 expression in tumor cells treated with etoposide, cisplatin and ultraviolet (UV) irradiation, and explore the effect of ID1 on chemotherapeutic drug- and UV-induced apoptosis.

To explore the effect of lycorine in inducing apoptosis of pulmonary carcinoma cell A549 and its mechanism. In the study, pulmonary carcinoma cell A549 were taken as the experimental subject and processed with different concentrations of lycorine (0, 0.5, 1.0, 2.0, 4.0 and 8.0 μmol x L(-1)). The MTT method was used to observe the cell proliferation. The apoptosis rate of A549 cells was determined by Annexin FITC/PI double staining. The microplate reader was used to detect the activities of Bcl-2, Bax and p53. The changes in mitochondrial membrane potential were measured by the flow cytometry. The expressions of apoptosis-related factors Bcl-2, Bax, p53 and Survivin were determined by Real-time PCR. The results showed that lycorine significantly inhibited the proliferation of A549 cells (P < 0.05), induced the apoptosis on A549 cells (P < 0.05), increased the activities of Bax and p53, reduced Bcl-2 activity and mitochondrial membrane potential, and notably changed the gene expressions of Bcl-2, Bax, p53 and Survivin (P < 0.05). In conclusion, lycorine can induce the apoptosis of A549 cells and be applied to treat pulmonary carcinoma. Its mechanism may be related to the activation of relevant factors in Bcl-2 signaling pathway.

To study the effect of sodium aescinate in inducing human breast cancer MCF-7 cells apoptosis and its possible mechanism. MTT assay was used to detect the inhibitory effect of sodium aescinate on the proliferation of MCF-7 cells. The morphological changes were observed under inverted microscope. DAPI nuclear staining was used to detect the changes in cell nucleus. Annexin V-FITC/PI flow cytometry was adopted to test the apoptosis rate. Changes in apoptosis-related proteins (PARP, cleaved caspase-8 and pro-caspase-3), cell survival-associated signal molecules (AKT and ERK) and their common upstream kinase SRC was detected by Western blotting. The result showed that after different concentrations of sodium aescinate were used to treat breast cancer MCF-7 cells, they inhibited the proliferation of MCF-7 cells in a dose-dependent manner, induced cell apoptosis (typical morphological changes in nucleus, significant increase in cell apoptosis rate). The expressions of cleaved PARP and caspase-8 increased, while the expression of pro-caspase-3 decreased, which further verified sodium aescinate's effect in inducing cell apoptosis. Sodium aescinate significantly inhibited the phosphorylation of cell survival-related signal molecules (AKT, ERK) and down-regulate the activation of their common up-stream kinase SRC. The findings indicated that sodium aescinate can block signals transiting to downstream molecules AKT, ERK, inhibit the proliferation of breast cancer cell MCF-7 cell apoptosis and induced cell apoptosis by suppressing the activation of SRC.

Evodiamine is one of the most important antitumor alkaloid from evodiamine. This study focused on the mechanism of evodiamine in inducing apoptosis of gastric cancer SGC-7901 cells through mammalian target of rapamycin (mTOR) signal pathway, in order to explore its antitumor mechanism and lay a foundation for clinical treatment of gastric cancer. The sole cytotoxic effect of evodiamine on SGC-7901 cells and human peripheral blood mononuclear cells (PBMCs) was observed by MTT assay. After the cells were respectively intervened with single evodiamine or evodiamine combined with z-VAD-fmk, the gene expressions of mTOR, p70S6K and 4EBP1 were analyzed by real-time PCR, and the protein expressions of mTOR and p-mTOR were detected by western blot. The result showed that evodiamine inhibited the apoptosis of SGC-7901 cells in a time-dependent manner, with no cytotoxic effect on human PBMCs. After the respective intervention with single evodiamine or evodiamine combined with z-VAD-fmk, the cells became round and floated in medium. Compared with the control group, both treatment methods can inhibit mTOR, 4E-BP1 and p70S6K gene expressions, with significant differences. Compared with single evodiamine, evodiamine combined with z-VAD-fmk showed a higher inhibitory rate in gene expression. According to the Western Blot result, evodiamine can inhibit the protein expressions of mTOR and p-mTOR regardless of the combination with z-VAD-fmk, with a higher inhibitory rate after z-VAD-fmk blocked caspase. In conclusion, evodiamine may promote the apoptosis of SGC-7901 cells through mTOR signal pathway.

To investigate the chemical compounds from aerial part of Rehmannia glutinosa, six compounds were isolated and deter- mined by extensive spectroscopic analysis as(+)-(7S, 8S, 8'S)-9-O-[β-D-glucopyranoyl] asarininone(1), 2α,3β,19α,23-tetrahydroxy-olean-12-en-28-oic acid(2),7,3'-dihydroxyl-5'-methoxyisoflavone (3), aeginetic acid (4), corchorifattty acid B (5), pinellic acid (6). Among them, compound 1 was a new natural product. Compounds 2, 3 and 5 were obtained from the Rehmannia genus for the first time. In vitro study showed that none of the six compounds exhibited obvious activities to BEL-7402 and HCT-8 at the concentration of 10 mg x L(-1).

To analyze and evaluate the clinical efficacy of heat-sensitive moxibustion for symptoms of large intestine cancer.

To observe the clinical effect of Huikangling Tablet (HT, extracted from Scabrous Patrinia root) on peripheral blood micrometastasis of differentiated thyroid carcinoma (DTC) patients.

To investigate the relationship between and underlying mechanistic pathway of clusterin (CLU) and chemo-resistance ofhepatocellular carcinoma (HCC) cells.

To explore the effects of low molecular weight heparin (LMWH) on cisplatin (DDP)- induced apoptosis in human hepatocellular carcinoma cell and the underlying mechanisms.