Malignant tumor is one of the principle diseases which threatens the health of human being, and its incidence rate has been dramatically increased in recent years.Modern medical model has transformed from biomedical model to the model of "biology-psychology-society",from experience-based medicine to evidence-based medicine (EBM).At the same time,individualization is also one of important principles of tumor combined therapy.EBM and individualization treatment are not to opposed to each other but to complement each other. This article expounded the relationship of EBM and individualization treatment in tumor therapy,and showed that both of these two principles must be grasped arid carried out in clinical work.

Biochemotherapy refers to the combination of biotherapy and chemotherapy,and it has been rapidly developed since its emergence.Biochemotherapy has brought both new therapies and new therapeutic ideas for the treatment of malignant tumors.In this article,we reviewed the recent advances in tumor biochemotherapies,including expansion of the indications,retaining of therapy even when tumor progressed(unique to biochemotherapy),and reversal of chemotherapy resistance by targeted therapy,the predicting response to tumor biochemotherapy,recent clinical trials of immunotherapy-based chemotherapy,and evaluation criteria for assessment of biochemotherapy response,and so on.

Objective To generate cytokine induced killer (CIK) by inducing lymphocytes cells from peripheral blood in vitro , and to study the phenotype and biological activities of CIK. Methods Lymphocytes cells were isolated fresh from peripheral blood of healthy donors by Ficoll Hypaque density centrifugation, and the cells obtained were resuspended in RPMI medium consisting of 10% fetal calf serum at 37℃, 5%CO 2 for 2h. On day 0, the nonadherent cells were activated with IFN ? (1 000U/ml) and the following days were stimulated with CD3mAb (3 75?g/ml) and rhIL 2 (600U/ml). Phenotype of CIK were analysed by FACS. The proliferation of CIK was tested using 3 H Thymidine, and the killing experiment using MTT tests. Results The proliferation peak of CIK was at day 20, and declined at day 30. The percentages of the cytotoxicity of CIK cells for stomach cancer cell line MGC803 and liver cancer cell line Bel7402 was 65 45%?5 68% and 68 37%?3 93% respectively. CIK cells expressed the phenotypes of CD3CD56, CD3, CD54, CD28CD54, CD11a, HLA DR and CD28. Conclusion IFN ?, CD3mAb and rhIL 2 can induce strong proliferation of peripheral lymphocytes to produce CIK cells expressing the phenotype of CD3CD56, CD3, CD54, CD28CD54, CD11a, HLA DR, CD28, which have strong cytotoxicity on tumor cells.

Objective　To investigate dynamic changes of the p53 gene and its protein during occurrence and metastasis of colorectal cancer and explore the relationship between p53 mutation and survival of the patients. Methods　p53 gene (exon 5-9) was examined by PCR, denaturing gradient gel electrophoresis (DGGE) and automated sequencing. Results　p53 alterations were found in exons 5 through 9 in 26 of the 41 patients (63%). Of the 26 patients, 6 had the alterations in the liver metastatic lesions but not in the original colorectal lesion. The other 20 had the alterations in both of the primary colorectal and hepatic metastatic lesions. Meanwhile, an additional mutation in the metastatic lesions was found in 3 cases. The analysis about the survival revealed that the patients with mutant p53 in the metastatic lesions had a longer survival as compared with those with wild type p53. Conclusion　In the process of liver metastasis of the colorectal cancer, p53 mutations mainly start in the primary colorectal lesion and then is kept and brought into the liver. It also might start from metastatic lesion in a few cases. For the patients who had liver metastasis of colorectal cancer and underwent hepatectomy, the survival is longer in mutant p53 group than in wild type p53 group.

To investigate the prognostic value of serum levels of tissue polypeptide specific antigen (TPS) in patients with hepatocellular carcinoma(HCC). Ninety six patients who had undergone hepatoma resections and 22 patients who received radio frequency ablations (RF) were followed up for 6～12 months.The serum levels of TPS were repeatedly determined.The RF group patients were divided into three subgroups: improved ,stable,and advanced.The median levels (U/L) of serum TPS in advanced subgroup were always higher than those in improved subgroup ( P

To investigate the value of tissue polypeptide specific antigen(TPS) in the diagnosis of hepatocellular carcinoma (HCC), the serum levels of TPS and alfa fetoprotein (AFP) were measured by TPS TM ELISA and enzyme immunoassay respectively in 96 patients with HCC, 30 patients with cirrhosis, 20 patients with hepatitis and 20 healthy controls.The diagnostic sensitivity of TPS and AFP is 89 6% and 73 0% respectively.There is a significant difference between them ( P

To investigate the expression of cytokeratin 18(CYK18) in hepatocellular carcinoma(HCC) cell membrane and the relationship between the serum levels of tissue polypeptide specific antigen (TPS) and the proliferating activity of HCC cells. The serum levels of TPS were determined by TPS TM ELISA in 96 patients with HCC. Four micrometer paraffin embeded sections of liver specimens from these patients were immunostained with the strept avidin biotin complex immunoperoxidase technique (IHC SABC). All of the HCC preparations were positively stained by CYK 18 and proliferating cell nuclear antigen (PCNA) with IHC SABC.The results of PCNA stainings were: + in 62 5%, in 26 0%,  in 8 3%,and  in 3 1% .The median levels of TPS in the four groups were: + 137 98 U/L,  685 3 U/L,  in 1 126 U/L and  4 672U/L respectively. There were significant differences among these groups ( P

Objective To explore the inhibitory effects of sorafenib combined with cisplatin (DDP) on human hepatocellular carcinoma cells HepG2 in vitro, and the possible underlying mechanisms. Methods The HepG2 cells were divided to 4 groups as control group, sorafenib group, cisplatin group and sorafenib-cisplatin group. Sorafenib and cisplatin were used in single agent or in combination against HepG2 in vitro. The inhibitory effects of sorafenib and/or cisplatin on proliferation of HepG2 were determined by MTT assay at 24h, 48h, 72h and 96h after the addition of the drugs to HepG2 culture. Cell cycle at 24h time point and apoptosis at 48h time point were examined by flow cytometry (FCM). At 24h time point, cells were labeled by Rhodamine123 and mitochondrial transmembrane potential (??m) was determined by FCM, while caspase-3 activity was assessed by caspase-3 colorimetric assay. Results MTT assay showed that sorafenib and cisplatin, when used as a single agent or in combination, could inhibit the growth of HepG2 cells and induce apoptosis in vitro, while synergistic effect was noted when lower doses of sorafenib and DDP were used in combination. It was also found that combined use of sorafenib and cisplatin arrested HepG2 cells at G0/G1 and G2 phase as shown by cell cycle analysis, and the highest apoptosis rate appeared in sorafenib-cisplatin combination group (P

Objective To observe and compare the anti-angiogenic effect of sorafenib, unfractionated heparin(UFH)and low molecular weight heparin (LMWH), singly used or in combination, with chick chorioallantoic membrane assay. Methods Sixty 8d-developed chick embryos were randomly divided into 6 groups (10 each): control group, sorafenib group, UFH group, LMWH group, sorafenib+UFH group, and sorafenib+LMWH group. Drugs were given respectively and incubation continued. The dosage of drugs for each embryo was 20 nmol of sorafenib, 5U of UFH and 5U of LMWH, respectively, and H-DMEM was applied to the embryo in control group in the same volume (2?l). After continuing incubation for another 72h, the anti-angiogenic effect in each group was observed and the vascular number in the chick chorioallantoic membrane was counted. Results Vascular number in single drug groups (sorafenib group: 8.9?1.9; UFH group: 7.6?2.3; LMWH group: 6.9?1.3) was significantly smaller than that in the control group (26.8?2.3, P

To investigate the therapeutic effects of recombinant humanized anti-HER2 antibody (Herceptin) on Her-2/neu-overexpressing metastatic human breast cancer, 7 patients with Her-2/neu-overexpressing metastatic human breast cancer were involved in this study. The results indicated that the therapeutic effective rate was 71. 4%. CR. PR, SD. PI) were seen in 2. 3, 1, 1 cases, respectively. No side reactions were observed. The results revealed that the therapeutic effect of Herceptin is intimately linked to Her-2/neu expression of breast cancer.