Objective To investigate the influence of the aberrant protein expression and mRNA transcription of transforming growth factor ? 1(TGF? 1) on the biological behavior of human bladder transitional cell carcinomas. Methods The expression of TGF? 1 was investigated in 74 specimens of TCCs by SP immunohistochemistry staining, and the level of TGF? 1 mRNA were determined in 43 cases of TCCs by the method of quantitative RT PCR. Results The positives expression rate of TGF? 1 was 89.2%. Superficial tumors had lower overexpressive rate of TGF? 1(33.3%) than the invasive TCCs(83.8%), P

Purpose:To investigate the relationships between the biological behavior of human transitional cell carcinomas(TCCs) and the protein expression of transforming growth factor ?1(TGF?1) as well as its'related receptors.Methods:The expression of TGF?1 ,T?RⅠ,T?RⅡ and PCNA were examined in 74 specimens of TCCs by S P immunohistochemistry staining.Results:The positive expression rate of TGF?1 , T?RⅠ and T?R Ⅱ were 89.2%,70.3% and 48.6%,respectively. Superficial tumors had lower overexpression rate of TGF?1 (33.3%) than muscle invasive TCCs (83.8%) ( P

Objective To investigate the expression of c-kit and analyze its relationship with proliferating cell nuclear antigen (PCNA) in RCC subtypes and its clinical progression. Methods Expression of c-kit protein was retrospectively studied with immunohistochemistry in paraffin sections from 137 cases of clear renal cell carcinoma (CCRCC), 82 papillary renal cell carcinoma (PRCC), 51 chromophobe renal cell carcinoma (ChRCC). Results The positive rate of c-kit in ChRCC was 94.1%(48/51), it was statistically higher than that in CCRCC (16. 1%, 22/137) and PRCC (28.1 %, 23/82)(P=0. 001 ). In ChRCC, the positive expression of c-kit was related with TNM stages. The positive expression of PCNA was related with the grade in CCRCC and PRCC. But there was no relationship between PCNA expression and grade of ChRCC. It also had the relationship with the metastasis in CCRCC. Conclusions The expression of c-kit in ChRCC is higher than in other subtype of RCC, and associated with tumor local progression. That makes c-kit as a helpful marker to discriminate different subtypes of kidney cancer.

Objective To study the effect of macrophage, its stimulating factor, granulocyte macrophage colony-stimulating factor (GM-CSF), the combination of GM-CSF and macrophage on the survival of rat deep epigastric perforator flap (DEP). Methods The stable animal model of DEP flap in Sprague-Dawley rat mimicing human deep inferior epigastric perforator flap in breast reconstruction was established. The rats were treated with subcutaneous injection of recombined rat GM-CSF or rat peritoneal macrophages, respectively, or combination of GM-CSF/ Macrophages. Normal saline was used as parallel negative control. The rats were sacrificed and flap specimens were harvested on day 7 after operation, the flaps survival area were measured by the method of rubbings and the survival proportion of flaps were calculated, Von Will brand factor were detected by immunohistochemistry and microvessel density (MVD), and were calculated with microscopic study, and collagen were stained and quantified by Masson staining. Results Survival proportion of flaps in group GM-CSF (53.08% ± 8. 76% ) was not different with that in macrophages group (47. 95% ± 4. 92% ), and both of these two groups were significantly higher than parallel negative control group (43.28% ± 5.27% ) but significantly lower than combination GM-CSF/ macrophages group ( 61.68% ± 6. 60% ). For MVD, flap in GM-CSF group ( 24. 82 ± 4. 18 ) was not significantly different with macrophages group (24.30 ± 3.02 ), and both of these two groups were significantly higher than group parallel negative control (21.37 ± 2.65 ) but significantly lower than combination GM-CSF/macrophages group ( 29. 82 ± 4. 74). Collagen deposition in the flaps in GM-CSF group (17. 25% ± 2. 85% ) were significantly higher than parallel negative control group (14.41% ± 2. 89% ), macrophages group ( 12. 69% ± 3.55% ) were lower than parallel negative control group but there was no significant difference. That in combination GM-CSF/macrophages group (20.31% ± 3.01% )was significantly higher than GM-CSF group ( P < 0. 05 ). Conclusion Treatment with rat GM-CSF or macrophage can significantly promote the survival of the flaps. Combined application of GM-CSF and macrophage could synergetically promote the survival of the flaps, the vasculogenesis and the collagen deposition.

Objective To prepare a gene chip for detecting polymorphisms on coding region of genes in hepatocellular carcinoma tissuses. Methods Genes harboring in loss regions with high frequency of hepatocellular carcinoma (HCC) were selected, the related information was inquired and the cSNP sequences were obtained in the SNP database of National Center for Biotechnology Information(NCBI).Then the appropriate primers and oligonucleotide probes were designed according to the SNP sites and the gene chip for the detection of SNPs were constructed. This chip includes 48 cSNPs of 25 hepatocellular carcinoma-related genes. The PCR products labeled by Dig-dUTP were hybridized with cSNP chip. Results The sensitivity, influence of probes and reiteration of the chip were detected. The results indicated that the chip was sensitive about 6?10~(-3) ng/?l. The signal of hybridization was down with lower concentrition of probes. By the chip, 7 of polymorphisms of caspase9 ( rs2308941) C→T and DOK2(rs2242241)T→G, 6 of polymorphisms of EGFL3(rs947345)A →G,caspase9 ( rs2308938)C→G and PHGDH(rs1801955)T→A, 5 of polymorphisms of E2F2(rs3218170) G→A,4 of polymorphisms of MUTYH(rs1140507)T→C and BNIP3L(rs1055806)G→T, 1 of polymorphism of TNFRSF1B (rs1061622)T→G were detected in the tissues of 10 HCC. Samples of caspase9 ( rs2308941G) and ( rs2308941A) were verified by PCR-SSCP and sequencing. Conclusion We prepare the cSNP chip of hepatocellular carcinoma-related genes, which can accelerate the discovery of polymorphic markers on hepatocellular carcinoma.

Abstract: The aim of this study was to prepare a high drug-carrying capacity micellar drug delivery system (CTD@Sol) of the polymer zebra tetracycline and to preliminarily investigate the feasibility of this drug delivery system for the treatment of breast cancer. Firstly, CTD@Sol was prepared using sol as the carrier material and CTD as the model drug, and its pharmacological properties such as appearance and morphology, particle size, potential and in vitro release were evaluated. The growth inhibitory and apoptotic effects of CTD@Sol on breast cancer (4T1) cells were investigated by MTT assay and Annexin V-FITC/PI double staining assay; the uptake efficiency of 4T1 to this delivery system was investigated by flow cytometry; and the in vivo tissue distribution of the delivery system and the targeting of tumour tissues were investigated by small animal in vivo imaging technique. The results showed that CTD@Sol appeared as a light pale blue creamy white colour, with an average particle size of (159.73 ± 1.96) nm, a PDI of 0.198 ± 0.006, Zeta potential of –(47.60 ± 1.77) mV, an encapsulation rate of (90.29 ± 1.69)% and a drug loading capacity of (45.00 ± 0. 84)%; the in vitro release and haemolysis experiments showed that the drug release rate of CTD@Sol in acidic environment (pH 5.5) was significantly faster than that in neutral environment (pH 7.4), suggesting that the system is acid-sensitive and has good biosafety under endocytosed pH conditions. Cellular uptake, cytotoxicity and apoptosis experiments showed that CTD@Sol was more lethal to 4T1 cells, and the sol-gel polymer micelles as a drug delivery vehicle could significantly improve the cellular uptake efficiency of the drug; in vivo experiments showed that the delivery system had a significant targeting effect on tumour tissues.In conclusion, this study has successfully produced a CTD@Sol drug delivery system with high drug loading capacity (>45%), good pharmacological performance, strong targeting and biosafety, which has the potential to be used in the treatment of breast cancer.

Objective: To investigate the strong expression (S+) of P53 and BCL2 proteins in MYC/BCL2 double-expression DLBCL (DEL) and whether they can be used for the prognostic evaluation and stratified diagnosis of DELs. Methods: Tissue microarray were made by filed FFPE blocks of 174 DLBCL cases. The translocation of MYC, BCL2 and BCL6 genes were detected by FISH, and the proteins were detected by IHC. Data of clinicopathologic features and follow up of patients were collected and OS (overall survival) and PFS (progression free survival) were analyzed by statistics. Results: Eight double-hit lymphomas (DHLs) were identified in all cases, and 45 DELs were selected from 166 remaining cases, which have no significant difference in OS and PFS compared with non-DEL cases (P=0.668 and P=0.790) . Of 42 DEL-cases with follow up data, 24 cases with P53+ or/and BCL2 (S+) are significantly shorter OS and PFS than others (P=0.003 and P=0.000) , in which the cases with P53+/BCL2 (S+) co-expression were the worst prognosis, and P53/BCL2 co-weaker positive DEL cases even have superior OS and PFS than those non-DELs. Although statistics showed that the cases of P53+ or/and BCL2 (S+) have a lower OS and PFS in total cases (P=0.063 and P=0.024) , it is not the case when the DEL-cases take out from total cases, that is the cases with P53+ or/and BCL2 (S+) are as similar OS and PFS as others in non-DEL group (P=0.590 and P=0.550) . Conclusion The strong expression of P53 and BCL2 proteins can be used as indicators of stratified diagnosis and poor prognosis of DEL.