OBJECTIVETo study the gene expression of transforming growth factor beta receptor II (TbetaR II) in pathological scar.

METHODSTwenty samples of pathological scar were collected from 20 burn or trauma patients hospitalized in the General Hospital of Ji'nan Military Command from 2007 to 2009. Twenty specimens of epidermal layer were obtained from the middle portion and the edge of pathological scars. Twenty normal skin specimens which were located more than 10 cm away from the lesion sites of 20 patients were collected as self-controls. Serum from 1-2 mL whole blood were obtained from each of the 20 patients for second self-control. Eight normal skin specimens from 8 patients without pathological scar, discarded from un-related operations, were also collected as negative-control. Positive expressions of TbetaR II in three different skin specimens were determined with biotin-streptavidin-peroxidase staining. Gene expressions of TbetaR II in all specimens were compared with PCR-single strand conformation polymorphism analysis and gene sequencing. Data were processed with Fisher's exact test.

RESULTSPositive expression of TbetaR II in pathological scar epidermis was lower than that in normal skin specimen of patients with pathological scar or normal skin specimen of patients without pathological scar, and TbetaR II was mainly located in the basal layer of epidermis. Positive expressions of TbetaR II were seldom found in acanthocytes, granular cells, and cuticle or even non-existing. No abnormality of TbetaR II was found in normal skin epidermis or serum samples of pathological scar patients or normal skin epidermis of patients without pathological scar. TbetaR II expressing in 8 specimens of epidermis of pathological scar showed abnormal electrophoresis pattern at poly A fragments hand and loss of one A base in DNA fragment (P = 0.044).

CONCLUSIONSThere may he abnormal gene expression of TbetaR II in pathological scar epidermis. Replantation of epidermis of scar may increase the risk of scar recurrence, while replantation of normal skin of patients with scar on wound may not increase the risk of scar recurrence.

Adolescent ; Adult ; Child ; Child, Preschool ; Cicatrix ; metabolism ; pathology ; Epidermis ; metabolism ; Female ; Gene Expression ; Humans ; Male ; Middle Aged ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Receptors, Transforming Growth Factor beta ; genetics ; metabolism ; Young Adult

In this research, the regulatory effects of T-lymphocytes on the expansion of hematopoietic cells in human bone marrow were studied. Anti-CD3 McAb and anti-CD8 McAb were used to eliminate the T-lymphocytes in bone marrow MNCs. Cell surface antigens were analysed by flow cytometry. Hematopoietic cells expanded with hematopoietic growth factors (HGFs) in a liquid culture system and the number of CD34(+) cell, CFU-GM and CFU-GEMM were determined. After cultured with HGFs for 20 days the total number of cells expanded by 75.8, 79.6, 77.4 and 67.0 folds respectively in three experimental groups (anti-CD3 McAb, anti-CD8 McAb and anti-CD3 + anti-CD8 McAb) and control group (MNC of bone marrow). The number of CFU-GM in the four groups were 173.67 +/- 18.90, 165.33 +/- 26.58, 170.33 +/- 21.50 and 79.67 +/- 8.33 respectively. The number of CFU-GEMM in the four groups were 431.33 +/- 34.56, 370.33 +/- 42.10, 386.67 +/- 10.02 and 177.67 +/- 26.86 respectively. There were significant differences in the number of CFU-GM and CFU-GEMM between experimental groups and control group. The results showed that the T-lymphocytes in bone marrow could inhibit the expansion of hematopoietic cells in vitro and the formation of CFU-GM and CFU-GEMM. The regulatory mechanism was to be explored.

OBJECTIVETo investigate the effect of curcumin (Cur) on radiosensitivity of nasopharyngeal carcinoma cell CNE-2 and its mechanism.

METHODThe effect of curcumin on radiosensitivity was determined by the clone formation assay. The cell survival curve was fitted by Graph prism 6. 0. The changes in cell cycle were analyzed by flow cytometry (FCM). The differential expression of long non-coding RNA was detected by gene chip technology. Part of differentially expressed genes was verified by Real-time PCR.

RESULTAfter 10 micro mol L-1 Cur had worked for 24 h, its sensitization enhancement ratio was 1. 03, indicating that low concentration of curcumin could increase the radiosensitivity of nasopharyngeal carcinoma cells; FCM displayed a significant increase of G2 phase cells and significant decrease of S phase cells in the Cur combined radiation group. In the Cur group, the GUCY2GP, H2BFXP, LINC00623 IncRNA were significantly up-regulated and ZRANB2-AS2 LOC100506835, FLJ36000 IncRNA were significantly down-regulated.

CONCLUSIONCur has radiosensitizing effect on human nasopharyngeal carcinoma CNE-2 cells. Its mechanism may be related to the changes in the cell cycle distribution and the expression of long non-coding IncRNA.

Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Curcumin ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; radiation effects ; Humans ; RNA, Long Noncoding ; genetics ; Radiation Tolerance ; drug effects

OBJECTIVEThe aim of this study was to evaluate the effect of anastrozole, a new generation aromatase inhibitor, on the lipid metabolism in postmenopausal Chinese women with early breast cancer, and observe the adverse reactions as well.

METHODSPostmenopausal women with early breast cancer patients took anastrozole 1 mg per day. The lipid profiles of total cholesterol, triglyceride, low density lipoprotein, and high density lipoprotein were assessed before taking the drug, 3 months, 6 months after taking medication, and later once a year, until the end of medication or follow-up. Patients taking lipid-lowering drugs were excluded. The adverse reactions during the process of taking medication was followed-up by telephone.

RESULTSTwo hundred and eighty-five postmenopausal breast cancer patients took part in the trial from Jan. 2003 to Jun. 2009. All patients had completed primary surgery and demonstrated a postmenopausal status. ER or PR positivity was confirmed by histopathology. Taking the medication from a minimum of one year to a maximum of 5 years, with a median time of 3.61 years. During the medication time, anastrozole significantly increased the levels of low density lipoprotein-cholesterol after 6 months of treatment, continuing to 5 years, from (3.08 ± 0.90) mmol/L to (3.59 ± 0.59) mmol/L, with a maximal increase of 18.2% higher than that before medication. Anastrozole significantly increased the levels of total cholesterol and high density lipoprotein-cholesterol after 1 years of treatment. Anastrozole significantly reduced the levels of triglycerides after 1 years of treatment. Anastrozole showed no significant effect on serum lipids in the patients with pre-existing hyperlipidemia. A more significant effect on blood lipids was observed in patients aged ≥ 60-years than that in patients less than 60 years of age. The rate of other adverse events were similar to that reported in foreign patients.

CONCLUSIONSFor the postmenopausal patients with breast cancer, taking anastrozole may lead to an abnormal lipid metabolism. Anastrozole significantly increases the levels of low density lipoprotein-cholesterol, total cholesterol and high density lipoprotein-cholesterol, and significantly reduces the level of triglycerides. The rate of other adverse events were similar to that reported in foreign patients. it is suggested that the blood lipid levels should be regularly assessed in patients with long-term anastrozole treatment. The rate of other adverse events similar to that reported with foreign patients, and patients tolerate this treatment well.

Age Factors ; Aged ; Aged, 80 and over ; Antineoplastic Agents, Hormonal ; therapeutic use ; Aromatase Inhibitors ; therapeutic use ; Breast Neoplasms ; blood ; complications ; drug therapy ; surgery ; Chemotherapy, Adjuvant ; Cholesterol ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Female ; Follow-Up Studies ; Humans ; Hyperlipidemias ; blood ; complications ; Lipid Metabolism ; drug effects ; Lipids ; blood ; Middle Aged ; Neoplasm Staging ; Nitriles ; therapeutic use ; Postmenopause ; Triazoles ; therapeutic use ; Triglycerides ; blood

Adenine ; analogs & derivatives ; therapeutic use ; Adolescent ; Adult ; Aged ; Creatinine ; blood ; Female ; Hepatitis B, Chronic ; blood ; drug therapy ; Humans ; Male ; Middle Aged ; Organophosphonates ; therapeutic use ; Phosphorus ; blood ; Retrospective Studies ; Young Adult

OBJECTIVETo investigate the changes in proliferation, invasiveness, clone sphere formation and chemosensitivity of human gastric cancer cell lines of KATO-III CD133(+) cells transfected with small interfering RNA (siRNA) against CD133 gene.

METHODSCD133(+) cells of KATO-III cell lines were isolated by magnetic activated cell sorting (MACS). CD133 siRNA was designed and synthesized, and then transfected into KATO-III CD133(+) cells. Cell fluorescence counting under confocal laser scanning microscope was used to determine the transfection efficiency after transfection with the CD133 FITC-siRNA. The knock-down effect of the CD133 gene and expression of epithelial-mesenchymal transition (EMT)-related factors were detected by RT-PCR and Western blotting. Cell counting kit-8 assay (CCK-8), transwell chamber and colony sphere forming assay were performed to measure the variation of cell proliferative, invasive, colony formation viability and chemosensitivity to 5-FU after the above-mentioned treatment.

RESULTSThe transfection efficiency was (87.7±8.1)%. The CD133 mRNA and protein expression levels in the interference group were lower than those in negative control group. Twenty-four, 48 and 72 hours after transfection, cells proliferation activity was significantly inhibited in the interference group compared with negative control group, (all P<0.01). Seventy-two hours after transfection, compared with negative control group, cells proliferation activity was reduced by (52.1±8.0)%. The invasive cell number reduced (41.7±6.0 vs. 130.3±11.0, P<0.05) and clone formation rate decreased significantly [(24.3±4.3)% vs. (45.1±6.4)%, P<0.01] in the interference group. EMT-related gene E-cadherin protein expression increased, while the Snail and N-cadherin protein expression reduced in the interference group (all P<0.01). The cells sensitivity to 5-FU was significantly enhanced in the interference group, and the cell inhibition rate of 5-Fu was (62.4±3.3)%, higher than that in negative control group [(21.5±2.2)%, P<0.01].

CONCLUSIONSThe expression of CD133 gene plays an important role in cell proliferation, invasiveness, colony formation and resistance to chemotherapy of KATO-III CD133(+) gastric cancer cells. It suggests that CD133 can be used as one of surface markers for detection of gastric cancer stem cells. Inhibition of CD133 expression may be a promising way for gastric cancer biotherapy.

AC133 Antigen ; Antigens, CD ; genetics ; metabolism ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Fluorouracil ; pharmacology ; Glycoproteins ; genetics ; metabolism ; Humans ; Peptides ; genetics ; metabolism ; RNA Interference ; RNA, Small Interfering ; genetics ; Stomach Neoplasms ; genetics ; metabolism ; pathology ; Transfection

Anthracycline-Taxane chemotherapy is widely used in neoadjuvant treatment for breast cancers. However, there is limited data reported in patients with triple negative breast cancer (TNBC). Here, we evaluated the pathologic responses and survival of neoadjuvant epirubicin and taxanes chemotherapy in patients with locally advanced TNBC to provide some useful information for clinical practice. A total of 43 patients with locally advanced TNBC were enrolled in this study. Patients were administered with epirubicin 75 mg/m(2) plus paclitaxel 175 mg/m(2) or docetaxel 75 mg/m(2) every 3 weeks for at least 2 cycles. The primary endpoint was pathologic complete response (pCR), which was defined as no residual invasive cancer, or only carcinoma in situ in both the excised breast and axillary lymph node, while relapse-free survival (RFS) and overall survival (OS) were secondary endpoints. Thirty-nine (90.7%) patients were at clinical stages IIB-IIIC. Thirty-seven (86%) completed 4-6 cycles of preoperative chemotherapy, and objective response rate (ORR) was 81.4% (35/43). Forty-two patients underwent radical surgery subsequently. The pCR rate was 14.3% (6/42). The most common adverse events in neoadjuvant chemotherapy were nausea/vomiting (88.4%, 38/43) and neutropenia (88.4%). After a median follow-up period of 34.0 months, 3-year RFS and OS rate was 53.6% and 80.1%, respectively. All events of recurrence and death occurred in non-pCR patients, in whom the 3-year RFS and OS rates were 44.3% and 76.6%, respectively. This study suggest that neoadjuvant chemotherapy with epirubicin plus taxanes has a relatively low pCR rate and high early recurrence risk in locally advanced TNBC, which indicates the necessity for more efficacious treatment. Further study is needed to validate these results.
Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; administration & dosage ; Chemoradiotherapy, Adjuvant ; methods ; Disease-Free Survival ; Epirubicin ; administration & dosage ; Female ; Humans ; Male ; Middle Aged ; Neoadjuvant Therapy ; methods ; Neoplasm Recurrence, Local ; pathology ; prevention & control ; Neoplasm, Residual ; pathology ; prevention & control ; Paclitaxel ; administration & dosage ; Taxoids ; administration & dosage ; Treatment Failure ; Treatment Outcome ; Triple Negative Breast Neoplasms ; drug therapy ; pathology

OBJECTIVETo study the clinical characteristics, outcome, prognostic factors and survival of patients with testicular germ cell tumors (TGCTs).

METHODS107 TGCT patients received chemotherapy after orchiectomy. The median age of the patients was 32 years. 30.8% (33/107) patients had seminomas with 14 (42.4%) stage I lesions. Seventy-four patients had non-seminomatous germ cell tumors (NSGCTT) with 21 (28.4%) stage I lesions. The response rate was analyzed with chi(2) test. The survival rate was calculated with Kaplan-Meier method and log-rank test. Therapy including chemotherapy, radiation and necessary salvage operation were performed after orchiectomy.

RESULTSClinical stage and pathological type were the main prognostic factors. The 3-, 5- and 10-year survival rates were 75.8%, 73.5%, 73.5% for all patients, 100%, 96.8%, 96.8% for seminoma and 63.5%, 61.7%, 61.7% for NSGCTTs, respectively. Sixty-four patients were evaluable for response. Seventeen (26.6%) patients achieved CR by chemotherapy alone and an additional 8 patients (12.5%) achieved CR by chemotherapy plus salvage operation or radiation. The 5-year survival rates were 91.7% and 26.2% for patients who achieved CR or not.

CONCLUSIONThe long-term outcome for stage I germ cell tumors is excellent. The treatment outcome and survival in patients with metastatic TGCTs can be greatly improved by adopting multi-modality therapy with combined chemotherapy as the chief means.

Adolescent ; Adult ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Bleomycin ; therapeutic use ; Child ; Child, Preschool ; Cisplatin ; therapeutic use ; Combined Modality Therapy ; Etoposide ; therapeutic use ; Follow-Up Studies ; Germinoma ; drug therapy ; secondary ; surgery ; Humans ; Lung Neoplasms ; drug therapy ; secondary ; Male ; Middle Aged ; Neoplasm Staging ; Orchiectomy ; Seminoma ; drug therapy ; secondary ; surgery ; Survival Rate ; Testicular Neoplasms ; drug therapy ; pathology ; surgery ; Treatment Outcome

OBJECTIVETo examine the association between CD133 expression and invasion of gastric cancer, and to elucidate whether CD133 can promote the invasion and metastasis of gastric cancer via epithelial-mesenchymal transition (EMT).

METHODSThe CD133(+) and CD133(-) KATO-III( cells were sorted by magnetic activated cell sorting (MACS). The invasion ability was detected by Transwell method. RT-PCR and Western blot were used to detect the expression of EMT-related factors in KATO-III( cells before and after CD133 was knocked out by siRNA method. The expressions of CD133 and EMT-related proteins of cancer and adjacent normal tissues in 50 patients with gastric cancer were detected by Western blot, and correlations among protein expressions were also analyzed.

RESULTSAs compared to CD133(-) cells, the number of broken-membrane cells was significantly higher (67.7±10.5 vs. 13.3±6.8, P=0.001) and the invasion ability was stronger (P<0.05) in CD133(+) cells, while the mRNA expression levels of Snail and N-cadherin were significantly higher in CD133(+) cells (0.311±0.015 vs. 0.223±0.016, P=0.040; 0.581±0.020 vs. 0.270±0.018,P=0.004), and the protein expression levels of Snail and N-cadherin were significantly higher in CD133(+) cells as well (0.513±0.015 vs. 0.179±0.023, P=0.030; 0.538±0.028 vs. 0.202±0.032, P=0.020), but E-cadherin mRNA and protein levels were significantly lower in CD133(+) cells (0.231±0.009 vs. 0.460±0.015, P=0.040; 0.426±0.030 vs. 0.748±0.027, P=0.040). After CD133 knock-out, the expressions of Snail and N-cadherin were down-regulated (P<0.05) and the expression of E-cadherin was up-regulated (P<0.05). As compared to normal mucosal tissues, the protein expression levels of Snail, N-cadherin and CD133 in gastric cancer tissues were significantly higher(0.635±0.119 vs. 0.485±0.116, P=0.029; 0.599±0.114 vs. 0.259±0.108, P=0.020; 0.754±0.154 vs. 0.329±0.134, P=0.001), while the protein expression of E-cadherin in gastric cancer tissues was lower (0.378±0.123 vs. 0.752±0.156, P=0.003). The protein expressions of Snail and N-cadherin were positively correlated with CD133 expression (r=0.278, P=0.048; r=0.406, P=0.003) and the protein expression of E-cadherin was negatively correlated with CD133 expression (r=-0.504, P=0.000).

CONCLUSIONCD133(+) cells in primary lesion of gastric cancer have relatively higher invasion ability, which may promote the metastasis of gastric cancer via up-regulation of EMT-related factors.

AC133 Antigen ; Adult ; Aged ; Aged, 80 and over ; Antigens, CD ; metabolism ; Cell Line, Tumor ; Epithelial-Mesenchymal Transition ; Female ; Glycoproteins ; metabolism ; Humans ; Male ; Middle Aged ; Neoplasm Invasiveness ; Neoplasm Metastasis ; Peptides ; metabolism ; Stomach Neoplasms ; metabolism ; pathology

OBJECTIVETo investigate the safety and tolerance of adjuvant dose-dense chemotherapy with paclitaxel and epirubicin for high-risk breast cancer.

METHODSFrom January 2004 to December 2006, 101 patients with high-risk breast cancer after surgical resection were enrolled into this study. The patients were divided into two groups: dose-dense and regular groups. Each patient received 6 cycles of chemotherapy with intravenous administration of paclitaxel (175 mg/m2, on D3) and epirubicin (60 mg/m2, on Dl and D2). The dose-dense group had repeated treatment every two weeks, while the regular group repeated it every three weeks. G-CSF was used in a dose of 3 microg/kg on D5-D9 during each cycle in the dose-dense group. While in the regular group, it was used only under the condition that grade II neutropenia occurred.

RESULTSThe toxicity could be evaluated in 101 patients. Major grade II-IV toxicities included: neutropenia, nausea, vomiting and alopecia. The incidence of grade III-IV neutropenia was 16.0% in the dose-dense group versus 54.9% in the regular group (P = 0.000); postponing of chemotherapy was 2.4% versus 6.0% (P = 0.027). Ninety-eight patients completed the chemotherapy as planed. After a median follow-up of 24 months, the median DFS and OS were not reached. The relapse-free rate and survival rate were 89.8% and 100% in the dose-dense group, which were 87.8% and 93.9% in the regular group. The relapse-free rate of the high-risk patients in the dose-dense group was 86.8% versus 81.3% in the regular group, and the corresponding survival rate was 100% versus 90.6%.

CONCLUSIONAdjuvant dose-dense chemotherapy with paclitaxel and epirubicin is safe, tolerable and promising for high-risk breast cancer.

Adult ; Antineoplastic Combined Chemotherapy Protocols ; administration & dosage ; adverse effects ; therapeutic use ; Breast Neoplasms ; drug therapy ; pathology ; surgery ; Chemotherapy, Adjuvant ; Epirubicin ; administration & dosage ; adverse effects ; Female ; Follow-Up Studies ; Granulocyte Colony-Stimulating Factor ; administration & dosage ; therapeutic use ; Humans ; Lymphatic Metastasis ; Mastectomy ; methods ; Middle Aged ; Nausea ; chemically induced ; Neoplasm Recurrence, Local ; Neoplastic Cells, Circulating ; Neutropenia ; chemically induced ; Paclitaxel ; administration & dosage ; adverse effects ; Survival Rate ; Vomiting ; chemically induced ; Young Adult