objective To investigate the clinicopathological features of mini-cancer of the stomach. Method In this study,out of 296 early gastric cancer cases there were 34 cases of early gastric cancer in which tumor diameter was≤10 mm,among those there were 5 cases with tumor size≤2 mm and 29 cases of the size 2～10 mm. Result Mini-cancer accunted for 2% of all early gastric cancers in this series:All these mini-cancers were of intramucosal cancer(100%),while that took up to 45%in control group in which tumors were between≥2 mm and≤10 mm:Tumors were high or moderately differentiated pathologically in 100%of mini-cancers and 55%in control group.None of mini-cancer patients had lymph node metastasis,however,1 of 29 patients in control group had lymph node metastasis.Both groups had no blood vessel and lymphatic vessel invasion:The differentiation concordance rate between superficial lesions and invasive fronts in mini-cancer was 100%,higher than 86%in control group. Conclusion Gastric mini-cancer is usually of high differentiation,low tumor invasion and low rate of lympy node metastasis than control group.Endoscopic therapy is applicable for most gastric mini-cancers.

Objective To investigate the expression and correlation of hypoxia-inducible factor-1?(HIF-1?),vascular endothelial growth factor(VEGF)and sFlt-1 in the preeclampsia placenta,and discuss their significance in the pathogenesis of preeclampsia.Methods Placentas were collected from 20 pregnant women with preeclampsia as study group and 15 normal pregnant women as control group.The expressions of HIF-1?,VEGF and sFlt-1 protein were semi-quantitatively analyzed with immunohistochemical assay and mRNA level was determined using reverse transcription polymerasc chain reaction(RT-PCR)technique. Results(1)the expression of HIF-1?and sFlt-1 protein in preeclampsia group obviously increased.Strong (+++)positive expression was observed in 9 and 11 cases respectively,significantly higher than in control group(2 and 3 cases)(P＜0.05),however,VEGF expression obviously reduced in preeclampsia group(P＜0.01).(2)the level of HIF-1?and sFlt-1 mRNA in preeclamptic placenta was 0.604?0.013, 0.898?0.041,significantly higher than 0.208?0.007 and 0.559?0.244 in normal placenta(P＜0.05). Although the level of VEGF mRNA increased in preeclampsia placenta,it was not significantly different from that in normal placenta(P＞0.05).The ratio of VEGF mRNA/sFlt-1 mRNA obviously reduced in preeclampsia group and was significantly lower than in control group(P＜0.05).(3)in preeclampsia group,HIF-1?mRNA expression was positively correlated with the expression of sFlt-1 mRNA(r=0.577, P＜0.05),and negatively correlated with the ratio of VEGF mRNA/sFlt-1 mRNA(r=-0.376,P＜0.05).Conclusion Abnormal high HIF-1?expression in preeclampsia placenta indicates that HIF-1?might play an important role in the pathogenesis of preeclampsia,possibly through affecting the cytotrophoblastic invasion and placental vascular reconstruction via the modulation of VEGF and sFlt-1 gene transcription.

Objective To explore the clinical characteristics and treatment of nodular panniculitis disease in children. Methods Clinical data of 13 cases with nodular panniculitis disease were reviewed retrospectively. Their etiology,clinical manifestation,misdiagnosis cause,pathologic characteristics, treatment and outcome were analyzed. Results Its clinical manifestation was multiform and showed mainly as fever and hypodermic nodule. Concomitant damages to digestive, respiratory, circulatory and renal system might occur in those children with the system type of this disorder. Conclusion Pediatric nodular panniculitis disease can be easily misdiagnosed and lack of specificity in the early stage, and complicates multiple organs damage.

Objective To investigate the endoscopic and pathological characteristics of Barrett's esophagus (BE).Methods Data of 152 patients who were diagnosed as having BE with endoscopy and pathology were retrospectively analyzed.Results BE was most commonly seen in patients of 40-60 years old.The clinical manifestations overlapped in different patients,including regurgitation and heartburn in 78 (51.32%),dysphagia in 9 (5.92%),retrosternal pain in 12 (7.89%),upper abdominal pain or discomfort in 67 (44.08%),and asymptomatic in 8 (5.26%).Long segment BE (LSBE) was determined in 7 patients (4.61%),and short segment BE (SSBE) in 145 (95.39%).The metaplasia pattern under endoscopy included island like in 98 (64.47%),tongue like in 39 (25.66%) and circumferential in 15 (9.87%).Stratified squamous epithelia in the lower part of the esophagus were replaced by columnar epithelia in all cases,and intestinal metaplasia occurred in 68 cases (44.74 %).Conclusion BE is most frequently seen in the middle-aged and can be diagnosed by endoscopy and pathology without special clinical manifestations.Island pattern occurs in most cases and is with lowest rate of intestinal metaplasia,which is associated with age.Patients with specialized intestinal metaplasia and dysplasia should be followed up for surveillance of cancer.

The aim of this study is to develop monoclonal antibody against human hepatocyte growth factor activator inhibitor 1 (HAI-1) for future study of HAI-1. The cDNA fragments of human hepatocyte growth factor activator inhibitor 1 (HAI-1) were subcloned to construct GST-HAI-1 fusion protein expression vectors. The vectors were transformed into E. coli and fusion protein expression was induced by IPTG. The GST-HAI-1 fusion proteins were separated on preparative SDS-PAGE and recovered by electroelution, and used to immunize BALB/c mice. Hybridomas producing monoclonal antibodies against human HAI-1 were prepared by cell fusion technique and characterized by ELISA, Western Blot and immunohistochemical staining. One hybridoma cell line, ZMC6, was obtained, which produces specific antibody against the expressed GST-HAI-1 fusion protein. The monoclonal antibody recognizes both the membrane-type and secretory-type HAI-1 proteins of colorectal tissue. The successful development of anti-HAI-1 antibody provides a powerful tool for further investigation on HAI-1's function.
Animals ; Antibodies, Monoclonal ; immunology ; Blotting, Western ; Glutathione Transferase ; genetics ; Immunohistochemistry ; Mice ; Mice, Inbred BALB C ; Proteinase Inhibitory Proteins, Secretory ; analysis ; genetics ; immunology ; Recombinant Fusion Proteins ; biosynthesis ; immunology

OBJECTIVETo analyze the mutational features of adenomatous polyposis coli (APC) gene and to explore the effect of mismatch repair (MMR) deficiency on its mutations in hereditary non-polyposis colorectal cancers (HNPCC).

METHODSPCR-based in vitro synthesized protein test (IVSP) assay and sequencing analysis were used to confirm somatic mutations of whole APC gene in 19 HNPCC patients.

RESULTSEleven cases with thirteen mutations were determined. The frequency of APC mutation was 58%(11/19). The exhibiting mutations consisted of 9 frameshift mutations and 4 nonsense ones, indicating the existence of more frameshift mutations (69%). All of frameshift mutations were deletion or insertion of 1-2 bp and most of them (7/9) happened at simple nucleotide repeat sequences, particularly within (A) n tracts (5/9). All of four nonsense mutations resulted from C to T transitions at CpG sites.

CONCLUSIONMutational inactivations of APC gene were detected in more than half of HNPCC patients in this study, indicating that APC mutation is a common molecular event in the tumorigenesis of HNPCC. According to the location of frameshift mutations at simple nucleotide repeat sequences and point mutations at CpG sites, it was suggested that endogenous mechanisms like MMR deficiency might exert an effect on the nature of APC mutations in most HNPCC.

Adenomatous Polyposis Coli ; genetics ; Adenomatous Polyposis Coli Protein ; genetics ; metabolism ; Carcinoma ; genetics ; Colorectal Neoplasms ; genetics ; pathology ; Colorectal Neoplasms, Hereditary Nonpolyposis ; genetics ; Genes, APC ; physiology ; Humans

OBJECTIVETo investigate whether the heat shock protein (HSP) 70 antisense oligomers can enhance the sensitivity of bladder cancer cell EJ to mitomycin C.

METHODSThe HSP70 mRNA of EJ cells was blocked by the 10 micromol/L HSP70 antisense oligomers, while its effect on cell growth was evaluated by methyl thiazolyl tetrazolium (MTT) and colony forming ability test.

RESULTSThe HSP70 expressions in HSP70 antisense treated group were lower than the corresponding sense and nonsense treated groups (P < 0.01). While, the increased sensitivity of EJ to mitomycin C was found in antisense treated group, compared with the corresponding sense and nonsense treated groups (P < 0.01).

CONCLUSIONThe sensitivity of bladder cancer cell EJ to mitomycin C was enhanced by the blockage of the HSP70 expression.

Cell Division ; drug effects ; Cell Line, Tumor ; HSP70 Heat-Shock Proteins ; antagonists & inhibitors ; biosynthesis ; genetics ; Humans ; Mitomycin ; pharmacology ; Oligonucleotides, Antisense ; pharmacology ; RNA, Messenger ; biosynthesis ; genetics ; Urinary Bladder Neoplasms ; genetics ; metabolism ; pathology

OBJECTIVETo establish a simple, rapid and economical method in detecting mutations of oncogene K-ras and to investigate its mutations in colorectal cancer tissues and its relationship with clinicopathologic characteristics of colorectal carcinoma.

METHODSForty colorectal cancer tissues were tested for K-ras mutations at codon 12 and codon 13 using polymerase chain reaction (PCR) followed by direct sequencing and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) followed by sequence analysis. The other 113 colorectal cancer tissues were tested for K-ras mutations at codon 12 and codon 13 using PCR-RFLP followed by sequence analysis only. The mutation results were analyzed with the corresponding clinical pathological data.

RESULTSAmong 40 colorectal cancer cases, none of K-ras mutations at codon 12 and codon 13 was detected by PCR followed by direct sequencing. However, K-ras mutations were found in 11 cases (11/40, 27.5%) by PCR-RFLP followed by sequence analysis, including 8 cases at codon 12 and 3 cases at codon 13 respectively. Among 153 colorectal cancer cases, point mutations were detected by PCR-RFLP followed by sequence analysis in 58 cases (37.9%). Point mutations at codon 12 were found in 46 cases and 12 cases at codon 13. Mutations with the highest frequency were G→A transitions (25/58, 43.1%) at codon 12. No significant correlation was observed between mutations of K-ras and gender, invasive depth, tumor differentiation, number of invaded lymph nodes, distant metastasis and clinical stage (P > 0.05). Mutation of oncogene K-ras at codon 12 and codon 13 was closely related with age and tumor location (P < 0.05). The incidence of K-ras mutation was significantly higher in younger patients and in patients with ascending colon cancer.

CONCLUSIONSPCR-RFLP followed by sequence analysis is a rapid, simple, sensitive and low-cost method. It is a suitable technology for detecting hot-spot mutations in the K-ras oncogene. Mutation of oncogene K-ras at codon 12 and codon 13 is a common molecular event in colorectal carcinogenesis, which might be related with age and tumor location.

Adult ; Aged ; Aged, 80 and over ; Colorectal Neoplasms ; genetics ; pathology ; Female ; Genes, ras ; genetics ; Humans ; Male ; Middle Aged ; Mutation ; Polymorphism, Restriction Fragment Length

OBJECTIVETo investigate the therapeutic effect of cationic liposome-mediated interleukin-12 gene delivery on established murine melanoma in vivo.

METHODSThe lipofectin encapsulated pCmIL-12 plasmid was given to C57BL/6 mice on the day 3,5,7,9 after inoculation of B16 melanoma cells. The tumor size, the survival time of mice and the NK cell activity were observed.

RESULTSThe pCmIL-12 plasmid coupled with cationic liposome inhibited the tumor growth and improved the survival of mice bearing established melanoma. The activity of NK cells was also enhanced after interleukin-12 gene delivery in vivo.

CONCLUSIONCationic liposome-mediated interleukin-12 gene delivery has significantly therapeutic effects on mice melanoma in vivo.

Animals ; Cations ; DNA ; therapeutic use ; Female ; Interleukin-12 ; genetics ; therapeutic use ; Killer Cells, Natural ; immunology ; Liposomes ; Melanoma, Experimental ; pathology ; therapy ; Mice ; Mice, Inbred C57BL ; Tumor Cells, Cultured

OBJECTIVETo investigate the pathological characteristics of HCV infection after liver transplantation.

METHODSThis is a retrospective analysis of the clinico-pathological changes of 73 liver biopsies obtained from 61 patients who had HCV infection (including HCV recurrence and reinfection) after liver transplantation in our center from September 2000 to September 2006.

RESULTSAbnormal enzyme test results due to HCV infection happened on the 9th to the 1553rd post-transplantation surgery day. The serum HCV RNA level was higher than 10(5) copies/ml in 19 cases and between 10(2)-10(5) copies/ml in the other 42 cases. The histological changes in the transplanted livers were hepatocellular degeneration, necrosis and apoptosis, portal infiltrations and fibrosis. They were classified into two stages (early stage and late stage) according to the onset of fibrosis which appeared within 90 days or later after their transplantation in our study. The incidence of predominant portal infiltrates and liver fibrosis in early stage and late stage was 5.7% (2/35) and 94.7% (36/38) (chi2=54.34, P<0.01) and 2.9% (1/35) and 97.4% (37/38) (chi2=61.47, P<0.01) respectively.

CONCLUSIONSPathological features of early stage and late stage hepatitis C infection in transplanted livers are different and they are also different from that in native livers. Liver biopsies are important in clinical staging, evaluation of the severity, and differential diagnosis of post-transplantation HCV infection.

Adult ; Aged ; Female ; Hepatitis C ; etiology ; pathology ; Humans ; Liver Transplantation ; adverse effects ; Male ; Middle Aged ; RNA, Viral ; Retrospective Studies