腺泡状软组织肉瘤1例报告

患者,男性,28岁。两天前感右侧腰部隐痛,呈持续性,疼痛无放射。入院前20天于当地医院查体时B超发观“右肾区肿物”,性质不清而就诊。既往无发热及腰痛等病史。 查体:心肺(一),腹部(一),双肾区叩痛(一)。 化验:血、尿常规无异常,ESR20mm/h。尿本——周氏蛋白阳性。

脊索瘤一例

脊索瘤(Chordoma)起源于胚胎期残留或异位的脊索组织,是一种较少见的恶性肿瘤。发生部位是胚胎期脊索组织所通过的体轴骨胳。常见于体轴的两端,55％发生于骶尾部,35％发生于颅底,少数发生于其它椎骨。本院曾收治一例发生于胸椎者,现报告如下:

Apoptosis Rate and Objective Diagnosis of Drug Resistance of Ovarian Cancer Cell Lines

Objective： To investigate whether the change of drug resistance degree could be evaluated by apoptotic rate in ovarian cancer cell lines. Methods： Human epithelia ovarian cancer cell line A2780 and its platinum （DDP） resistance cell line AD4 were used. They were divided into 4 groups respectively （A2780-DDP group, A2780-DDP＋VRM group, AD4-DDP group and AD4-DDP＋VRM group）. 3-（4, 5- dimethylthiazol-2-yl）-2, 5-diphenyl-2H-tetrazolium bromide （MTT） was used to measure the multiple of drug resistance. The expression of drug-resistance genes （mdrl, TopoⅡα and GSTπ） was detected by using reverse transcription polymerase chain reaction （RT-PCR）. Semi-quantity assay was proceed by rate the of multidrug resistance genes to G3 PDH gene. Apoptosis was measured by DNA gel electrophoresis and flow cytometry respectively. The advantages and disadvantage of evaluating drug-resistance with these three methods were analyzed. Results： The 50% inhibition concentration （IC50） of A2780 and AD4 was 19.2 μg/mL and 66 μg/mL respectively, and the resistance fold of the AD4 was 3.4. Some drug-resistance genes could be detected by RT-PCR in A2780 and AD4 cell lines. The expression of mdrl was only （0.09±0.03）×10^-2 ： 1 and （0.10±0.02） × 10^-2：1 respectively （rate to G3 PDH gene） with the difference being not significant between them. The expression of TopoⅡα in the A2780 cells was （2.60±0.12）×10^-2：1 and （0.11±0.03）× 10^-2：1 in the AD4 cells respectively with the difference between them being significant. On the contrary, the expression of GSTπ in A2780 cells was lower than in AD4 cells, and the ratio was （0.11±0.03）×10^-2：1 and （3.13±0.14）×10^-2：1 respectively with tile difference being significant between them. There was no significant difference among the genes expression after the drugs were given for 6 h, 12 h and 24 h. couldn＇t reflect the change of drug-resistance timely. DNA gel electrophoresis used to detect apoptosis was only a qualitative analysis. Different drug resistance degrees may be detected by flow cytometry as early as few hours after drugs were given, which realized the earlier and quantities detection of drug resistance. Conclusion： Detection of apoptosis with flow cytometry may not be affected by the variety of drug-resistance genes, suggested this was a general, quantitative and objective method to reflect drug resistance.

猪胃类癌一例

1979年8月份以来,我们结合屠宰家畜肿瘤发病情况的调查,在公司所属有关厂(场)对屠宰加工中的猪胃进行了比较详细的检验和检查,先后检出了猪胃溃疡、胃息肉、胃肿瘤共350余例,其中一例为猪胃类癌。

胃类癌(附5例报告)

类癌是一种含有从消化管嗜铬细胞衍化来的嗜银细胞的肿瘤,具有特殊的组织结构,并在瘤细胞内常含有能够还原银盐的嗜银颗粒;瘤体生长缓慢,较其它癌瘤之浸润和转移性均低;转移者常伴有类癌综合症。本瘤好发于胃肠道,且以兰尾、直肠、迥盲肠最多。发生于胃者在日本仅次于兰尾,)欧美较低。本文报告胃类癌5例,结合有关文献略作讨论。

EFFECTS OF RETINOIC ACID ON PROLIFERATION AND DIFFEREN-TIATION OF A HUMAN OVARIAN CARCINOMA CELL LINE:3AO

Objective To observe the effects of retinoic acid (RA) on the proliferation and differentiation of a human ovarian carcino-ma cell line: 3AO cells. Methods 3AO cell proliferation was evaluated by viable cell count, percentage of cells in each cycle phase were analyzed by flow cytometric analysis, alkaline phosphatase (AKP) activity was determined as described , and CA125 expression was measured by ELISA. Results RA could inhibit the proliferation of 3AO cells accompanied with morphological changes in a dose-dependent manner. Cell cycle analysis indicated that RA inhibition of 3AO cells growth occurred through induction of G1 arrest with a concomitant reduction in the proportion of cells in S phase, AKP activity increased significantly after treatment with RA(0.1 μmol/L) for 1-5 days. Dose-response studies revealed that the AKP activity increased to a different extent as a function of RA concentrations. Furthermore, RA could suppress the expression of CA125 tumor marker in 3AO cells.Conclusion RA could markedly inhibit the proliferation and induce the differentiation of 3AO cells. for 1-5 days. Dose

Glycogen synthase kinase-3β positively regulates the proliferation of human ovarian cancer cells

Although glycogen synthase kinase-3 （GSK-3） might act as a tumor suppressor since its inhibition is expected to mimic the activation of Wnt-signaling pathway, GSK-3β may contribute to NF-κB activation in cancer cells leading to increased cancer cell proliferation and survival. Here we report that GSK-3β activity was involved in the proliferation of human ovarian cancer cell both in vitro and in vivo. Inhibition of GSK-3 activity by pharmacological inhibitors suppressed proliferation of the ovarian cancer cells. Overexpressing constitutively active form of GSK-3β induced entry into the S phase, increased cyclin D1 expression and facilitated the proliferation of ovarian cancer cells. Furthermore, GSK-3 inhibition prevented the formation of the tumor in nude mice generated by the inoculation of human ovarian cancer cells. Our findings thus suggest that GSK-3β activity is important for the proliferation of ovarian cancer cells, implicating this kinase as a potential therapeutic target in ovarian cancer.

The Effect of the MDM2-p53 Loop on the Sensitivity of Ovarian Cancer Cells to Cisplatin

OBJECTIVE To explore whether MDM2 transfection can alter the MDM2-p53 autoregulatory feedback loop so as to change the sensitivity of ovarian cancer cell lines to cisplatin. METHODS The ovarian cancer cell line A2780 expressing wild-type P53 and the ovarian cancer cell line SKOV-3 with the p53 null type were stably transfected with pCMV-MDM2 or pCMV as a control. The blocked expression of P53 was determined by Western blots. Cytotoxicity was assessed using the MTT assay and the trypan blue exclusion assay. Flow cytometry was used to detect changes in the cell cycle and removal of platinum -DNA adducts was measured by atomic absorption spec-troscopy. RESULTS (1) Parental A2780 and A2780-V cells (IC50= 15.14±1.39 μmol) have similar cisplatin sensitivities, whereas sensitivity to cisplatin in A2780-M cells (IC50=7.98±1.32 μmol) was 2 to 3 fold greater (P=0.001). The trypan blue exclusion assay demonstrated that cisplatin killed a higher percentage of A2780-M cells compared to A2780-V cells. There was no significant change following MDM2 transfection in SKOV-3 cells. (2) After cisplatin treatment, A2780-M cells showed a pronounced S-phase arrest, however, A2780 cells with the intact wild-type P53, arrested primarily at the G2/M transition. (3) Platinum uptake was similar for all of the A2780 cell lines after ciaplatin treatment, but the removal of plat-inum-DNA adducts was reduced in the A2780-M cells compared with A2780-V cells. CONCLUSION MDM2 increases cisplatin cytotoxicity in ovarian cancer cells by blocking the expression of p53 through the MDM2-p53 autoregulatory feedback loop.

Nestin in gastrointestinal and other cancers: Effects on cells and tumor angiogenesis

Nestin is a class Ⅵ intermediate filament protein that was originally described as a neuronal stem cell marker during central nervous system (CNS) development, and is currently widely used in that capacity. Nestin is also expressed in non-neuronal immature or progenitor cells in normal tissues. Under pathological conditions, nestin is expressed in repair processes in the CNS, muscle, liver, and infarcted myocardium. Furthermore, increased nestin expression has been reported in various tumor cells, including CNS tumors, gastrointestinal stromal tumors, pancreatic cancer, prostate cancer, breast cancer, malignant melanoma, dermatofibrosarcoma protuberances, and thyroid tumors. Nestin is reported to correlate with aggressive growth, metastasis, and poor prognosis in some tumors; however, the roles of nestin in cancer cells have not been well characterized. Furthermore, nestin is more specifically expressed in proliferating small-sized tumor vessels in glioblastoma and gastric, colorectal, and prostate cancers than are other tumor vessel markers. These findings indicate that nestin may be a marker for newly synthesized tumor vessels and a therapeutic target for tumor angiogenesis. It has received a lot of attention recently as a cancer stem cell marker in various cancer cells including brain tumors, malignant rhabdoid tumors, and uterine, cervical, prostate, bladder, head and neck, ovarian, testicular, and pancreatic cancers. The purpose of this review is to clarify the roles of nestin in cancer cells and in tumor angiogenesis, and to examine the association between nestin and cancer stem cells. Nestin has the potential to serve as a molecular target for cancers with nestin-positive cancer cells and nestin-positive tumor vasculature.

ROLE OF ERK1/2 KINASE IN CISPLATIN-INDUCED APOPTOSIS IN HUMAN OVARIAN CARCINOMA CELLS

Objective To investigate the role of extracellular regulated kinase (ERK1/2) pathway in cisplatin-induced apoptosis in human ovarian carcinoma cells. Methods Cisplatin-induced apoptosis were stained with DAPI and was assessed microscopically in human epithelial adenocarcinoma ovarian cell line SKOV3 cells. ERK activation was determined by Western blotting using an anti-phospho-ERK antibody to detect ERK activity. The effect of PD98059 on ERK activity induced by cisplatin was detected by MTT assay. Results Marked apoptosis of SKOV3 cells resulted from 48 hours treatment with 20 μg/mL cisplatin. Strong activation of ERK was led to by 15 μg/mL cisplatin. Dose response and time course of cisplatin induced apoptosis in SKOV3 cells. Cisplatin-induced ERK activation occurred at 12 hours and increased to highest induction at 24 hours by Western blotting. The effect of PD 98059 on ERK activity induced by cisplatin at the concentration of 100 μmol/L PD 98059. Statistically significant decreased in cell survival were observed with 100 μmol/L PD 98059 at 15 and 20 μg/mL cisplatin (P< 0.05). Conclusions Cisplatin activates the ERK signaling pathway in ovarian cancer cell line SKOV3. Inhibition of ERK acti-vity enhances sensitivity to cisplatin cytotoxity in ovarian cancer cell line SKOV3. Evaluation of ERK activity could be useful in predicting which ovarian cancer will response most favorably to cisplatin therapy.

The Effect of 17 β-Estradiol on Invasion by the Ovarian Clear Cell Adenocarcinoma Cell Line ES-2 and the Molecular Mechanism Involved

OBJECTIVE To assess the effect of 17 β-estradiol（E2） on cell proliferation, cell invasiveness and its regulation of MTA3, Snail and matrix metalloproteinase 2 （MMP-2） expression in the ovarian clear cell adenocarcinoma cell line ES-2, and to further investigate the mechanism involved. METHODS We first investigated expression of ERα, ERβ, PR and E-cadherin of ES-2 cells by RT-PCR and Western blots. Before all experiments, the ES-2 cells were grown in medium depleted of steroid for more than 7 days. Following treatment with 10^-7,10^-8 and 10^-9 M E2, cell viability of the ES-2 cells was determined by the MTT method, and the cell cycle distribution and apoptosis were examined by flow cytometry （FCM）. Invasion and mobility assays were performed using modified Boyden chambers. MTA3, Snail and MMP-2 mRNA expression was measured by RT-PCR, and Snail, MMP-2 protein levels were determined by IHC. MMP-2 activity was assayed by zymography. RESULTS RT-PCR and Western Blots showed that theexpression of ERα and E-cadherin mRNA and protein in the ES-2 cells was negative, while ERβ and PR expression was positive. E2 at 10^-7,10^-8 or 10^-9M stimulated cell proliferation. A level of 10^-8M E2 reduced the proportion of G0-G1 phase cells and increased the proportion of cells in the S phase, but it had no effect on apoptosis. Invasiveness and mobility of the ES-2 cells was significantly increased by 10^-8M E2. Treatment with 10^-8M E2 led to reduced MTA3 mRNA expression, and elevated Snail and MMP-2 mRNA and protein levels. CONCLUSION E2 enhanced invasion by the ES-2 cells. The effects observed maybe mediated by down-regulation of MTA3 and up-reguation of Snail and MMP-2.

Human ovarian neoplasm cell CD147 stimulates production and activation of matrix metalloproteinases in co-cultures with mouse fibroblasts

Objective: To investigate the expression of CD147 on human ovarian neoplasm cell lines and its influence on production and activation of matrix metallproteinases(MMPs). Methods: The expression of CD147 on different human ovarian neoplasm cell lines was studied by western blotting. Co-culture was carried out to investigate the stimulative effect of the positive expression CD147 cell HO-8910 on the production of MMPs of fibroblast cell in vitro. Zymography and immune blotting were used to study the production and activity of positive MMPs, at the time, to explore the relation between CD147 and MMPs. Results: CD147 was positively presented in 2 ovarian neoplasm cell lines(HO-8910,3-AO), but in SKOV3, TC-1,NIN3T3 cell was negative. MMP-2 and MMP-9 were detected by HO-8910 cell line, mouse fibroblast cell and co-culture cells; but the expression in co-culture cell is obviously higher than individual cultures of each type alone.CD147 stimulated MMPs in dose-dependent manner. Conclusion: CD147 causes increased production and activation of MMP-2, MMP-9.CD147 is probably a indirect marker of some ovarian cancer cells with invasion and metastasis.

Effects of carbon dioxide pneumoperitoneum on metastasis of ovarian carcinoma cell line SKOV_3

The long suspicion of the potential harm of carbon dioxide （CO2） pneumoperitoneum exists in laparoscopic cancer surgery. For better understanding of this problem, we targeted this study at the effects of CO2 pneumoperitoneum on the invasive ability of ovarian carcinoma cell line and the possible mechanism within it. To study the effects of CO2 pneumoperitoneum on carcinoma cell, SKOV3 cells were divided into 2 groups, respectively exposed to pneumoperitoneal CO2-insuffiation and normal conditions. To study the possible mechanism, SKOV3 cells were divided into 3 groups, one was exposed to CO2 pneumoperitoneum, one to N2 and the other to normal conditions served as control. The in vitro adhesive and invasive ability of the cells was analyzed through 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyl tetrazolium bromide （MTT） assay and Boyden filters metastasis model; the expressions of vascular endothelial growth factor C （VEGF-C） and matrix metalloproteinase 9 （MMP9） were determined by reverse transcription polymerase chain reaction（RT-PCR）, and Western blot. We found that the adhesive ratio of SKOV3 cells exposed to CO2 was significantly higher than that of the control group; cells exposed to CO2 invaded the matrigel with a greater number （P〈0.01）; the expression of VEGF-C exposed to both CO2 and N2 was significantly increased compared with control group （P〈0.05）; the MMP9 expression level of CO2 group was higher than that of N2 group, P〈0.05. We concluded that carbon dioxide pneumoperitoneum may improve the adhesive and invasive ability of ovarian carcinoma cell line in vitro and CO2 can also be an independent factor to stimulate the expression of MMP9.

Growth inhibition of interleukin-2 receptor gene-transduced peripheral blood lymphocytes on human ovarian cancer cells

Objective To investigate the growth inhibition of interleukin 2 receptor (IL 2R) gene transduced peripheral blood lymphocytes (PBLs) on human ovarian cancer cells Methods Interleukin 2 (IL 2) and IL 2R genes were transfected into human ovarian cancer cell line 3AO and PBLs, respectively, using the same Fugene vector Twenty four hours later transfected and nontransfected PBLs were cocultured with transfected and nontransfected 3AO for 48 hours Cytotoxity of PBLs on 3AO was detected by the MTT assay Results The morphology of IL 2 transduced 3AO and IL 2R transduced PBLs remained unchanged 3AO cells could be transfected with the IL 2 gene and expressed IL 2 mRNA, and PBLs could be transfected with the IL 2R gene and expressed IL 2R mRNA IL 2 transduced 3AO cells enhanced their response to the cytotoxity of PBLs Furthermore, growth inhibition of PBLs to 3AO cells increased significantly when the IL 2R was transfected into PBLs and when the IL 2 gene was transfected into 3AO cells and the two were combined Conclusions IL 2R gene transduced PBLs are able to enhance their cytotoxity on IL 2 gene transduced ovarian cancer cells This method may be a new way to investigate IL 2 gene therapy for ovarian cancer