类肿瘤型舍格伦综合征诊断问题的初步探讨

目的 探讨类肿瘤型舍格伦综合征的临床特点和诊断方法。方法 对 2 2例腮腺区类肿瘤型舍格伦综合征、5 0例腮腺多形性腺瘤和 2 5例腮腺腺淋巴瘤 ,进行各项临床资料内容的卡方检验及逐步判别分析。结果 (1)类肿瘤型舍格伦综合征好发于 40 5 9岁的女性 ,局部表现为涎腺区肿块 ,质中、表面光滑、有酸胀和时大时小现象 ,还有口干、眼干和关节酸痛等全身症状 ,抗炎治疗有效。 (2 )建立了类肿瘤型舍格伦综合征、多形性腺瘤和腺淋巴瘤的判别函数。结论 判别函数的建立为类肿瘤型舍格伦综合征的诊断与鉴别诊断提供了一种简单。

联合免疫抑制疗法治疗类肿瘤型舍格伦综合征的疗效研究

目的 :评价联合免疫抑制疗法在治疗类肿瘤型舍格伦综合征中的临床应用。方法 :临床表现为类肿瘤型的舍格伦综合征患者共 2 2名。免疫抑制剂选用的是强的松和氯喹。根据临床表现 ,将治疗效果分为优、良、差 3级。结果 :强的松和氯喹联合治疗类肿瘤型舍格伦综合征的总有效率可达 95 .5 %。结论

肺类癌型微小瘤的临床病理及其形态发生分析

目的 描述肺类癌型微小瘤的病理特征和免疫表型 ,探讨其发生的形态学基础。方法 对 3例支气管扩张症 (支扩 )伴发微小瘤进行临床病理学观察 ,另 11例支扩和 2例正常肺作对照 ;应用免疫组织化学EnVision法检测其特异性标志物和标记气道上皮内神经内分泌细胞 (NECs)。结果 肺类癌型微小瘤多为散发多灶性镜下结节 ,呈簇状、巢状或索团状 ,分布于支扩受损的支气管壁旁、细小支气管周围和瘢痕化的组织中 ;由短梭形或小圆形细胞构成 ,核呈圆形、椭圆或长椭圆形 ,染色深 ;胞质弱嗜酸性 ;细胞嗜银性强 ;强表达神经元特异性烯醇化酶 (NSE)、嗜铬素、降钙素、胃泌素等神经内分泌性标志物 ,小灶性表达绒毛膜促性腺激素 (HCG)、促肾上腺皮质激素 (ACTH)、5 羟色胺(5 HT) ,弱表达细胞角蛋白 (CK)、上皮膜抗原 (EMA)、S 10 0。微小瘤旁气道黏膜上皮NECs明显增生 ,比不伴微小瘤的支扩肺和正常肺气道黏膜上皮内NECs计数的差异均具有统计学意义 (P值均 <0 .0 0 1)。结论 肺微小瘤具有周围型典型性类癌的病理特征和免疫表型 ,可能是典型性类癌发生的早期阶段。

Protocol of Interventional Treatment for Hepatocellular Carcinoma

To establish a reasonable protocol for interventional treatment ofhcpatocellular carcinoma (HCC). Methods: The data of 1000 HCC patients treated by different kinds ofinterventional treatments were reviewed with their results of biochemistry, imaging, pathology andsurvival rate evaluated. The values as well as the pros and cons of these various kinds ofinterventional treatments were compared in order to find an optimal protocol. Results:Segmental-transcatheter oil chemoembolization (S-TOCE) could more effectively eradicate the tumoryet inflicting less damage on the noncancerous hepatic tissue and giving much higher survival ratethan the conventional transcatheter oil chemoembolization (C-TOCE). Precutaneous ethanol injection(PEI) in combination with chemoembolization could eliminate the residual tumor and significantlyincrease the survival rate without damaging the noncancerous hepatic tissue. The living quality orsurvival rate could be improved by choosing different ways of interventional treatments to cut downthe complications. Conclusion: The selection of different interventional treatments should bo doneaccording to the size and type of HCC. Active management is indicated for different complicationspresenting along with HCC.

Inhibitory effect of human telomerase antisense oligodeoxyribonucleotides on the growth of gastric cancer cell lines in variant tumor pathological subtype

AIM: To investigate the inhibitory effect of specialized human telomerase antisense oligodeoxyribonucleotides on the growth of well (MKN-28), moderately (SGC-7901)and poorly (MKN-45) differentiated gastric cancer cell lines under specific conditions and its inhibition mechanism,and to observe the correlation between the growth inhibition ratio and the tumor pathologic subtype of gastric cancer cells.METHODS: Telomerase activity in three gastric cancer cell lines of variant tumor pathologic subtype was determined by modified TRAP assay before and after the specialized human telomerase antisense oligodeoxyribonucleotides were dealt with under specific conditions. Effect of antisense oligomer under specific conditions of the growth and viability of gastric cancer cell lines was explored by using trypan blue dye exclusion assay, and cell apoptosis was detected by cell morphology observation, flow cytometry and TUNEL assay.RESULTS: Telomerase activity was detected in well,moderately and poorly differentiated gastric cancer cell lines (the quantification expression of telomerase activity was 43.7TPG, 56.5TPG, 76.7TPG, respectively).Telomerase activity was controlled to 30.2TPG, 36.3TPG and 35.2TPG for MKN-28, SGC-7901 and MKN-45 cell lines respectively after treatment with human telomerase antisense oligomers at the concentration of 5 μmol/L, and was entirely inhibited at 10 μmol/L, against the template region of telomerase RNA component, whereas no inhibition effect was detected in missense oligomers (P＜0.05). After treatment with antisense oligomers at different concentrations under specific conditions for 96 h, significant growth inhibition effects were found in MKN-45 and SGC-7901gastric cancer cell lines (the inhibition ratio was 40.89%and 71.28%), but not in MKN-28 cell lines (15.86%). The ratio of inactive SGC-7901 cells increased according to the prolongation of treatment from 48 to 96 h. Missense oligomers could not lead to the same effect (P＜0.05).Apoptosis of SGC-7901 and MKN-45 cells was detected not only by morphology and TUNEL assay but also by flow cytometry. The apoptotic rate reached 33.56% for SGC-7901 cells and 44.75% for MKN-45 cells.CONCLUSION: The viability and proliferation of gastric cancer cells can be inhibited by antisense telomerase oligomers. The growth inhibition of gastric cancer cells is correlated with concentration, time and sequence specialty of antisense oligomers. The inhibition mechanism of antisense human telomerase oligomers depends not only on the sequence specialty but also on the biological characteristics of gastric cancer cell lines.

Anti-tumor immunity,autophagy and chemotherapy

Autophagy or self-digestion of cells is activated upon various stressful stimuli and has been found to be a survival and drug resistance pathway in cancer.However,genetic studies support that autophagy can act as a tumor suppressor.Furthermore,defective autophagy is implicated in tumorigenesis,as well.The precise impact of autophagy on malignant transformation has not yet been clarified,but recent data suggest that this complex process is mainly directed by cell types,phases,genetic background and microenvironment.Relation of autophagy to anticancer immune responses may indicate a novel aspect in cancer chemotherapy.

EXPRESSION OF mRNA FOR MEMBRANE-TYPE 1, 2, AND 3 MATRIX METALLOPROTEINASES IN HUMAN LARYNGEAL CANCER

To investigate correlation of expressions of membrane-type 1, 2, and 3 matrix metalloproteinases (MT1, MT2, and MT3-MMP) to the invasion and metastases in laryngeal cancer. Methods Reverse transcription-polymerase chain reaction (RT-PCR) was used to examine the mRNA level of MT1, MT2, and MT3-MMP in 24 patients with laryngeal cancer. The relationships of these three MT-MMP expressions to clinico-pathology were analyzed by statistics. Results The expressions of MT1, MT2, and MT3-MMP were significantly higher in laryngeal cancer tissues than those in para-tumorous tissues (P < 0.01) and had a close relationship with invasive depth (P < 0.05). But no significantly different expressions of these three MT-MMPs were found in different primary location and different histological grade of laryngeal cancer (P > 0.05). The expression of MT1-MMP was obviously higher in patients with metastatic lymph nodes than that in patients without metastatic lymph nodes (P < 0.05). Conclusion MT1, MT2, and MT3-MMP play an important role in the progression of laryngeal cancer, and MT1-MMP may serve as a reliable marker in estimating invasive and metastatic potency of laryngeal cancer. Suppressing expressions of MT1, MT2, and MT3-MMP early may inhibit the invasion and metastases of laryngeal cancer.

Membrane redistributions through multi-intercellular exchanges and serial trogocytosis

Trogocytosis is a rapid transfer between cells of membranes and associated proteins. Trogocytic exchanges have been investigated between different cell types, mainly in two-cell systems, involving one donor and one acceptor cell type. Here, we studied trogocytosis in a more complex system, involving not only several immune cell subsets but also multiple tumor cells. We show that CD4~ T cells, CD8＋ T cells and monocytes can acquire membrane patches and the intact proteins they contain from different tumor cells by multiple simultaneous trogocytoses. The trogocytic ca- pabilities of CD4~ and CD8~ T cells were found to be similar, but inferior to that of autologous monocytes. Activated peripheral-blood mononuclear cells （PBMCs） may also exchange membranes between themselves in an all-autolo- gous system. For this reason, monocytes are capable of acquiring membranes from multiple tumor cell sources, and transfer them again to autologous T cells, along with some of their own membranes （serial trogocytosis）. Our data illustrate the extent of membrane exchanges between autologous activated immune effector cells and their environ- ment, and how the cellular content of the local environment, including ＂bystander＂ cells, may impact the functions of immune effector cells.

Significance of regenerating islet-derived type Ⅳ gene expression in gastroenterological cancers

The regenerating islet-derived members （Reg）, a group of small secretory proteins, which are involved in cell proliferation or differentiation in digestive organs, are upregulated in several gastrointestinal cancers, functioning as trophic or antiapoptotic factors. Regenerat- ing islet-derived type Ⅳ （RegⅣ）, a member of the Reg gene family, has been reported to be overexpressed in gastroenterological cancers. RegIV overexpression in tumor cells has been associated with carcinogen- esis, cell growth, survival and resistance to apoptosis. Cancer tissue expressing RegIV is generally associated with more malignant characteristics than that with- out such expression, and RegⅣ is considered a novel prognostic factor as well as diagnostic marker in some gastroenterological cancers. We previously investigated the expression levels of RegⅣ mRNA of 202 surgical colorectal cancer specimens with quantitative real-time reverse-transcriptase polymerase chain reaction and reported that a higher level of RegⅣ gene expression was a significant independent predictor of colorec- tal cancer. The biologic functions of RegⅣ protein in cancer tissue, associated with carcinogenesis, anti- apoptosis and invasiveness, are being elucidated by molecular investigations using transfection techniques or neutralizing antibodies of RegIV, and the feasibility of antibody therapy targeting RegIV is being assessed. These studies may lead to novel therapeutic strate- gies for gastroenterological cancers expressing RegⅣ. This review article summarizes the current information related to biological functions as well as clinical impor- tance of RegⅣ gene to clarify the significance of Reg~ expression in gastroenterological cancers.

Clinicopathological features of early gastric cancer with duodenal invasion

The incidence of early gastric cancer （EGC） with duodenal invasion is extremely low, although advanced gastric cancer that arises in the antrum occasionally invades the duodenum. We investigated the clinicopathological features of EGC with duodenal invasion and provided strategies for clinical management.A Medline search was performed using the keyword early gastric cancer＂ and ＂duodenal invasion＇： Additional articles were obtained from references within the papers identified by the Medline search. We revealed that EGC with duodenal invasion was of the superficial spreading type of tumor. Tumors 〉 60 mm in size invaded the duodenum more extensively, and the distance of duodenal invasion from the pyloric ring was further in the elevated type than in the depressed type of tumor.There was no significant difference between the length of duodenal invasion and the histological type of the tumor. Gastric cancer located adjacent to the pyloric ring, even if cancer invasion was confined to the mucosa or submucosa, was more likely to invade the duodenum.The present study reveals that the elevated type of EGC is associated with more extensive duodenal invasion when the tumor size is 〉 60 ram, thus highlighting the importance of identification of duodenal invasion in these cases. We also reveal that sufficient duodenal resection with a cancer-free distal surgical margin should be performed in cases of duodenal invasion.

Increased risk of hyperglycemia associated with the use of everolimus in patients with cancer: a systematic review and meta-analysis

Everolimus is an orally administered rapamycin analogue that has been approved to treat several types of solid tumors. However, some patients develop hyperglycemia after being treated with everolimus. In this meta-analysis, we aimed to evaluate the incidence and risk of hyperglycemia in patients with cancer who received everolimus. We searched the medical literature, as index in the Cochrane Library, PubMed, EMBASE, and abstracts from the top scientific meetings （AACR, ASCO, and ESMO）. Our meta-analysis included the randomly controlled trials published before November 2014. We calculated overall incidence, relative risk （RR） and 95% confidence intervals （CI） using fixed-effects or random-effects models, depending on the heterogene- ity among the trials. A total of 3377 patients （everolimus： 1971; control： 1406） from 8 randomized clinical trials were included in the meta-analysis. In the everolimus groups, the incidence of all grades of hyperglycemia was 20.0% （95% CI： 11.0%-29.0%）, while the incidence of high-grade hyperglycemia was 6.0% （95% CI： 3.0%-8.0%）. Patients treated with everolimus had an in- creased risk of hyperglycemia as compared with that of controls （all-grade RR： 2.94, 95% CI： 2.34-3.70; high-grade RR： 4.66, 95% CI： 2.75-7.89）. Everolimus significantly increased the risk of hyperglycemia. This risk may depend on the tumor type and the everolimus dosage.

Effect of Aspirin on DMBA-induced mammary gland carcinogenesis and its anti-tumor mechanism in MCF-7 breast cancer cell

The effects of Aspirin on tumor chemoprevention and inhibition have been debated and researched in recent years and its effects on colorectal cancer are quite clear.For breast cancer,however,conclusions are inconsistent and the anti-tumor mechanism of Aspirin is not clear yet.In our study,we used DMBA-induced mammary gland carcinogenesis model to assess the chemoprevention effect of Aspirin on mammary precancerous lesions.After SD rats were treated with Aspirin,the total numbers of precancerous lesion in experimental groups were 16（40 mg/kg Aspirin） and 13（20 mg/kg Aspirin）,while the number in control group was 35.In vitro,we found that Aspirin inhibited cell proliferation in human breast cancer cell line MCF-7 by SRB assay with no apparent cytotoxity under the doses of 10,8,6,4 and 2 mM,the inhibitory rates were 86.96%,54.56%,24.83%,14.24% and 4.49%,respectively.In mechanism research,the results of gene microarray assay demonstrated that 4 mM and 2 mM Aspirin were effective in changing gene expression profile in MCF-7 cells.The expression of cell cycle regulator,cyclin A,was significantly down-regulated under the same doses,while the down-regulation of Cdk2 was only remarkable at 4 mM.Our findings reveal that Aspirin is effective in tumor inhibition during initial phase in rats.In MCF-7 cells,Aspirin reduces cell proliferation without significant cytotoxity and its possible mechanism involves altering tumor-related gene expression and regulating cell cycle process.

Non-coding RNAs regulate tumor cell plasticity

Tumor metastasis is one of the most serious challenges for human cancers as the majority of deaths caused by cancer are associated with metastasis,rather than the primary tumor.Recent studies have demonstrated that tumor cell plasticity plays a critical role in tumor metastasis by giving rise to various cell types which is necessary for tumor to invade adjacent tissues and form distant metastasis.These include differentiation of cancer stem cells(CSCs),or epithelial-mesenchymal transition(EMT)and its reverse process,mesenchymal-epithelial transition(MET).A growing body of evidence has demonstrated that the biology of tumor cell plasticity is tightly linked to functions of non-coding RNAs(ncRNAs),especially microRNAs(miRNAs)and long non-coding RNAs(lncRNAs).Therefore,understanding the mechanisms how non-coding RNAs regulate tumor cell plasticity is essential for discovery of new diagnostic markers and therapeutic targets to overcome metastasis.