结直肠癌患者血清IL-17和TGF-β浓度及其相关性的初步研究

  目的   研究血清IL-17和TGF-β浓度变化与结直肠癌（colorectal cancer,CRC）发生发展的相关性及其临床意义。   方法   健康志愿者30例、无远处转移并行手术治疗的结直肠癌患者59例及术后发生远处转移的44例患者被纳入本研究,依次为A（对照组）、B、C组,平均年龄分别为（53.8±20.8）岁、（62.0±11.8）岁、（64.0±15.7）岁,所有患者均经病理学检查确诊为结肠或直肠癌。B组59例,其中结肠癌26例为B1组,直肠癌33例为B2组;C组44例,其中结肠癌23例为C1组;直肠癌21例为C2组。测定A、B和C组血清IL-17和TGF-β浓度,其中分别测定B组术前术后血清IL-17和TGF-β浓度。   结果   血清IL-17浓度测定结果显示,B组术前高于术后,C组高于B组（术前和术后）,B、C组均高于A组,B组术前术后比较、B组和C组比较及B、C组与对照组比较差异均有统计学意义（P < 0.05）。B组术前、术后血清TGF-β水平比较差异无统计学意义（P>0.05）,A组和B组比较差异无统计学意义（P>0.05）。C组高于B组,B、C组均高于A组,C组和B组比较,B、C组和A组比较,差异均有统计学意义（P < 0.05）。B组结肠癌（B1组）和直肠癌（B2组）组比较、C组结肠癌（C₁）和直肠癌（C₂）组比较,血清IL-17和TGF-β水平差异均无统计学意义（P>0.05）。   结论   血清IL-17水平和结直肠癌的发生、发展密切相关,随着结直肠癌进展和肿瘤负荷增加,血清IL-17水平升高。血清TGF-β水平和结直肠癌转移显著相关,在结直肠癌的转移机制中可能起到重要作用。      

TGF-βRII/hMSH6与结直肠癌关系的研究进展

TGF-βRII基因突变会丧失对细胞生长和分化的调节,使细胞向癌变发展。hMSH6基因的突变会造成复制后错配修复功能丧失、整个基因组的不稳定、产生突变体,增加肿瘤易感性。本文就国内外对TGF-βRII/hMSH6与结直肠癌发生发展关系的研究进展作一综述。     

术前炎性因子水平对82例行结直肠癌根治术患者预后影响研究

摘 要：［目的］ 探讨术前炎性因子水平对行结直肠癌根治术患者预后情况的影响。［方法］ 82例行结直肠癌根治术的患者作为研究对象,对其术前炎性因子水平及预后情况进行回顾性研究,进行相关性分析。对有差异的因素进行Logistic多因素回归分析。 ［结果］ 病理分期及各项术前炎性因子水平均会对患者3年生存率产生影响,差异有统计学意义（P<0.05）。Logistic多因素回归分析结果显示,TNF-α、IL-6、IL-8表达水平以及GPS评分是影响患者预后的独立危险因素。 ［结论］ 术前炎性因子对于预测结直肠癌根治术后患者预后具有一定意义,应作为常规检测指标。     

术后腹腔热灌注化疗对结直肠癌患者胃肠功能、免疫功能及炎性因子的影响

目的 探讨术后腹腔热灌注化疗对结直肠癌患者胃肠功能、免疫功能及炎性因子的影响。方法 根据术后化疗方法的不同将108例腹腔镜结直肠癌根治术患者分为对照组和观察组,每组54例,对照组患者采用静脉化疗,观察组患者采用腹腔热灌注化疗。比较两组患者的胃肠功能指标[胃动素(MTL)、胃泌素(GAS)]、免疫功能指标(CD4⁺、CD8⁺水平及CD4⁺/CD8⁺)、炎性因子[C反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)]水平及不良反应发生情况。结果 化疗后,两组患者的MTL、GAS水平均低于本组化疗前,观察组患者的MTL、GAS水平均高于对照组,差异均有统计学意义(P﹤0.05)。化疗后,两组患者的CD4⁺水平及CD4⁺/CD8⁺均高于本组化疗前,CD8⁺水平均低于本组化疗前,观察组患者的CD4⁺水平及CD4⁺/CD8⁺均高于对...     

PGE2诱导产生的CXCL1促进结直肠癌的血管形成

已知慢性炎症可以通过刺激血管形成而促进肿瘤生长，约15％的恶性肿瘤的发生与慢性炎症有关。慢性炎症导致炎性细胞上调表达IL-1α／15、IFN-γ及TNF-α等细胞因子，而这些炎性细胞因子又会诱导另一些炎性介质如环加氧酶-2（COX-2）及炎性趋化因子的表达。以前的研究表明COX-2具有促进肿瘤血管形成的作用。作为COX-2的主要代谢产物之一的PGE2，在人结直肠癌及家族性息肉患者腺瘤中的含量明显上升，在结直肠癌的发展中起重要作用。     

腹腔镜结直肠癌根治术对老年结直肠癌患者免疫功能的影响

目的 探究腹腔镜结直肠癌根治术对老年结直肠癌患者免疫功能的影响.方法 将200例结直肠癌患者根据手术方式不同分为对照组与观察组,每组100例.对照组进行常规手术治疗,观察组进行腹腔镜结直肠癌根治术治疗,比较两组患者T淋巴细胞亚群水平、炎性因子水平、手术相关指标及并发症发生率.结果 治疗后,两组患者肿瘤坏死因子-α(TN...     

IGFBP-2与结直肠癌的研究进展

胰岛素样生长因子结合蛋白2（IGFBP-2）是胰岛素样生长因子系统的一员,IGFBP-2在神经胶质瘤、结直肠癌、前列腺癌、卵巢癌、乳腺癌等多种恶性肿瘤细胞株、患者血清及其肿瘤组织中均有表达或表达水平升高。大量的临床实验及流行病学研究涉及了IGFBP-2与结直肠癌之间的关系,全文就目前IGFBP-2与结直肠癌的研究进展作一综述。     

结直肠癌中Ets-1和整合素α6β4的表达及临床意义

目的：检测结直肠癌中转录因子Ets-1和整合素α6β4的表达,探讨其在结直肠癌浸润转移中的作用及临床意义。方法：选取2007年6月至2008年6月间天津医科大学总医院外科40例结直肠癌手术标本为研究对象,分别采用荧光实时定量PCR和免疫组织化学方法检测肿瘤和切端组织中Ets-1和整合素α6β4的mRNA和蛋白表达水平,并结合临床病理资料进行统计学分析。结果：Ets-1和整合素α6β4在肿瘤组织中的mRNA表达水平和蛋白表达水平均高于切端组织 （P<0.05）;Ets-1 mRNA的表达与肿瘤的组织学类型、肿瘤部位、大小及分化程度未见相关性 （P>0.05）,伴淋巴结转移者Ets-1 mRNA的表达明显高于不伴淋巴结转移者, 其差异具有统计学意义 （P<0.05）, Ets-1 mRNA表达与大肠癌浸润深度及Dukes分期存在正相关, 伴随肿瘤浸润深度和临床分期的增加, Ets-1 mRNA表达明显增加, 其差异有统计学意义 （P<0.05）; 淋巴结转移者的Ets-1蛋白阳性率为91.3% （21/23）,无淋巴结转移者为58.8% （10/17）,两者差异具有统计学意义 （P<0.05）,伴随肿瘤浸润深度和Dukes分期的增加, 肿瘤组织中Ets-1蛋白阳性率也显著增加 （P<0.05）, 而Ets-1蛋白表达水平与病理类型及分化程度未见相关性 （P>0.05）; 结直肠癌中Ets-1的表达与整合素α6β4的表达呈正相关 （P<0.05）。结论： 检测结直肠癌内Ets-1和整合素α6β4的表达可作为评价肿瘤侵袭转移、 判断预后的重要指标, Ets-1可能成为结直肠癌基因治疗新的靶点。     

直肠癌患者血清中白介素 ８、ＴＮＦ-α和Ｔ细胞亚群的临床研究

目的　探讨直肠癌患者免疫状态及其与肿瘤临床病理特征的关系。方法　分别采用流式细胞仪和ＥＬＩＳＡ双抗夹心法检测４３例直肠癌患者血清中单个核细胞ＣＤ４、ＣＤ８以及白介素-８（ＩＬ-８）、肿瘤坏死因子α（ＴＮＦ-α）含量,并与正常人进行对照。结果　直肠癌患者外周血Ｔ细胞亚群ＣＤ４、ＣＤ４／ＣＤ８明显低于对照组（Ｐ＜０.０１）,并且随着Ｄｕｋｅｓ分期的增加而逐渐降低;ＣＤ８、ＩＬ-８和ＴＮＦ-α明显高于对照组（Ｐ＜０.０１）,并且随着Ｄｕｋｅｓ分期的增加而逐渐升高。结论　直肠癌患者存在免疫功能低下,血清中Ｔ细胞亚群以及ＩＬ-８、ＴＮＦ-α含量与直肠癌Ｄｕｋｅｓ分期具有相关性。     

血吸虫肠病相关性结直肠癌的研究进展

日本血吸虫感染曾经是中国较为严重的流行病，同时也是引起结直肠癌(colorectal cancer,CRC)发生的原因之一。CRC的患者若有血吸虫病感染史，术前肠道具有血吸虫感染相关的影像学表现，术后病理证实肿瘤附近有虫卵沉积，则可定义为血吸虫肠病相关性CRC（colorectal cancer with schistosomiasis，CRCS）。探究血吸虫肠病到CRCS之间演变的炎癌转化机制，对于改善CRCS预后尤为重要。笔者结合国内外的最新研究报道，对CRCS发病机制、病理特征以及临床研究进展进行综述，以期为CRCS防治提供帮助，亦为炎癌转化研究提供新的思路。     

Inflammatory cytokines in human pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal types of cancer with poor prognosis. Despite extensive efforts, the current treatment methods have limited success. Therefore, novel therapeutic approaches are required. The pancreatic tumor microenvironment is rich in growth factors and inflammatory cytokines that support tumor growth, and it is highly immunosuppressive. Up-regulation of cytokine pathways has been shown to modulate PDAC progression and immune evasion; therefore targeting cytokines may have therapeutic benefits. In this review we provide an overview of current understanding of pro- and anti-inflammatory cytokines in pancreatic cancer and their potential as therapeutic targets.     

Inflammatory breast carcinoma: A distinct entity?

Sixty-four patients with the diagnosis of either inflammatory or locally advanced breast cancer were analyzed with respect to age, menopausal status, estrogen receptor protein (ERP) measurements, characteristics on clinical presentation, disease-free interval (DFI), and overall survival. There were no significant differences between the two groups in the patients' clinical presentation, DFI, or overall survival time. Patients with inflammatory carcinoma were significantly younger as well as more likely to be pre- or perimenopausal than patients with locally advanced breast cancer. Of those patients who had ERP measurements performed, patients with inflammatory breast cancer had a significantly decreased incidence of ERP(+) tumors in comparison to patients with locally advanced breast cancer. These results suggest that inflammatory carcinoma of the breast behaves as an ERP(-) subtype of locally advanced breast carcinoma rather than a truly distinct entity.     

宫颈癌相关干细胞的研究进展

目的:总结目前宫颈癌相关干细胞的研究进展.方法:应用Medline和CNKI期刊全文数据库检索系统,以“宫颈肿瘤、干细胞、干细胞通路”为主题词,检索2000-01-2012-05相关文献,纳入标准:1)正常宫颈干细胞;2)宫颈癌相关肿瘤干细胞,包括肿瘤干细胞和肿瘤相关间质干细胞;3)干细胞通路与宫颈癌治疗抵抗.根据纳入标准符合分析的文章有31篇.结果:1)正常宫颈干细胞为宫颈基底层下的储备细胞.2)宫颈肿瘤干细胞具有明确的分子表型标志,如醛脱氢酶(+);亦有研究认为,侧群细胞即宫颈癌干细胞,表达多药耐药蛋白ABCG2/BCRP1;宫颈癌细胞系和新鲜肿瘤组织中分离筛选出的宫颈癌干细胞呈肿瘤球样悬浮增殖,富于表达自我更新相关基因如Nanog、Oct-4和Sox-2等,且致瘤性明显增强.间充质干细胞是一种机体内部间质内广泛存在的非造血系成体干细胞,有多向分化能力,在肿瘤组织中是否存在及相互作用目前研究较少.宫颈癌组织中能分离出具有多向分化潜能的间充质干细胞,其核型正常,可分化为骨骼、软骨和脂肪细胞等;而上皮间质转化基因的激活能诱导出肿瘤干细胞表型.3)宫颈癌的发生、进展过程中能发现干细胞相关通路的活化及参与,如Hedgehog通路、TGF-β通路等,通过靶向调节信号通路的关键分子,能明显抑制肿瘤细胞的增殖,降低其自我更新能力,从而达到提高治疗敏感性的目的.结论:通过对宫颈癌相关干细胞及其信号通路的研究,有望为宫颈癌治疗提供新的理论依据和临床靶点,从而为根治肿瘤提供可能.     

鼻咽癌放射抗拒相关microRNAs研究进展

鼻咽癌是一种起源于鼻咽部上皮组织的鳞状细胞恶性肿瘤,在东南亚和中国华南地区具有很高的发病率,目前放疗已成为鼻咽癌的首选治疗方式。放射抗拒是鼻咽癌放疗成功的主要障碍,寻找鼻咽癌放射抗拒相关的生物标志物,明确放射抗拒的产生机制,对治疗具有重大意义。MicroRNAs通过结合靶mRNA的3’UTR 从而诱导其翻译抑制或降解,调节蛋白的表达,参与放疗反应相关的所有重要的细胞过程如DNA损伤反应与修复、细胞凋亡、增殖以及血管生成的调节。近年来鼻咽癌放射抗拒相关microRNAs的研究成为热点,本文就microRNAs及其潜在的作用机制进行综述。     

Colonic carcinoma associated with an abnormal collagen table. Collagenous colitis

A case of cecal adenocarcinoma with the typical histopathologic features of collagenous colitis throughout the resected colon is described in a 67-year-old woman. Collagenous colitis has not previously been reported in association with adenocarcinoma of the colon and the relationship of these findings appears to be unprecedented. A review of 100 randomly selected Duke's B adenocarcinomas of the colon revealed no similar case.     

Colostomy carcinoma in ulcerative colitis

A 52-year-old female who was diagnosed with ulcerative colitis in 1976 underwent emergency ascending colostomy construction in February 1983. Six years later, a biopsy of the colostomy revealed an adenocarcinoma. The patient subsequently underwent total proctocolectomy and ileal J pouch-anal anastomosis in January 1990. The lesion was surrounded by colonic dysplasia and positioned at the leading edge of the extraabdominally herniated bowel. A moderately differentiated adenocarcinoma with a mucinous component and no lymph node involvement, was detected. This rare condition may advance our understanding of carcinogenesis in this disease by focusing on the effect of stomal effluent with intestinal flora and malignant changes.     

Severe colitis associated with docetaxel use: A report of four cases

Diarrhea is a common side effect of chemotherapy. Pseudomembranous colitis is a well known complication of antibiotic treatment that can also be observed, albeit rarely, with certain chemotherapeutic agents. We present four cases of severe colitis in patients undergoing treatment with taxane-based chemotherapy for pancreatic, lung and breast cancer. None of them had recently received antibiotics. One patient presented with a bowel perforation and three had endoscopic findings of pseudomembranous colitis. Two of these three patients had negative stool toxin assays for Clostridium difficile. In the patient presenting with perforation, an emergency left hemicolectomy was performed and the pathological findings in the colon were acute inflammation and ischemic necrosis; the other three patients were treated with oral vancomycin and/or oral or intravenous metronidazole leading to complete resolution of the symptoms. Apart from pseudomembranous colitis, we describe patients presenting with neutropenic enterocolitis as well as ischemic colitis after docetaxel use. These cases provide some insight into the spectrum and varied clinical presentations of severe colitis associated with taxane-based chemotherapy.     

Cells and cytokines involved in the pathogenesis of sarcoidosis

Granulomatous inflammation develops under the regulatory influence of cytokines produced by local mononuclear phagocytes, T cells, dendritic cells, fibroblasts, and other local cells. In sarcoidosis, granulomatous inflammation is characterized by dominant expression of T helper 1 (Th1) cytokines such as IFN gamma and interleukin (IL)-2 with low levels of expression of T helper 2 (Th2) cytokines such as IL4 and IL5. Recent studies show that the cytokine IL12, the most important regulator of Th1 immune responses currently known, is upregulated at sites of inflammation in sarcoidosis. In particular, enhanced expression of IL12 is seen in sarcoid lung and lymph node, along with dysregulated production of IL12 by stimulated and unstimulated sarcoid alveolar macrophages. The known dependence of granulomatous inflammation on type 1 cytokines (IFN gamma, IL12) in many experimental models of granulomatous disease makes it likely that these cytokines function in a similar fashion in the initiation and maintenance of granulomatous inflammation in sarcoidosis. Whether these same type 1 cytokines drive granulomatous inflammation in patients with extensive fibrocystic lung disease remains unknown. TGF beta, a known inhibitor of IL12 and IFN gamma production, is produced at higher levels by lung cells from those patients who undergo remission of their disease, suggesting that TGF gamma is important in downregulating granulomatous inflammation in sarcoidosis. These studies offer new insight into the molecular mechanisms of granuloma formation in sarcoidosis and provide a framework for developing new therapeutic strategies for the treatment of this disease.