人肺巨细胞癌PLA-801C和PLA-801D的体内自发转移性再研究

目的　了解人肺巨细胞癌亚系PLA -80 1C和PLA- 80 1D目前的体内自发转移特性,为进行下一步研究提供具体数据及所需模型。方法　采用肿瘤细胞动物皮下接种的方法,建立肿瘤自发性转移动物模型,实验结束时处死动物行病理学检查,统计成瘤率及转移率。结果　两株细胞的成瘤率均为10 0 %。腋窝皮下接种组PLA- 80 1C和PLA -80 1D的淋巴结转移率分别为0 ,33 .33% ,肺转移率分别为10 0 % ,6 6. 6 7%。左后腿皮下接种PLA 80 1D的裸鼠淋巴结及肺部的转移率分别为16. 6 7% ,4 1 .6 7%。已与前人所验证的结果明显不同。结论　本文分析了这两株细胞的成瘤性和转移性变化的原因,并认为这两株细胞在转移特性上仍存在明显差异,仍具有用于肿瘤转移领域研究的重要价值。     

人鼻咽癌CD133+干细胞的生物学特性及意义人鼻咽癌CD133+干细胞的生物学特性及意义

背景:有研究表明肿瘤细胞株中存在肿瘤干细胞,是肿瘤复发、转移的根源,但人鼻咽癌细胞株CNE-2中肿瘤干细胞的表达及生物学特性至今少有报道.目的:观察人鼻咽癌CD133+干细胞生物学特性及意义.方法:采用流式细胞仪检测人鼻咽癌细胞株CNE-2中CD133的表达情况.免疫磁珠分选技术获得人鼻咽癌CD133+干细胞,分别采用无血清培养法、CCK-8法、平板克隆形成试验及裸鼠体内成瘤实验检测CD133+干细胞的体外增殖及体内成瘤能力,并将其与CD133-及未分选鼻咽癌细胞进行比较,以了解CD133+干细胞的生物学特性.结果与结论:免疫磁珠富集的CD133+细胞在无血清培养基中呈悬浮生长,并可以形成肿瘤干细胞球.CD133+细胞与CD133-细胞比较具有较高的克隆形成能力(P < 0.01);CD133+细胞在裸鼠体内的成瘤率高于CD133-细胞(P < 0.05).结果证实,鼻咽癌CD133+干细胞能在体外分离培养,形成干细胞球,增殖能力强,在裸鼠体内具有极强的成瘤能力.     

人鼻咽癌CD133^＋干细胞的生物学特性及意义

背景：有研究表明肿瘤细胞株中存在肿瘤干细胞,是肿瘤复发、转移的根源,但人鼻咽癌细胞株CNE-2中肿瘤干细胞的表达及生物学特性至今少有报道。目的：观察人鼻咽癌CD133^＋干细胞生物学特性及意义。方法：采用流式细胞仪检测人鼻咽癌细胞株CNE-2中CD133的表达情况。免疫磁珠分选技术获得人鼻咽癌CD133^＋干细胞,分别采用无血清培养法、CCK-8法、平板克隆形成试验及裸鼠体内成瘤实验检测CD133^＋干细胞的体外增殖及体内成瘤能力,并将其与CD133-及未分选鼻咽癌细胞进行比较,以了解CD133^＋干细胞的生物学特性。结果与结论：免疫磁珠富集的CD133^＋细胞在无血清培养基中呈悬浮生长,并可以形成肿瘤干细胞球。CD133^＋细胞与CD133-细胞比较具有较高的克隆形成能力（P〈0.01）;CD133^＋细胞在裸鼠体内的成瘤率高于CD133-细胞（P〈0.05）。结果证实,鼻咽癌CD133^＋干细胞能在体外分离培养,形成干细胞球,增殖能力强,在裸鼠体内具有极强的成瘤能力。     

MCF7细胞中肿瘤干细胞的增殖特征

背景:肿瘤干细胞学说认为,肿瘤干细胞是肿瘤不断增殖的根源,并与肿瘤的浸润转移、耐药现象密切相关。目的:在单细胞水平研究体外传代培养的MCF7细胞中肿瘤干细胞含量变化规律,认识肿瘤干细胞在体外培养环境下的增殖特点。方法:利用单细胞分离种植-成瘤性克隆方法对传代培养后不同时间点MCF7细胞中肿瘤干细胞的比例连续检测,流式细胞仪同步检测相应细胞样本中CD44+CD24-/low亚群的含量变化。结果与结论:传代后培养的MCF7细胞在不同时间点其肿瘤干细胞比例及CD44+/CD24-/low亚群比例均呈现有规律的变化。但CD44+/CD24-/low亚群变化更为显著(36.84%到81.95%),而肿瘤干细胞含量仅在小范围波动(38.54%～47.39%)。结果提示传代培养的MCF7细胞中,肿瘤干细胞具有通过调节自身增殖来保持其比例相对稳定的特点;CD44+/CD24-/low亚群并不代表或者富集MCF7细胞株中的肿瘤干细胞亚群。     

CXCR4对骨肉瘤细胞株的裸鼠肺转移的影响

[目的]研究趋牝因子受体CXCR4对不同转移潜能骨肉瘤细胞株的裸鼠肺转移的影响.[方法]采用单细胞克隆技术,从人骨肉瘤细胞系MG-63中分离培养出2株不同CXCR4表达的骨肉瘤细胞株,免疫组化检潮其CXCR4的表达水平,将骨肉瘤细胞株分剐接种于裸鼠的颈背部皮下并于4周后处死裸鼠,观察肺部转移情况.[结果]分离培养出2株骨肉瘤细胞株,其CXCR4蛋白的表达水平为B8＞G5,各组裸鼠的肺组织转移灶数为B8＞G5,与CXCR4蛋白的表达呈正相关.[结论]骨肉瘤细胞高度的肺转移能力与CXCR4的高表达密切相关.     

MCF7细胞中肿瘤干细胞的增殖特征

背景：肿瘤干细胞学说认为,肿瘤干细胞是肿瘤不断增殖的根源,并与肿瘤的浸润转移、耐药现象密切相关。目的：在单细胞水平研究体外传代培养的MCF7细胞中肿瘤干细胞含量变化规律,认识肿瘤干细胞在体外培养环境下的增殖特点。方法：利用单细胞分离种植-成瘤性克隆方法对传代培养后不同时间点MCF7细胞中肿瘤干细胞的比例连续检测,流式细胞仪同步检测相应细胞样本中CD44＋CD24-/low亚群的含量变化。结果与结论：传代后培养的MCF7细胞在不同时间点其肿瘤干细胞比例及CD44＋/CD24-/low亚群比例均呈现有规律的变化。但CD44＋/CD24-/low亚群变化更为显著（36.84%到81.95%）,而肿瘤干细胞含量仅在小范围波动（38.54%～47.39%）。结果提示传代培养的MCF7细胞中,肿瘤干细胞具有通过调节自身增殖来保持其比例相对稳定的特点;CD44＋/CD24-/low亚群并不代表或者富集MCF7细胞株中的肿瘤干细胞亚群。     

人胎脑皮层神经干细胞的体外培养及鉴定

目的 从36周人胎脑皮层分离培养神经干细胞并鉴定。方法 采用无血清培养和单细胞克隆技术,从36周自愿水囊引产人胎脑皮层中分离出具有单细胞克隆能力的细胞,并观察神经干细胞体外培养、传代、分化潜能,采用免疫组化和免疫荧光技术检测克隆细胞的神经巢蛋白和各种分化细胞的特征性抗原的表达。结果 从36周人胎脑皮层中成功分离出具有自我更新和多分化潜能的神经干细胞,在无血清培养时细胞呈悬浮状态生长,形成神经球,该细胞具有连续克隆能力,可传代培养,呈Nestin免疫反应阳性;在含血清培养时神经干细胞分化,并表达神经元细胞和星形胶质细胞的特异性抗原。结论 36周人胎脑皮层仍能培养出具有自我复制和分化潜能的神经干细胞。     

纤连蛋白在血液系统的研究进展

纤连蛋白（Fibronectin，FN）是细胞外基质中重要的黏附分子，与其整合素受体共同参与造血干／祖细胞的增值、分化及细胞黏附介导的耐药。随着对骨髓造血微环境的不断认识，细胞黏附介导的耐药在血液系统肿瘤耐药中起重要的作用。FN在血小板黏附与聚集中也起重要的作用，FN可能是独立于Fbg、vWF之外介导血小板黏附与聚集的重要蛋白分子。本文就FN的分类、结构、功能及其与血液系统关系等方面的研究进展作一综述。     

肿瘤干细胞研究进展

传统发育生物学理论认为,肿瘤是由成熟细胞突变而来,每个肿瘤细胞都有相同、无限增值、分化和成瘤的能力。最近研究发现,肿瘤生长是肿瘤组织中极少量具无限增殖潜能的肿瘤干细胞(tumor stem cell)增殖的结果。越来越多的证据表明,肿瘤内存在类似正常干细胞的具自我更新能力的肿瘤起始细胞(initiated cell),其是肿瘤发生、发展和转移的根源[1,2]。干细胞理论近年研究发现,几乎所有正常组织都存在一小群可分化为其他不同类型细胞的原始细胞,这类细胞具自我更新、多向分化潜能及永生性三大特性,被称为干细胞。干细胞可分为3种类型:①胚胎干细胞…     

KAI1基因在不同转移潜能人肺癌细胞株中的表达

目的：探讨人肺癌细胞转移潜能与KAI1基因表达的关系。方法：应用real-timeRT-PCR技术检测不同转移潜能的人肺癌细胞株和正常人成纤维细胞株MRC-5中KAI1基因mRNA的表达水平及差异。结果：人肺癌细胞株中KAI1基因mRNA表达水平均显著低于正常肺成纤维细胞株MRC-5;不同转移潜能人大细胞肺癌细胞株中KAI1基因mRNA表达水平有明显差异。结论：KAI1基因表达降低与人肺癌细胞的转移潜能高低有关。     

microRNAs as cancer biomarkers

Abstract

Since their discovery in 1993, microRNAs (miRNAs) have been identified as important gene regulators in many biological processes and as key molecular players in human disease, including cancer where they show specific pathogenic deregulation. Their remarkable chemical stability, the availability of very sensitive miRNA detection methods and the fact that miRNAs can be extracted from and detected in various kinds of clinically relevant samples, such as solid tissues, body fluids and secretions make them excellent candidate biomarkers. However, no miRNA has yet entered the level of practical clinical relevance. We present a brief background and some key aspects and challenges of miRNAs as cancer biomarkers, we discuss shortfalls and identify possible routes towards the use of miRNAs as reliable biomarkers for cancer.     

Breast cancer presenting as periostitis

A previously healthy 69-year-old woman presented with progressive and unremitting distal leg pain that was confirmed by biopsy to be periostitis. Ten months after the onset of symptoms, carcinoma of the breast was diagnosed. Surgical removal of the neoplasm was followed by complete relief of leg pain within 24 hours. Hypertrophic osteoarthropathy must be considered in adult patients presenting with unexplained joint or distal extremity symptoms, and a vigilant search for underlying malignancy should be undertaken.     

Splice variants as cancer biomarkers

Inherited and acquired changes in pre-mRNA splicing have been documented to play a significant role in human disease development and many cancer-associated genes are regulated by alternative splicing. Loss of fidelity, variation of the splicing process, even controlled switching to specific splicing alternatives may occur during tumor progression and could play a major role in carcinogenesis. Splice variants that are found predominantly in tumors have clear diagnostic value and may provide potential drug targets. Moreover, understanding the process of aberrant splicing and the detailed characterization of the splice variants may prove crucial to our understanding of malignant transformation. This review discusses the basic mechanism of alternative splicing, alternative splicing in cancer-associated genes, tools to identify splice variants, and the development of clinical tests based on alternatively spliced biomarkers.     

Mitochondrial DNA as a cancer biomarker

As part of a national effort to identify biomarkers for the early detection of cancer, we developed a rapid and high-throughput sequencing protocol for the detection of sequence variants in mitochondrial DNA. Here, we describe the development and implementation of this protocol for clinical samples. Heteroplasmic and homoplasmic sequence variants occur in the mitochondrial genome in patient tumors. We identified these changes by sequencing mitochondrial DNA obtained from tumors and blood from the same individual. We confirmed previously identified primary lung tumor changes and extended these findings in a small patient cohort. Eight sequence variants were identified in stage I to stage IV tumor samples. Two of the sequence variants identified (22%) were found in the D-loop region, which accounts for 6.8% of the mitochondrial genome. The other sequence variants were distributed throughout the coding region. In the forensic community, the sequence variations used for identification are localized to the D-loop region because this region appears to have a higher rate of mutation. However, in lung tumors the majority of sequence variation occurred in the coding region. Hence, incomplete mitochondrial genome sequencing, designed to scan discrete portions of the genome, misses potentially important sequence variants associated with cancer or other diseases.     

Shock as a complication of cancer

Shock is a syndrome in which multiple etiologies converge on a pathway of response which, although preservative and compensatory early on, rapidly becomes irreversible and fatal. The mechanisms of this response are under intense investigation, though little therapeutic improvement has accompanied our understanding. The patient with malignancy is at risk for developing shock both as a result of his disease and therapy for his disease, yet he is by no means alone in his vulnerability. Technologic advances may still bring more effective support to the shock patient, while immunologic advances may ultimately provide support to the shock patient, while immunologic advances may ultimately provide answers and cure.     

Allogeneic immune replacement as cancer immunotherapy

The graft-versus-leukaemia (GVL) reaction that occurs after allogeneic haematopoietic cell transplantation (HCT) can cure patients with a variety of haematological malignancies. A heightened appreciation of the GVL effect has resulted in the development of reduced intensity transplant approaches, where antitumour effects occur predominantly as a consequence of the transplanted donor immune system. The recent success of these transplants in patients with acute and chronic leukaemias has led to trials investigating for graft-versus-tumour (GVT) effects in patients with treatment-refractory metastatic solid tumours. This review discusses evidence that immune replacement following allogeneic HCT is a potent form of cancer immunotherapy for patients with haematological and non-haematological malignancies.     

Allogeneic immune replacement as cancer immunotherapy

The graft-versus-leukaemia (GVL) reaction that occurs after allogeneic haematopoietic cell transplantation (HCT) can cure patients with a variety of haematological malignancies. A heightened appreciation of the GVL effect has resulted in the development of reduced intensity transplant approaches, where antitumour effects occur predominantly as a consequence of the transplanted donor immune system. The recent success of these transplants in patients with acute and chronic leukaemias has led to trials investigating for graft-versus-tumour (GVT) effects in patients with treatment-refractory metastatic solid tumours. This review discusses evidence that immune replacement following allogeneic HCT is a potent form of cancer immunotherapy for patients with haematological and non-haematological malignancies.