表皮-钙黏附素和Snail蛋白的表达与大肠癌侵袭转移及预后的关系

目的 研究表皮-钙黏附素(E-CD)和Snail蛋白在大肠癌组织中的表达及其与大肠癌侵袭、转移和预后之间的关系.方法 采用免疫组化EnVision法,检测E-CD和Snail蛋白在30例正常大肠黏膜、30例大肠腺瘤及142例大肠癌组织中的表达.结果 E-CD蛋白在正常大肠黏膜组织中的强阳性表达率为90.0%,明显高于其在大肠腺瘤和大肠癌组织中的强阳性表达率(63.3%和41.5%,P<0.05).Snail蛋白在大肠癌组织中的阳性表达率为52.1%,明显高于其在正常大肠黏膜和大肠腺瘤组织中的阳性表达率(6.7%和26.7%,P<0.05).E-CD蛋白的表达与大肠癌的分化程度、浸润深度、静脉侵犯、淋巴管侵犯、淋巴结转移以及Duke's分期有关(均P<0.05),而与患者的年龄、性别、肿瘤大小以及病理组织学类型无关(均P0.05).Snail蛋白的表达与大肠癌的分化程度、浸润深度、静脉侵犯、淋巴管侵犯、淋巴结转移、病理组织学类型以及Duke's分期有关(均P<0.05),而与患者的年龄、性别以及肿瘤大小无关(均P>0.05).E-CD蛋白与Snail蛋自在大肠癌组织中的表达呈负相关(r=-0.508).E-CD蛋白阳性表达者的术后1、3和5年生存率明显高于阴性表达者(P<0.05),Snail蛋白阴性表达者的术后1、3和5年生存率明显高于阳性表达者(P<0.05).淋巴结转移、Duke's分期、E-CD和Snail蛋白的表达可作为大肠癌独立的预后指标(均P<0.05).结论 E-CD和Snail蛋白的表达与大肠癌的侵袭、转移和预后明显相关,E-CD蛋白表达降低和Snail蛋白表达增强的大肠癌患者病期晚、预后差.     

Twist和E-cadherin蛋白在口腔鳞状细胞癌中的表达及临床意义

目的:研究转录因子Twist和上皮细胞钙黏蛋白(E-cadherin)在口腔鳞状细胞癌(OSCC)中的表达,探讨其与OSCC发生发展的关系.方法:采用免疫组化SP法分别检测Twist和E-cadherin在20例正常口腔黏膜组织和78例OSCC组织中的表达,用Spearman秩相关分析Twist和E-cadherin在OSCC组织中表达的相关性.结果:Twist在OSCC组织中的表达明显高于正常口腔黏膜组织(P<0.05);E-cadherin蛋白在OSCC组织中的表达明显低于正常口腔黏膜组织(P<0.05);E-cadherin在Ⅲ、Ⅳ期OSCC组织中的表达低于Ⅰ、Ⅱ期(P<0.05);E-cadherin在淋巴结转移患者的OSCC组织中的表达低于无转移者(P<0.05);Twist在Ⅲ、Ⅳ期OSCC组织中的表达高于Ⅰ、Ⅱ期(P<0.05);Twist在淋巴结转移患者的OSCC组织中的表达高于无转移者(P<0.05);OSCC组织中Twist的表达与E-cadherin的表达呈显著负相关(r=-0.639,P<0.05).结论:Twist与E-cadherin在OSCC组织中异常表达,且两者的表达高度相关,提示两者可能参与OSCC的发生、发展、浸润和转移,联合检测Twist和E-cadherin对OSCC的预防诊治及预后评估具有较大的临床价值.     

CDX2和Survivin及E—cadherin在大肠癌中的表达及其相关性

目的 研究肠道特异性转录因子2(CDX2)、存活素(survivin)、上皮型钙黏附分子(E-eadherin)在大肠癌、大肠腺瘤、正常大肠黏膜中的表达及其与大肠癌生成、侵袭转移之间的关系;探讨CDX2、survivin、E-cadherin之间的关系.方法 选取临床资料完整的40例大肠癌、30例大肠腺瘤和30例正常大肠黏膜,采用免疫组化S-P法研究CDX2、survivin、E-cadherin的表达.结果 CDX2、E-eadherin、survivin在大肠癌中的表达与在正常大肠黏膜、大肠腺瘤中的表达差异有显著性(P＜0.01);大肠腺瘤中survivin表达明显高于正常大肠黏膜(P＜0.05);CDX2、E-eadherin、survivin在大肠癌中的表达与Dukes分期有关(P＜0.05);CDX2、E-cadherin在大肠癌中的表达与淋巴结转移有关(P＜0.05);大肠癌中CDX2与survivin表达呈负相关(P＜0.01);大肠癌中CDX2与E-cadherin表达正相关(P＜0.01).结论 联合检测CDX2、survivin、E-cadherin的表达可为大肠癌的早期发生、侵袭转移的研究提供依据,对大肠癌诊断、治疗、预后判定有一定价值.     

CD44V6和E-cadherin在大肠癌中的表达及预后意义

目的探讨大肠癌中CD44 V6和E-cadherin蛋白表达的意义.方法应用免疫组化Evision法检测80例大肠癌中CD44 V6和E-cadherin蛋白的表达,并分析其与临床病理参数的关系.结果 80例大肠癌中,CD44 V6蛋白在77.5%的大肠癌中呈阳性,显著高于正常大肠黏膜组织的阳性率,(P＜0.001);E-cad蛋白在46.3%的大肠癌中呈阳性,显著低于正常大肠黏膜组织的阳性率,(P＜0.001);CD44 V6高表达和E-cad低表达与大肠癌Dukes分期、浆膜浸润、淋巴结转移呈显著正相关,(P＜0.05),而与年龄和组织学类型无关;CD44 V6和E-cad表达呈负相关(P＜0.001).结论 CD44 V6和E-cadherin表达与大肠癌浸润转移密切相关,CD44 V6阳性和E-cad阴性者更具有侵袭性和转移性,提示预后差.联合检测CD44 V6和E-cadherin有助于判断大肠癌的预后.     

Bmi-1、Ki67在大肠肿瘤组织中的表达及其意义

背景与目的:多梳基因家族成员的Bmi-1基因被认为是一种癌基因,在多种肿瘤组织中均有表达,而增殖细胞核抗原Ki67是反映细胞增殖程度的重要参考指标.本研究旨在通过检测大肠肿瘤组织中Bmi-1、Ki67蛋白表达情况及意义,并探讨两者在大肠癌中的表达的相关性.方法:采用免疫组织化学方法检测Bmi-1、Ki67蛋白在60例大肠癌、30例大肠腺瘤及20例正常大肠粘膜组织中的表达情况及其与大肠癌临床病理特征及患者生存率的关系,并探讨大肠癌中Bmi-1蛋白表达与Ki67蛋白的相关性.结果:Bmi-1蛋白在大肠癌、大肠腺瘤及正常肠粘膜组织中高表达率分别为25.0%、6.7%、0%,而Ki67蛋白的高表达率分别为18.3%、3.3%、0%;Bmi-1、Ki67蛋白在大肠癌中表达明显高于腺瘤组及正常组(P<0.05);采用卡方检验显示,Bmi-1蛋白高表达与有无远处转移密切相关(P<0.01).而与TNM分期有关(P<0.05).采用Logistic回归分析显示只有远处转移与Bmi-1蛋白高表达有关(P<0.01,OR>1).卡方检验显示,Ki67蛋白高表达与患者年龄、有无远处转移及TNM分期密切相关(P<0.05),Logistic回归分析显示只有患者年龄与Ki67蛋白高表达有关(P<0.05,OR<1);Kaplan-Meier生存分析显示Bmi-1、Ki67蛋白高表达患者生存率明显低于低表达患者(P<0.05);大肠癌组织中Bmi-1蛋白表达与Ki67蛋白表达相关性无统计学意义(r=0.224,P>0.05).结论:Bmi-1、Ki67蛋白表达与大肠癌的发生、转移及预后关系密切,可作为评估患者浸润转移及预后的参考指标:Bmi-1蛋白对Ki67蛋白表达可能有间接的调控作用.     

P-p38和uPA蛋白在大肠癌中的表达及临床意义

目的：研究P-p38和uPA蛋白的表达与大肠癌生物学行为及预后的关系。方法：应用免疫组织化学（ SP）法检测P-p38和uPA在62例大肠癌、25例大肠腺瘤及18例正常大肠黏膜组织中的表达。结果：大肠癌组织中P-p38和uPA阳性表达率分别为79.0%和74.2%,均明显高于大肠腺瘤及正常大肠黏膜组织,差异有显著统计学意义（ P<0.05）。P-p38和uPA表达与大肠癌的分化程度、淋巴结转移、Dukeˊs分期及浸润肌层的深度密切相关（ P<0.05）,且两者表达成明显正相关（ P<0.05）。P-p38和uPA表达阳性者术后5年生存率明显低于阴性者,差异有显著意义（ P<0.05）。结论：P-p38和uPA 的高表达预示着大肠癌的低分化,并共同促进了肿瘤的侵袭、转移。联合检测P-p38和uPA 的表达情况对于评估大肠癌的发展及预后具有重要意义。     

鼻咽癌原发与转移性淋巴结E-cadherin 和TGF-β1表达相关性的探讨

目的:探讨E-钙黏附蛋白(E-cadherin)、转生长因子(TGF-β1)蛋白在鼻咽癌组织中的表达情况及临床病理意义.方法:采用免疫组织化学染色S-P法检测57例鼻咽癌组织、36例淋巴结转移癌组织和20例癌旁鼻咽黏膜慢性炎组织中E-cadherin、TGF-β1蛋白的表达水平.结果:1)E-cadherin在颈部淋巴结转移癌中的阳性表达率为47.2%(17/36),显著低于鼻咽癌组织(80.7%,46/57,P=0.001)和鼻咽黏膜慢性炎组织(90.0%,18/20,P=0.02);TGF-β1在颈部淋巴结转移癌中阳性表达率高于鼻咽黏膜慢性炎组织(P=0.041).2)在鼻咽癌组织中E-cadherin及TGF-β1的表达与临床分期有关(均P<0.05);有淋巴结转移组的鼻咽癌组织中TGF-β1阳性率明显高于无淋巴结转移组(P=0.044).3)鼻咽癌中E-cadherin与TGF-β1的表达呈负相关(P<0.05).结论:E-cadherin蛋白表达下调或TGF-β1蛋白表达增多可能是导致鼻咽癌癌细胞侵袭转移的重要因素.     

COX-2、E-Cadherin、VEGF在大肠癌中的表达及意义

[目的]探讨COX-2、E-cadherin、VEGF在大肠癌中的表达及意义。[方法]采用免疫组织化学Envision法检测85例大肠癌和10例正常大肠黏膜组织中COX-2、E-cadherin、VEGF的表达。[结果]85例大肠癌中COX-2、E-cadherin、VEGF的阳性率分别为77.6%、34.1%和67.1%,和正常大肠黏膜相比有显著差异(P<0.01)。大肠癌中COX-2、VEGF、E-cadherin的表达在不同Dukes’分期、淋巴结转移状态均有显著差异(P<0.01)。E-cadherin和VEGF的表达在不同浸润深度下也均有差异(P<0.05)。E-cadherin与VEGF、COX-2的表达均呈负相关(r=0.28,r=0.41,P<0.01);COX-2与VEGF的表达正相关(r=0.51,P<0.01)。[结论]COX-2、E-cadherin、VEGF在大肠癌的发生、发展中起着重要作用,三者联合检测可为大肠癌恶性程度和预后的判断提供有效证据。     

S100A4和E-Cad在大肠癌中的表达与侵袭转移的关系

目的:探讨S100A4和E-Cad蛋白表达与大肠癌侵袭转移及预后的关系.方法:应用免疫组织化学方法检测101例大肠癌组织和20例癌旁正常粘膜、34例淋巴结转移癌、17例肝转移癌及10例大肠腺瘤中S100A4和E-Cad的表达情况.结果:S100A4蛋白在大肠癌组织中表达明显高于正常组织和腺瘤(P＜0.05),S100A4蛋白的袁达与有无淋巴结转移、肝转移及Dukes分期有关(P＜0.05);E-Cad蛋白在大肠癌组织中表达明显低于正常组织和腺瘤(P＜0.05),E-Cad蛋白的表达与有无淋巴结转移、肝转移及大肠癌分化、分期有关(P＜0.05),生存分析采用Log-rank检验:生存期均无统计学意义(P＞0.05),两种蛋白在大肠癌组织中的表达呈负相关(P＜0.05).结论:S100A4蛋白在大肠癌组织中表达增强和E-Cad表达减弱与大肠癌侵袭转移有关.     

nm23 VEGF-C及VEGFR-3在大肠癌中的表达及意义

目的:探讨nm23、VEGF-C及其受体VEGFR-3在大肠癌中的表达和三者间的相互关系,及其在大肠癌淋巴结转移和肿瘤进展中的意义.方法:采用免疫组化SP法检测97例大肠癌组织和97例正常大肠组织中nm23、VEGF-C及VEGFR-3的表达.结果:1)A、B期大肠癌及无淋巴结转移的大肠癌组织中nm23的阳性表达率分别为68.9%、68.2%,C、D期及有淋巴结转移的大肠癌组织中nm23阳性表达率分别为30.6%、25.8%,A、B期高于C、D期,无淋巴结转移高于有淋巴结转移,差别有统计学意义(P<0.05);VEGF-C阳性表达率在C、D期及有淋巴结转移的大肠癌组织中分别为75.0%、77.4%,在A、B期及无淋巴结转移的大肠癌组织中分别为49.2%、50.0%,两者比较,差别有统计学意义(P<0.05);VEGFR-3在C、D期及有淋巴结转移的大肠癌中的阳性表达率分别为63.9%、67.7%,在A、B期及无淋巴结转移的大肠癌组织中分别为41.0%、40.9%,差别有统计学意义(P<0.05.2)nm23与分化程度、肠壁侵犯深度、有无淋巴结转移及Duckes分期有关(P<0.05),VEGF-C及VEGFR-3与分化程度、淋巴结转移及Duckes分期有关(P<0.05).3)nm23在正常大肠组织和大肠癌组织中的阳性表达率分别为83.5%、54.6%,差别有统计学意义(P<0.05),VEGF-C在正常大肠组织和大肠癌组织中的阳性表达率分别为29.9%、58.8%,差别有统计学意义(P<0.05),VEGFR-3在正常大肠组织和大肠癌组织中的阳性表达率分别为21.6%、49.5%,两者比较,差别有统计学意义(P<0.05).结论:nm23与VEGF-C和VEGFR-3在大肠癌中的表达呈负相关关系,nm23基因时大肠癌有抑制作用,VEGF-C和VEGFR-3与大肠癌的侵袭和转移密切相关,三者的联合检测可作为评价大肠癌病情、推测预后及指导治疗的重要参考指标.     

Religiosity and Physical and Emotional Functioning Among African American and White Colorectal and Lung Cancer Patients

The literature suggests that religiosity helps cope with illness. The present study examined the role of religiosity in functioning among African Americans and Whites with a cancer diagnosis. Patients were recruited from an existing study and mailed a religiosity survey. Participants (N = 269; 36% African American, 56% women) completed the mail survey, and interview data from the larger cohort was utilized in the analysis. Multivariate analyses indicated that in the overall sample religious behaviors were marginally and positively associated with mental health and negatively with depressive symptoms. Among women, religious behaviors were positively associated with mental health and negatively with depressive symptoms. Religiosity was not a predictor of study outcomes for men. Among African Americans, religious behaviors were positively associated with mental health and vitality. Among Whites, religious behaviors were negatively associated with depressive symptoms. These findings suggest a mixed role of religious involvement in cancer outcomes. The current findings may have applied potential in the areas of emotional functioning and depression.     

New and emerging radiosensitizers and radioprotectors

The combination of chemotherapy and radiation has led to clinical breakthroughs in several disease sites, and current work continues to define optimum combinations of proven chemotherapy as well as more recently available, noncytotoxic agents. Administration of systemic therapies allows modulation of radiation response to improve tumor control (radiosensitization) or to prevent normal tissue toxicity (radioprotection). Substantial progress has been made in identifying the targets of standard chemotherapeutic radiation sensitizers and protectors as well as in the introduction of a new generation of molecularly targeted therapies in combination with radiation. We have reviewed the most recent, predominantly early phase clinical trials combining systemic agents with radiation. Although the proof of an improved schedule ultimately needs to come from well-run Phase III trials, the search among schedules could be shortened by the use of surrogate endpoints such as presence of active drug metabolites in the tumor. This has been accomplished only in a few cases and needs to become a more standard part of radiation sensitizer and protector trials.     

Fruit and vegetables and cancer risk

The possibility that fruit and vegetables may help to reduce the risk of cancer has been studied for over 30 years, but no protective effects have been firmly established. For cancers of the upper gastrointestinal tract, epidemiological studies have generally observed that people with a relatively high intake of fruit and vegetables have a moderately reduced risk, but these observations must be interpreted cautiously because of potential confounding by smoking and alcohol. For lung cancer, recent large prospective analyses with detailed adjustment for smoking have not shown a convincing association between fruit and vegetable intake and reduced risk. For other common cancers, including colorectal, breast and prostate cancer, epidemiological studies suggest little or no association between total fruit and vegetable consumption and risk. It is still possible that there are benefits to be identified: there could be benefits in populations with low average intakes of fruit and vegetables, such that those eating moderate amounts have a lower cancer risk than those eating very low amounts, and there could also be effects of particular nutrients in certain fruits and vegetables, as fruit and vegetables have very varied composition. Nutritional principles indicate that healthy diets should include at least moderate amounts of fruit and vegetables, but the available data suggest that general increases in fruit and vegetable intake would not have much effect on cancer rates, at least in well-nourished populations. Current advice in relation to diet and cancer should include the recommendation to consume adequate amounts of fruit and vegetables, but should put most emphasis on the well-established adverse effects of obesity and high alcohol intakes.     

VEGF及KDR在大肠腺瘤和腺癌中的表达及意义

目的：探讨VEGF和KDR在大肠腺瘤和大肠腺癌中的表达及临床病理特征的关系。方法：大肠腺瘤和大肠腺癌组织标本各100例,采用免疫组织化学染色法检测VEGF和KDR在标本中的表达情况。结果：VEGF和KDR在大肠腺癌组中的阳性表达明显高于大肠腺瘤组（P〈0.05）;在正常大肠黏膜均未见VEGF和KDR表达的阳性染色;VEGF阳性表达组中KDR的阳性表达率为70%,显著高于VEGF阴性表达组中KDR的阳性表达率16%,两组比较有统计学意义（P〈0.01）。结论：大肠腺癌组织中KDR的表达与肿瘤大小、转移情况、浸润深度密切相关;VEGF和KDR在大肠腺瘤中的表达与患者的年龄、性别及分型均无相关性,而与增生程度相关（P〈0.05）。在大肠腺癌患者中VEGF及KDR表达更高,二者具有协同效应。     

肾上腺素能β受体与肿瘤生长及转移

大量研究表明肿瘤细胞可表达β受体，而一些神经递质、药物和社会心理因素可能通过β受体影响肿瘤的生长和转移，β受体激动剂、β受体阻滞剂以及抑郁等社会心理因素可加强或削弱这种作用。这为表达β受体肿瘤的治疗开辟了新的道路，提供了新的治疗靶点。     

Occupational and environmental radiation and cancer

Epidemiologic evidence on the relation between occupational and environmental radiation and cancer is reviewed. Studies of pioneering radiation workers, underground miners, and radium dial painters revealed excess cancer deaths and contributed to the setting of radiation protection standards and to theories of carcinogenesis. Occupational exposures today are generally much lower than in the past, thus any associated increases in cancer will be difficult to detect. Pooling investigations of these more recently exposed workers, however, has the potential to validate current estimates of risk used in radiation protection. New information on the effects of chronic radiation exposure also may come from studies in the former Soviet Union of Chernobyl clean-up workers and of workers at the Mayak nuclear facilities. Studies of environmental radiation exposures, other than radon, are largely inconclusive, due mainly to the difficulties in detecting the low risks associated with low dose exposures. Thyroid cancer, however, has been linked to environmental radiation from the Chernobyl accident and from nuclear weapons tests. Low-level radiation released during normal operations at nuclear plants has not been found to increase cancer rates in surrounding populations. Radon, a human carcinogen, is the most ubiquitous exposure to human populations; remediating high residential-radon levels is recommended, recognizing that the exposure can never be removed completely because it occurs naturally.     

Cell and tissue interactions in carcinogenesis and metastasis and their clinical significance

This review describes a new vision for future directions in the study of metastatic cancer biology and pathology. It is based upon clinical and experimental observations on the constituent cell lineages within a neoplasm and on tumour-host interactions. The vision incorporates information from studies in population biology, developmental biology and experimental pathology as well as investigations upon human malignant disease. The assembled information reveals that invasion and metastasis are supra-cellular manifestations of "emergent behavior" among combinations of normal and malignant cell lineages in vivo. Emergent behavior is a combinatorial interactive process in which a population displays new traits which cannot be achieved by individuals acting separately and which subside when the specific population mix disaggregates. Disruption of such pathological interactions in the field of a developing primary or secondary tumour is, therefore, required to disable the malignant population and arrest progression without tissue destruction. These conclusions originate, in part, from principles which govern the sociobiology and group behavior of bees, ants, fish, birds and human societies. In all these social organisms, external factors can disrupt signaling mechanisms and induce expanding self-perpetuating rogue behavior, leading to social disintegration. These principles also apply to cellular societies composing higher animals, which likewise need intrinsic rules to maintain social order and avoid anarchy, and recognition of this is essential for advancing future research on the mechanisms involved in carcinogenesis and metastasis. Summarised evidence is presented here to support the conclusion that miscommunications between cells and tissues in the region of the developing tumour and its metastases are the main direct perpetrators of malignant disease. Genetic lesions (mutations, deletions, translocations, reduplications, etc.), commonly seen in cancers, can significantly disrupt important molecular pathways in the networks of communications needed to sustain orderly tissue/organ structure and function. However, genetic lesions can also, themselves, be induced by abnormal cell interactions initiated by extrinsic carcinogenic agents such as chemicals, viruses, hormones and radiation. The evidence shows that, irrespective of the initiating cause, it is this miscommunication in the region of a developing tumour and its metastases that is ultimately responsible for the emergence and progression of the disease. The article describes how this information collectively, provides a framework for designing specific novel therapeutic approaches targeting the cell and tissue interactions driving tumour metastasis and its manifold effects on the whole body.     

Vitamin D and melanoma and non-melanoma skin cancer risk and prognosis: A comprehensive review and meta-analysis

Vitamin D is formed mainly in the skin upon exposure to sunlight and can as well be taken orally with food or through supplements. While sun exposure is a known risk factor for skin cancer development, vitamin D exerts anti-proliferative and pro-apoptotic effects on melanocytes and keratinocytes in vitro. To clarify the role of vitamin D in skin carcinogenesis, we performed a review of the literature and meta-analysis to evaluate the association of vitamin D serum levels and dietary intake with cutaneous melanoma (CM) and non-melanoma skin cancer (NMSC) risk and melanoma prognostic factors. Twenty papers were included for an overall 1420 CM and 2317 NMSC. The summary relative risks (SRRs) from random effects models for the association of highest versus lowest vitamin D serum levels was 1.46 (95% confidence interval (CI) 0.60–3.53) and 1.64 (95% CI 1.02–2.65) for CM and NMSC, respectively. The SRR for the highest versus lowest quintile of vitamin D intake was 0.86 (95% CI 0.63–1.13) for CM and 1.03 (95% CI 0.95–1.13) for NMSC. Data were suggestive of an inverse association between vitamin D blood levels and CM thickness at diagnosis. Further research is needed to investigate the effect of vitamin D on skin cancer risk in populations with different exposure to sunlight and dietary habits, and to evaluate whether vitamin D supplementation is effective in improving CM survival.