外周血黏附分子CD24在结直肠癌筛查中的作用

目的:探讨外周血CD24在结直肠癌及大肠息肉筛查中的作用。方法:应用流式细胞仪分别检测新发结直肠癌患者、大肠息肉患者及健康对照者外周血白细胞中的CD24表达情况。进一步根据病理类型将大肠息肉患者分为炎症性息肉、增生性息肉、腺瘤性息肉及腺瘤性息肉伴不典型增生四组,比较组间差异。结果:结直肠癌患者（15.56±5.28）、大肠息肉患者（12.05±3.43）外周血白细胞中CD24的荧光强度显著高于健康对照（9.42±1.48）（P＜0.01）。炎症性息肉（10.75±1.80）、增生性息肉（12.14±3.11）、腺瘤性息肉患者（10.77±2.67）外周血白细胞中CD24的荧光强度无统计学差异,腺瘤性息肉伴不典型增生组患者（17.08±5.12）外周血白细胞中CD24的荧光强度显著高于前三组（P＜0.01）。结论:非侵入性的外周血CD24表达水平的检测对于结直肠癌的筛查可能有一定的意义。     

C-myc在结直肠癌和息肉中的表达及其意义

[目的]探讨c-myc在结直肠癌发生、发展中的作用及其与临床病理特征的相关性。[方法]采用免疫组织化学SP法检测60例结直肠癌组织、60例结直肠息肉组织、30例结直肠癌旁组织中c-myc蛋白表达。[结果]结直肠癌、结直肠腺瘤性息肉组织中c-myc蛋白表达阳性率明显高于结直肠增生性息肉及癌旁黏膜组织。c-myc蛋白高表达与结肠癌发病部位、肿瘤分化程度、Dukes分期、淋巴结转移有关（P均〈0.05）。c-myc蛋白高表达与结直肠腺瘤性息肉大小以及息肉有蒂或无蒂相关（P〈0.05）。[结论]c-myc表达与结直肠癌发生、发展有关。主题词：结直肠息肉;结直肠肿瘤;c-myc;免疫组织化学     

CD151和MMP-7在结直肠癌中的表达及其临床意义

  目的  探讨人类白细胞分化抗原151（CD151）和基质金属蛋白酶-7（MMP-7）在结直肠癌中的蛋白表达,及其与结直肠癌发生、发展、转移的关系。  方法  采用免疫组织化学染色法检测结直肠癌组织中CD151和MMP-7的蛋白表达,阐明二者与患者临床病理特征之间的关系。  结果  CD151和MMP-7在大肠正常组织中表达的阳性率分别为5%（1/20）和15%（3/20）,在结直肠癌组织中表达的阳性率分别为78%（39/50）和72%（36/50）,CD151和MMP-7在大肠正常组织和结直肠癌组织中的表达差异有统计学意义（χ2=31.086,P<0.05;χ2=18.811,P<0.05）。两种蛋白的阳性表达率与结直肠癌患者的年龄、性别、部位无关联（P>0.05）,但与淋巴结转移、浸润深度、远隔器官转移、肿瘤分化程度、Dukes分期有密切关系（P<0.05）。结直肠癌中CD151和MMP-7两种蛋白的表达强度具有相关性（r_s=0.314,P=0.026）。  结论  CD151和MMP-7在结直肠癌组织中异常高表达并与其发生、发展及浸润转移有密切关系,联合检测可作为判断结直肠癌生物学行为的重要指标。      

EGFR、VEGF和PTEN在结直肠癌中表达及与其临床病理特征的关系

目的探讨结直肠癌中表皮生长因子受体（EGFR）、血管内皮生长因子（VEGF）和张力蛋白同源物基因（PTEN）蛋白表达及与其临床病理特征的关系。方法应用免疫组织化学技术,检测98例结直肠癌和20例正常结直肠黏膜组织中的EGFR、VEGF和PTEN蛋白表达,并结合临床病理特征进行分析。结果 8例结直肠癌中EGFR、VEGF和PTEN蛋白阳性表达率分别为61.2%（60/98）、66.3%（65/98）和48.0%（47/98）。结直肠癌中EGFR和VEGF表达阳性率显著高于正常结直肠黏膜组织（χ2=21.05,χ2=15.90,P〈0.05）,而PTEN表达阳性率显著低于正常结直肠黏膜组织（χ2=14.72,P〈0.05）。EGFR、VEGF和PTEN表达与结直肠癌Dukes分期、浆膜浸润和淋巴结转移相关（P〈0.05）。结直肠癌中EGFR表达与VEGF表达呈正相关（χ2=8.36,P〈0.05）,EGFR和VEGF表达与PTEN表达呈负相关（χ2=19.73,χ2=22.85,P〈0.05）。结论 EGFR、VEGF和PTEN表达与结直肠癌浸润和转移密切相关,可作为判断结直肠癌预后的客观指标。     

CD44V6在结直肠癌组织中的表达及临床意义

目的：探讨CD44V6表达与结直肠癌发生、发展及转移的关系。方法：采用S－P免疫组织化学方法，检测78例原发性结直肠腺癌、14例结直肠腺瘤癌变、57例结直肠腺瘤、30例结直肠增生性息肉和24例结直肠正常黏膜中CD44V6的表达情况。结果：腺瘤、腺瘤癌变和腺癌组织中CD44V6阳性表达率分别为78．95％、100．00％和56．41％，明显高于增生性息肉和正常黏膜组织的阳性表达率（14．81％）。CD44V6阳性表达与腺癌淋巴结转移、Dukes分期和病理分级无相关性。结论：CD44V6表达与结直肠癌的发生有关，可作为诊断结直肠癌前病变和早期癌的生物学指标。     

CD10蛋白在结直肠癌组织中的表达及其临床意义

目的：研究CD10蛋白在结直肠癌组织中的表达及其与结直肠癌的各临床病理指标之间的关系,探讨其在结直肠癌发生、发展中的作用。方法：收集78例结直肠癌组织标本及22例癌旁正常组织样本,运用免疫组化EliVision法检测CD10蛋白的表达,并采用卡方检验分析其表达强度及分布比例与结直肠癌临床病理指标的关系。结果：CD10蛋白在结直肠癌组织和正常结肠黏膜组织中的阳性表达率分别为46.2%（36/78）和0,差异有统计学意义（P < 0.01）。结直肠癌组织中CD10蛋白表达比例与各临床病理指标均无明显相关（P > 0.05）。结直肠癌组织中CD10蛋白表达强度与患者性别、年龄、肿瘤部位、分化程度、浸润深度无明显相关（P > 0.05）,而与肿瘤的临床分期、有无脉管侵犯及淋巴结转移有关（P < 0.05）,中晚期结直肠癌CD10蛋白表达强度高于早期肿瘤（P=0.033）,周围淋巴结转移阳性的结直肠癌CD10蛋白表达强度高于淋巴结阴性病例（P=0.023）,存在脉管受侵犯的结直肠癌CD10蛋白表达强度高于无脉管受侵病例（P=0.004）。结论：CD10蛋白在结直肠癌组织中呈高表达,且表达强度与肿瘤的临床分期、有无脉管侵犯及淋巴结转移有关,可能有促进结直肠癌发展和浸润转移的作用。     

CD10蛋白在结直肠癌组织中的表达及其临床意义

目的：研究CD10蛋白在结直肠癌组织中的表达及其与结直肠癌的各临床病理指标之间的关系，探讨其在结直肠癌发生、发展中的作用。方法：收集78例结直肠癌组织标本及22例癌旁正常组织样本，运用免疫组化EliVision法检测CD10蛋白的表达，并采用卡方检验分析其表达强度及分布比例与结直肠癌临床病理指标的关系。结果：CD10蛋白在结直肠癌组织和正常结肠黏膜组织中的阳性表达率分别为46.2%（36/78）和0，差异有统计学意义（P < 0.01）。结直肠癌组织中CD10蛋白表达比例与各临床病理指标均无明显相关（P > 0.05）。结直肠癌组织中CD10蛋白表达强度与患者性别、年龄、肿瘤部位、分化程度、浸润深度无明显相关（P > 0.05），而与肿瘤的临床分期、有无脉管侵犯及淋巴结转移有关（P < 0.05），中晚期结直肠癌CD10蛋白表达强度高于早期肿瘤（P=0.033），周围淋巴结转移阳性的结直肠癌CD10蛋白表达强度高于淋巴结阴性病例（P=0.023），存在脉管受侵犯的结直肠癌CD10蛋白表达强度高于无脉管受侵病例（P=0.004）。结论：CD10蛋白在结直肠癌组织中呈高表达，且表达强度与肿瘤的临床分期、有无脉管侵犯及淋巴结转移有关，可能有促进结直肠癌发展和浸润转移的作用。     

CD133 β-catenin和APC在结直肠癌组织中的表达及其与预后的关系

  目的  探讨CD133、β-catenin和APC蛋白在结直肠癌发生发展中的作用, 分析三者的表达和临床病理特征与结直肠癌患者预后的关系。   方法  应用组织芯片及免疫组织化学法检测74例结直肠腺瘤、135例结直肠癌及癌旁正常黏膜组织中CD133、β-catenin和APC蛋白的表达; 结合随访资料进行单因素Kaplan-Meier生存分析及多因素Cox回归分析。   结果  CD133在结直肠癌中阳性率为45.9%, 高于腺瘤(9.5%)及癌旁正常黏膜(0, P < 0.05), 其表达与腺瘤不典型增生程度及结直肠癌组织分级具有相关性(P < 0.05);β-catenin胞质/胞核阳性表达在结直肠癌(93.3%)和腺瘤(85.1%), 高于癌旁正常黏膜(14.8%, P < 0.05), β-catenin膜表达缺失率在结直肠癌(45.2%)高于腺瘤(4.1%)及癌旁正常黏膜(5.2%, P < 0.05), 且与淋巴结转移及Dukes分期有关(P < 0.05);APC阳性表达率在癌旁正常黏膜(100%)、腺瘤(90.5%)和结直肠癌(34.8%)呈逐级降低(P < 0.05), 在结直肠癌APC表达缺失组, β-catenin胞质/胞核表达与CD133表达呈正相关(P < 0.05)。单因素和多因素生存分析均筛选出Dukes分期、β-catenin膜表达缺失为影响结直肠癌患者预后的高风险因素及独立预后影响因素(P < 0.05)。   结论  CD133、β-catenin、APC参与了结直肠癌的发生发展, CD133表达与β-catenin及APC之间存在密切联系, 三者的检测对结直肠癌的早期诊断、生物学行为及预后评估有一定意义。      

NOB1在结直肠癌中的表达及其临床意义

目的：研究NOB1编码蛋白在结直肠癌及正常结直肠黏膜（距癌组织边缘5cm以上）、结直肠良性息肉中的表达特征.探讨结直肠癌中NOB1表达的临床病理意义.方法：利用免疫组织化学SABC法检测87例结直肠癌组织、22例正常结直肠黏膜组织18例结直肠息肉组织中NOB1的表达.结果：NOB1在结直肠癌,结直肠良性息肉及正常结直肠黏膜中的阳性表达率分别为74.7％、44.4％、13.6％,三组进行比较,差异有统计学意义（P＜0.01）.细胞分化差的结直肠癌NOB1蛋白阳性率表达高（P＜0.05）与患者年龄,性别,肿瘤浸润深度及淋巴结转移无明显相关性.结论：NOB1蛋白在结直肠癌中表达升高,并与大肠癌临床病理学特征有关.     

APC、β-catenin及c-myc在大肠腺瘤-癌组织序列中的表达及其意义

目的 探讨大肠腺瘤性息肉病基因(adenomatous polysis coil,APC)、β-环形蛋白(β-catenin)及原癌基因蛋白c-myc的表达在大肠肿瘤发生发展中的作用及其与临床病理参数之间的关系.方法 应用免疫组织化学SP法检测APC、β-catenin及c-myc在大肠正常黏膜、大肠腺瘤和大肠腺癌组织中的表达.结果 ①正常黏膜、大肠腺瘤和大肠腺癌中APC蛋白的表达率为97.3%、25.0%、24.6%.腺瘤与腺癌组均低于正常黏膜组(P＜0.01),腺瘤与腺癌组差异不显著(P＞0.05).②β-catenin在正常黏膜组为胞膜表达,腺瘤与腺癌组呈胞质/核异位表达,异位表达率为10.8%、75.0%、98.2%,3组之间有显著性差异(P＜0.01).③正常黏膜、大肠腺瘤和大肠腺癌中c-myc的表达率为10.8%、40.6%、70.2%.3组之间有显著性差异(P＜0.01).④大肠腺癌中β-catenin蛋白的异常表达随着肿瘤大小、组织学分级、Dukes分期的改变呈逐渐增高趋势,有淋巴结转移者β-catenin蛋白阳性表达率(100.0%)高于无淋巴结转移者(96.4%),但无显著性差异(P＞0.05).结论 APC的失表达、β-catenin的异常表达及c-myc的过表达与大肠肿瘤的发生发展有关,β-catenin的异常表达可能与大肠腺癌的恶性行为有关.     

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.     

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。     

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.     

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.     

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。     

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.