早期三阴性乳腺癌与非三阴性乳腺癌VEGF和MVD表达的比较

目的探讨血管内皮生长因子（vascularendothelialgrowthfactor,VEGF）、微血管密度（microvesseldensity,MVD）在早期三阴性乳腺癌组织中与非三阴性乳腺癌组织中的表达水平。方法采用免疫组化染色法检测我院2007年1～12月行根治性手术切除、经病理证实的乳腺癌组织蜡块89例（其中早期三阴性乳腺癌21例,非三阴性乳腺癌68例）癌组织中VEGF的表达及MVD值,分析VEGF的表达及MVD值在早期三阴性乳腺癌和非三阴性乳腺癌组织中的差别,以及VEGF和MVD之间的关系。结果早期三阴性乳腺癌癌组织中VEGF表达的阳性率高于非三阴性乳腺癌（71．43％vs25．00％,P〈O．001）。MVD在早期三阴性乳腺癌与非三阴性乳腺癌组间的差异无统计学意义（P=0．105）。结论VEGF表达与乳腺癌血管生成密切相关,VEGF及MVD在三阴性乳腺癌中的生物学意义值得进一步探讨。     

乳腺癌血管内皮生长因子的表达及意义

目的探讨血管内皮生长因子（VEGF）在乳腺癌中的表达及其与血管生成，肿瘤转移等参数之间的关系。方法对101例浸润性乳腺癌组织的VEGF表达进行了免疫组化检测。结果正常乳腺组织及良性病变组织均无VEGF表达。乳腺癌VEGF表达与组织分化（P＜0．05），淋巴结转移（P＜0．005），远处转移（P＜0．005）及早期死亡（P＜0．005）密切相关，与乳腺癌组织微血管密度（MVD）亦呈显著相关性（P＜0．05）；与患者年龄，肿瘤大小无关（P＞0．05）。结论VEGF是促进乳腺癌血管生成的主要因素。VEGF阳性的乳腺癌组织分化差，易发生转移，预后不良。     

血管内皮生长因子及微血管密度在卵巢浆液性肿瘤中的表达

目的探讨卵巢浆液眭肿瘤组织中的血管生成状况。方法采用免疫组织化学方法检测76例卵巢浆液性肿瘤中微血管密度（MVD）及血管内皮生长因子（VEGF）表达状况并分析二者间相关关系。结果良性、交界性及恶性浆液性卵巢肿瘤组织中MVD值及VEGF表达呈逐渐增高趋势,MVD值分别为7．8±2．4、17．5±3．3及27．6±7．5,VEGF的表达分别为（16．1±3．9）％、（36．7±14．2）％及（52．3±22．8）％,各组间差异有统计学意义。浆液性卵巢癌高、中及低分化组织MVD值分别为18．3±3．4、24．2±3．1及32．3±6．4,VEGF的表达分别为（30．9±16．2）％、（48．0±18．4）％及（62．1±21．3）％,各组间差异有统计学意义。浆液性卵巢癌FIGOⅢ～Ⅳ期及Ⅰ～Ⅱ期的MVD值分别为28．9±4．7及22．0±4．7,VEGF的表达分别为（55．1±22．9）％及（40．18±18．0）％,差异均有统计学意义。浆液性卵巢癌中VEGF的表达与肿瘤组织中的MVD值呈正相关关系（r=0．576）。结论血管生成在浆液性卵巢肿瘤的发生、发展中起重要促进作用。     

乳腺癌组织中HIF-1α的表达水平及其与肿瘤血管生成相关性研究

目的:探讨缺氧诱导因子1α（hypoxia inducible factor 1α,HIF-1α）在乳腺正常组织、不典型增生、原位癌、浸润性癌组织中的表达水平,分析其与浸润性乳腺癌临床病理指标及肿瘤血管生成之间的关系。方法:收集20例正常乳腺组织、23例不典型增生、34例原位癌、80例浸润性乳腺癌组织标本,用免疫组化SP法检测各组中HIF-1α的表达,分析其在浸润性乳腺癌中的表达与肿瘤大小、腋窝淋巴结受累情况、TNM分期、组织学分级、激素受体等临床病理指标之间的关系。并用CD34标记肿瘤新生血管,分析HIF-1α表达对肿瘤血管生成的影响。结果:HIF-1α在正常乳腺组织中未见阳性表达,在乳腺不典型增生组织、原位癌组织、浸润性癌组织中表达阳性率分别为8.7%（2/23）、47.1%（16/34）及73.8%（59/80）,表达率依次增高,乳腺原位癌组织与不典型增生组织之间、乳腺浸润癌组织与原位癌组织之间差异具有统计学意义（P＜0.01）。在浸润性乳腺癌中,HIF-1α的表达在不同肿瘤直径、组织学分级及淋巴结转移分组中差异具有统计学意义（P均＜0.05）。浸润性导管癌HIF-1α阳性组MVD值（11.74±4.398）明显高于HIF-1α表达阴性组（9.093±2.856）,差异有统计学意义（P＜0.05）。HIF-1α表达与MVD值呈正相关性（r=0.633,P＜0.05）。结论:HIF-1α在浸润性乳腺癌组织中表达水平升高,其表达上调与乳腺癌新生血管生成密切相关。     

HER-2阴性乳腺癌中VEGF、COX-2的表达及相关性研究

目的:研究血管内皮生长因子（VEGF）、环氧化酶-2（COX-2）在91例HER-2阴性乳腺癌组织中的表达及相互关系,分析其与临床病理特征及预后的关系。方法:采用免疫组化SABC法,检测91例HER-2阴性乳腺癌组织中VEGF、COX-2蛋白的表达,并与临床病理特征进行相关性分析。结果:HER-2阴性乳腺癌组织中VEGF阳性表达率为94.5%,其中47.2%为高表达（+++）,VEGF的表达与肿瘤大小、淋巴结转移相关（P<0.05）。HER-2阴性乳腺癌组织中COX-2阳性表达率为86.8%,其中34.0%为高表达（+++）,COX-2的表达与患者年龄、组织学分级、肿瘤大小、淋巴结转移及TNM分期无关（P>0.05）。VEGF与COX-2的表达呈正相关（r=0.1798,P=0.018）,VEGF/COX-2均高表达的患者淋巴结转移率高。结论:VEGF、COX-2在HER-2阴性乳腺癌组织中均高表达且两者呈正相关,联合检测VEGF、COX-2的表达对HER-2阴性乳腺癌预后判断可能具有重要价值。     

大鼠实验性肺鳞癌癌变各阶段间质微血管密度及 VEGF、 FLK-1表达的动态变化

目的：观察化学致癌物诱发大鼠肺鳞癌癌变过程中间质微血管密度（ microvessel density,MVD）变化及血管内皮细胞生长因子（ vascular endothelial growth faetor,VEGF）及其受体（ FLK 1）表达的变化,探讨上述指标与肺癌发生发展的关系。方法： Wistar大鼠 80只,其中 70只用致癌质碘油溶液左肺叶支气管灌注, 10只对照。第 15～ 75天分批处死动物,取左肺组织。应用免疫组织化学 S P法检测大鼠肺鳞癌癌变各阶段组织的 VEGF、 FLK 1的蛋白表达,在 vWF染色切片上检测 MVD。结果：随大鼠肺鳞癌的发生发展, VEGF、 FLK 1表达均逐渐增强, MVD计数逐渐增高。不典型增生 MVD（ 8.92± 3.80）、 VEGF阳性系数（ 1.25± 0.95）,原位癌 MVD（ 39.5± 12.6）、 VEGF（ 2.25± 1.07）,早期浸润癌 MVD（ 58.5± 18.4）、 VEGF（ 3.03± 0.93）之间比较,其差异分别具有高度显著性 (P<0.01)。原位癌 FLK 1阳性系数（ 2.00± 0.93）和早期浸润癌 FLK 1阳性系数（ 2.63± 1.54）比较,其差异具显著性（ P< 0.05）。 VEGF表达与 MVD（ r="0.983" 7, P< 0.01）和 FLK 1表达（ r="0.968" 8, P< 0.01）呈高度正相关。 FLK 1在肿瘤细胞、血管内皮细胞及血管平滑肌细胞内都有表达,且在肿瘤细胞内的表达强度高于血管内皮细胞。结论：新生血管形成是大鼠肺鳞癌发生发展的重要现象。 VEGF、 FLK 1与肿瘤血管生成、肿瘤的浸润扩散密切相关。 VEGF通过旁分泌及自分泌途径参与肿瘤血管生成和肿瘤的发生发展。     

环氧化酶-2、血管内皮生长因子在乳腺癌组织中表达及其对血管生成的影响

目的研究环氧化酶-2（COX-2）、血管内皮生长因子（VEGF）在乳腺癌组织中的表达，并探讨其对血管生成的作用。方法应用免疫组织化学SP法检测30例乳腺癌组织标本和20例正常乳腺组织标本中COX-2、VEGF的表达，并用血管内皮细胞标记物CD34单克隆抗体标记行免疫组织化学染色，观察肿瘤微血管生成状况。结果COX-2在70．0％（21／30）乳腺癌组织中过表达，VEGF在56．7％（17／30）乳腺癌组织中过表达，与正常组织相比差异均有统计学意义；COX-2和VEGF表达相关；COX-2和VEGF表达均与肿瘤微血管生成相关。结论COX-2和VEGF过表达均与乳腺癌血管生成有关。     

尿纤溶酶原激活物及血管内皮生长因子在食管癌中的表达及对肿瘤血管形成的影响

目的探讨尿纤溶酶原激活物（uPA）、血管内皮生长因子（VEGF）在食管癌中的表达及对肿瘤血管生成的影响。方法采用免疫组织化学sP法检测正常食管黏膜上皮组织（18例）及食管癌组织（68例）中uPA、VEGF的表达,检测CD。用以标记肿瘤微血管密度（MVD）,根据MVD均值分为高、低MVD组,分析食管癌uPA、VEGF的表达和临床病理特征的关系及对肿瘤血管形成的影响。结果uPA蛋白在正常食管黏膜上皮组织、食管癌组织中的阳性率分别为27．8％（5／18）和70．6％（48／68）,差异有统计学意义（X^2=11．63,P〈0．05）;VEGF蛋白在正常食管黏膜上皮组织、食管癌组织中的阳性率分别为22．2％（4／18）和63．2％（43／68）,差异有统计学意义（X^2=9．78,P〈0．05）。食管癌组织中uPA与VEGF表达有一致性（X^2=9．72,P〈0．05）。MVD平均为42．38±11．62,高MVD组uPA、VEGF蛋白表达显著高于低MVD组（X^2值分别为6．13和10．12,均P〈0．05）。uPA、VEGF蛋白表达与年龄、性别、病理类型无关（均P〉0．05）,均与临床病理分期、分化程度和淋巴结转移相关（P〈0．05）。结论食管癌组织中uPA、VEGF蛋白高表达,可能促进肿瘤血管形成,提示预后不良。     

腋淋巴结阴性乳腺癌新生血管形成活性的研究

背景与目的：观察腋淋巴结阴性乳腺癌血管内皮细胞生长因子（vascular endothelial growth factor,VEGF)的表达和微血管密度（microvessel density,MVD)的分布,并探讨VEGF和MVD与肿瘤大小（T）、组织学分级、雌激素受体水平（ER）、及复发转移的关系,同时评价检测VEGF和MVD对预后预测的价值。方法：用Ⅷ因子抗体与抗VEGF多克隆抗体分别对62例腋淋巴结阴性乳腺癌作病理切片的免疫组织化学染色,在显微镜下判断VEGF染色程度以及进行微血管计数。随访预后情况。结果：MVD和VEGF与组织学分级和复发转移有关（P＜0．05）。VEGF表达阳性患者和高MVD患者的总生存率和无瘤生存率均明显低于VEGF表达阴性患和低MVD患者的相应生存率（P＜0．01）。尤其在VEGF表达阳性且MVD也高的患者更明显（P＜0．005）。VEGF和MVD之间也明显相关（P＜0．01）。结论：VEGF与MVD与腋淋巴结阴性乳腺癌患者的预后相关,均可作为有价值的预后预测指标,两者联合应用对预后判断更有价值。VEGF是促进肿瘤新生血管形成的重要因素。     

乳腺癌VEGF的表达和微血管形成的关系及意义

目的 :探讨血管内皮生长因子 (VEGF)与肿瘤内微血管形成的关系 ,以及微血管密度 (MVD)与乳腺癌淋巴结转移和预后的关系。方法 :采用免疫组化 S- P法对 4 0例人乳腺浸润性导管癌组织中的 VEGF和 MVD进行检测。结果 :VEGF阳性者 MVD值显著高于阴性者 ,VEGF表达和MVD与乳腺癌淋巴结转移关系密切。结论 :VEGF与乳腺癌血管生成密切相关 ,VEGF和 MVD表达的增高对乳腺癌淋巴结转移有促进作用 ,MVD和 VEGF均可作为反映乳腺癌生物学行为的指标之一     

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.