p27kip1,VEGF在大肠粘液腺癌中的表达及其意义

目的 研究细胞周期素依赖性激酶抑制剂ｐ－２７ｋｉｐ１、血管内皮生长因子（ＶＥＧＦ）在大肠粘液腺癌中的表达及其与组织分级、浸润及转移的关系。方法 应用免疫组化染色及半定量分析的方法,检测４０例大肠粘液腺癌中的ｐ－２７ｋｉｐ１、ＶＥＧＦ表达及其特征。分析它们的阳性表达与肿瘤的病理组织分级、临床Ｄｕｋｅ’ｓ分期的相关性。结果 ｐ２７Ｋｉｐ１随着肿瘤分级、分期增高（恶性程度增高）,阳性表达率逐渐下降;而Ｖ     

血管内皮生长因子及其受体在大肠癌中的表达

研究血管内皮生长因子及其受体大肠癌中的表达及其临床意义。「方法」应用免疫组化ＳＰ法检测１５５例大肠癌标本ＶＥＧＦ及ＫＤＲ蛋白的表达。分析ＶＥＧＦ和ＫＤＲ与临床病理因素,微血管计数及预后的关系。「结果」ＶＥＧＦ和ＫＤＲ的表达与大肠癌浸润深度、淋巴结转移、血管侵犯、脏脏转移、Ｄｕｋｅｓ’分期密相关,而与组织学分型和肿瘤大小无关。ＶＥＧＦ和ＫＤＲ的表达密切相关。ＶＥＧＦ和ＫＤＲ表达阳性者ＭＶＣ显著高于阴     

大肠癌微血管密度和血管内皮生长因子表达的研究

目的 探讨大肠癌间质微血管密度（ＭＶＤ）和血管内皮生长因子（ＶＥＧＦ）表达与肿瘤浸润和转移和关系。方法 应用ＣＤ３４抗体和ＶＥＧＦ抗体,采用免疫组化Ｓ－Ｐ法对５６例手术切除的大肠癌患者进行血管标记和染色,并取１０例正常组织对照。结果 有淋巴结转移组大肠癌ＭＶＤ、ＶＥＧＦ表达强度与无淋巴结转移组、正常对照组组间比较,均有显著性差异（Ｐ〈０．０１）,且ＭＶＤ与ＶＥＧＦ表达两者呈相关（ｒ＝０．９２）。结     

胃癌VEGF和nm23表达与血管生成的关系及其临床意义

目的 探讨血管内皮细胞生长因子（ＶＥＧＦ）和ｎｍ２３与血管生成及胃癌发展的关系。方法 采用免疫组织化学Ｓ－Ｐ法对４０例胃癌组织中的ＶＥＧＦ、ｎｍ２３蛋白表达和微血管密度（ＭＶＤ）进行检测,分析其与胃癌组织学类型、浸润深度、淋巴结转移和预后的关系。结果 ＶＥＧＦ阳性者（ＭＶＤ）值显著高于阴性者（Ｐ〈０．０１）,ＶＥＧＦ表达率和ＭＶＤ值与胃癌浸润深度、淋巴结转移呈正相关（Ｐ〈０．０５）,ｎｍ２３高表达     

肝门部胆管癌组织中VEGF和血管生成相关性的研究

目的：探讨肝门部胆管癌组织中血管内皮细胞生长因子（ＶＥＧＦ）和血管生成的相关性。方法：应用逆转录多聚酶链反应（ＲＴ－ＰＣＲ）和免疫组化技术对２６例肝门部胆管癌、癌周组织及１２例正常组织中ＶＥＧＦｍＲＮＡ和蛋白及微血管密度（ＭＶＤ）进行了检测。结果：２６例肝门部胆管癌组织中ＶＥＧＦｍＲＮＡ阳性表达率为７６．９％（２０／２６）;癌周组织阳性表达率为２８．９％（７／２６）;正常组织表达率为８．３％（１／１２）,三者差异有显著性（Ｐ＜０．０１）。ＶＥＧＦｍＲＮＡ阳性表达与ＶＥＧＦ蛋白表达具有一致性;ＶＥＧＦｍＲＮＡ阳性者ＭＶＤ值显著高于阴性者（Ｐ＜０．０１）;ＶＥＧＦｍＲＮＡ表达和ＭＶＤ与肝门部胆管癌的分化程度、浸润转移密切相关（Ｐ＜０．０５）;而与发生部位、病理类型、肿瘤大小、临床分型无关（Ｐ＞０．０５）。结论：ＶＥＧＦ在肝门部胆管癌发生和浸润转移过程中发挥重要作用,肿瘤血管生成与肝门部胆管癌浸润转移密切相关。     

血管内皮生长因子（VEGF）在恶性肿瘤中的表达及其临床意义

ＶＥＧＦ于１９８３年由Ｓｅｎｇｅｒ等发现 ,分子量３４ ４２ＫＤ ,以二巯键连接的糖蛋白二聚体形式存在 ,是一种对热酸稳定的外分泌蛋白 ,可在健康人体多数组织中检出 ,但表达量甚微。人ＶＥＧＦ是一种多功能细胞生长因子 ,可以形成４种不同长度的多肽 ,称为ＶＥＧＦ２０６、１８９、１６５和１２１。ＶＥＧＦ有三种受体 ,即Ｆｌｔ １、ＫＤＲ和ＦＬＫ ４ ,均有酪氨酸激酶活性。近年来许多研究表明 ,ＶＥＧＦ是内皮细胞的有丝分裂原 ,诱导内皮细胞的生长 ,并且是有效的血管形成促进因子 ,诱导增加血管的通透性 ,与肿瘤生长、浸润、转移的…     

舌鳞癌血管内皮细胞生长因子表达的意义

研究舌磷癌组织中血管内皮细胞生长因子（ｖａｓｃｕｌａｒ ｅｎｄｏｔｈｅｌｉａｌ ｇｒｏｗｔｈ ｆａｃｔｏｒ,ＶＥＧＦ）的表达及其临床意义。方法用免疫组化Ｓ－Ｐ法和Ｗｅｉｄｎｅｒ法分别对５５例舌鳞细胞癌（简称舌鳞癌,下同）,标本进行血管内皮细胞生长因子测定和肿瘤微血管数（ｍｉｃｒｏｖｅｓｓｅｌ ｑｕａｎｔｉａｔｉｏｎ,ＭＶＱ）计数。结果舌鳞癌组织中,ＶＥＧＦ表达阳性率为４９．１％。ＶＥＧＦ阳性病例Ｍ     

Ⅱ期结直肠癌组织ＶＥＧＦ-Ａ与ＭＶＤ检测的临床意义

目的　探讨Ⅱ期结直肠癌组织血管内皮生长因子Ａ（ＶＥＧＦ-Ａ）与微血管密度（ＭＶＤ）检测的临床意义。方法　用免疫组化ＰＶ６０００法检测５６例Ⅱ期结直肠癌组织及１３例正常组织的ＶＥＧＦ-Ａ表达与ＭＶＤ,分析其与患者临床病理特征的关系以及对生存的影响。结果　（１）肿瘤组织ＶＥＧＦ-Ａ表达和ＭＶＤ明显高于正常组织（６４.３％ｖｓ．０,２３.６９±５.７７９ｖｓ．７.９±１.２７;Ｐ均＝０.０００）;原发肿瘤＞５ｃｍ癌组织ＶＥＧＦ-Ａ表达明显高于＜５ｃｍ者（８５.０％ ｖｓ．５２.８％,Ｐ＝０.０３4）,发生复发或转移患者的癌组织ＶＥＧＦ-Ａ和ＭＶＤ明显高于未发生复发或转移者（５７.１％ ｖｓ．２８.９％,Ｐ＝０.０３９;２８.９４±４.２０８ｖｓ．２２.４１±５.４２８,Ｐ＝０.０００）;年龄＞６０岁患者的癌组织ＭＶＤ明显高于≤６０岁患者（２７.３６±５.６５８ｖｓ．２１.６７±４.９５９,Ｐ＝０.００１）,低分化患者癌组织ＭＶＤ明显高于中高分化者（２７.６５±６.３２９ｖｓ．２３.１６±５.４１６,Ｐ＝０.０１３）;ＶＥＧＦ-Ａ阴性组与弱阳性组及强阳性组ＭＶＤ值的差异均有统计学意义（２１.８０±４.６０ｖｓ．２４.５１±５.０７,Ｐ＝０.０２７;２１.８０±４.６０ｖｓ．２５.７９±３.７８,Ｐ＝０.００６）,ＶＥＧＦ-Ａ弱阳性组和强阳性组ＭＶＤ值的差异无统计学意义（２４.５１±５.０７ｖｓ．２５.７９±３.７８,Ｐ＝０.６６６）。（２）５６例Ⅱ期结直肠癌患者１、３、５年生存率分别为９８.２３％、８７.３７％和７５.９６％;癌组织ＶＥＧＦ-Ａ表达与患者ＤＦＳ（χ^２ ＝８.５７０,Ｐ＝０.０１４,ｒ＝－０.２９２）和ＯＳ（χ^２＝６.５０２,Ｐ＝０.０３９,ｒ＝－０.２８１）相关,ＶＥＧＦ-Ａ表达越强,ＤＦＳ和ＯＳ越短;癌组织ＭＶＤ与患者的ＤＦＳ相关（χ^２＝６.８０６,Ｐ＝０.０３２,ｒ＝－０.２１３）,ＭＶＤ越高,ＤＦＳ越短,但是与ＯＳ无明显相关性（χ^２＝１.９０２,Ｐ＝０.１６８,ｒ＝－０.０２２）。结论　Ⅱ期结直肠癌组织ＶＥＧＦ-Ａ表达和ＭＶＤ与患者的临床病理特征有一定的关系,可能是判断预后的重要参考指标。     

血管内皮生长因子在食管癌中的表达和临床意义

目的探讨食管癌血管内皮生长因子（ＶＥＧＦ）、血管生成与食管癌临床病理特点的关系。方法采用免疫组织化学技术,检测５０例食管癌组织ＶＥＧＦ蛋白表达和微血管密度（ＭＶＤ）。分析ＶＥＧＦ和ＭＶＤ的关系及其与食管癌组织学分型、浸润度、生长方式、淋巴结转移和预后的关系。结果ＶＥＧＦ阳性者ＭＶＤ值显著高于阴性者,ＶＥＧＦ及ＭＶＤ与食管癌浸润深度、淋巴结转移密切相关,与组织学分型、生长方式也有明显相关性。结论ＶＥ     

血管内皮生长因子在大肠癌中的表达及预后价值

目的：研究血管内皮生长因子（ＶＥＧＦ）在朋肠癌中的表达及其与临床病理特征的关系。方法：采用免疫组织化学方法检测８０例大肠癌手术标本肿瘤组织内的血管内皮生长因子（ＶＥＧＦ）和微血管计数（ＭＶＤ）。结果：ＶＥＧＦ表达阳性率为６１．２％,ＶＥＧＦＤ表达阳性的肿瘤组织其ＭＶＤ明显高于阴性者（Ｐ＜０．０５）。ＶＥＧＦ表达与肿瘤的浸润性生长、浆膜浸润、淋巴结转移和肝转移有明显相关性（Ｐ＜０．０５）。此外,ＶＥ     

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.