骨肉瘤中Rb、p16、CDK4、cyclinD1蛋白的表达及其意义

目的 探讨骨肉瘤中Ｒｂ、ｐ１６、ＣＤＫ４、ｃｙｃｌｉｎＤ１的蛋白表达、相互关系及其意义。方法 应用免疫组化方法对４０例骨肉瘤组织中Ｒｂ、ｐ１６、ＣＤＫ、ｃｙｃｌｉｎＤ１的蛋白表达状况进行检测。结果 ４０例骨肉瘤Ｒｂ、ｐ１６蛋白表达缺失分别为７２．５％（２９／４０和）２２．５％（９／４０）;１１例ｐＲｂ阳性的骨肉瘤中的８例ｐ１６阴性,２９例ｐＲｂ阴性的骨肉瘤中２８例ｐ１６阳性;５２．５％（２１／４０     

p16和cyclinD_1蛋白在膀胱移行细胞癌中的表达及意义

 目的探讨ｐ１６、ｃｙｃｌｉｎＤ１蛋白表达与膀胱移行细胞癌（ＴＣＣ）临床分期、病理分级及预后的关系。方法采用免疫组化Ｓ－Ｐ法检测 ５９例膀胱ＴＣＣ中ｐ１６、ｃｙｃｌｉｎＤ１蛋白的表达。结果膀胱ＴＣＣ 组织中 ｐ１６蛋白阳性表达率为 ４２．４％，随临床分期、病理分级增高而下降，ｃｙｃｌｉｎＤ１蛋白阳性表达率为 ６１％，随临床分期增高而上升；ｐ１６、ｃｙｃｌｉｎＤ１蛋白表达间呈负相关；ｐ１６阳性组和 ｃｙｃｌｉｎＤ１阴性组复发率明显低于 ｐ１６阴性组和ｃｙｃｌｉｎＤ１阳性组；ｐ１６阳性组和 ｃｐｃｌｉｎＤ１阴性组 ３年存活率明显高于 ｐ１６阴性组和 ｃｙｃｌｉｎＤ１阳性组。结论ｐ１６、ｃｙｃｌｉｎＤ１蛋白检测可作为膀胱ＴＣＣ辅助诊断及预后判断的参考指标。     

非霍奇金淋巴瘤CyclinD1和p34^cdc2蛋白的检测

为了研究非霍奇金淋巴瘤（ＮＨＬｓ）中细胞周期调节因子ＣｙｃｌｉｎＤ１和ｐ３４＾ｃｄｃ２蛋白表达与肿瘤分化程度和免疫分型的关系,对４０例ＮＨＬｓ进行ＣｙｃｌｉｎＤ１和ｐ３４＾ｃｄｃ２蛋白免疫组化（ＳＰ法）染色。在４０例ＮＨＬｓ中,有１９例（４７．５％）ＣｙｃｌｉｎＤ１阳性表达２３例（５７．５％（ｐ３４＾ｃｄｃ２阳性表达。１０例淋巴结良性病变中６例生发中心细胞ＣｙｃｌｉｎＤ１和ｐ３４＾ｃｄｃ２弱 是必     

p16、CyclinD1、Cdk4、Rb基因在胰腺癌中的表达及其意义

目的：探讨ｐ１６,ＣｙｃｌｉｎＤ１,Ｃｄｋ４,Ｒｂ在胰腺癌中的作用及其相互关系。方法：免疫组织化学检测ｐ１６,ＣｙｃｌｉｎＤ１,Ｃｄｋ４,Ｒｂ蛋白在胰腺癌中的表达,原位杂交检测ｐ１６和ＣｙｃｌｉｎＤ１在胰腺癌中的存在状况。结果：ｐ１６在胰腺癌中低表达,ＣｙｃｌｉｎＤ１呈正相关关系。结论：胰腺癌发生机制涉及ｐ１６,ＣｙｃｌｉｎＤ１,Ｃｄｋ４和Ｒｂ调节环路中多个基因的异常,ｐ１６低表达和ＣｙｃｌｉｎＤ     

胃粘膜病变中多种肿瘤相关基因产物的表达

目的　探讨胃粘膜病变中ｐ１６、ｐ２１、ｐ５３ 蛋白、ｃｙｃｌｉｎＤ１和ＰＣＮＡ表达异常的意义。方法　免疫组织化学（Ｓ－ Ｐ）方法和显微摄像计算机图象分析技术。结果　２２７ 例胃粘膜病变中ｐ１６ 阳性１５２ 例（６６．９％ ）;ｐ２１阳性１３５ 例（５９．５％ ）;ｐ５３阳性２５例（１１．０％ ）;ｃｙｃｌｉｎＤ１ 阳性９７ 例（４２．７％ ）。结论　提示ｐ１６、ｐ２１ 蛋白的低表达和ｐ５３ 蛋白、ｃｙｃｌｉｎＤ１的过表达在胃粘膜细胞增殖癌变过程中起重要作用。     

非霍奇金淋巴瘤中Cyclin D1和p34~(cdc2)蛋白的检测

为了研究非霍奇金淋巴瘤（ＮＨＬｓ）中细胞周期调节因子ＣｙｃｌｉｎＤ１ 和ｐ３４ｃｄｃ２ 蛋白表达与肿瘤分化程度和免疫分型的关系,对４０ 例ＮＨＬｓ 进行ＣｙｃｌｉｎＤ１ 和ｐ３４ｃｄｃ２ 蛋白免疫组化（ＳＰ法）染色。在４０ 例ＮＨＬｓ 中,有１９ 例（４７．５ ％）ＣｙｃｌｉｎＤ１ 阳性表达,２３ 例（５７．５ ％）ｐ３４ｃｄｃ２ 阳性表达。１０ 例淋巴结良性病变中６ 例生发中心细胞ＣｙｃｌｉｎＤ１ 和ｐ３４ｃｄｃ２ 弱阳性表达。低分化ＮＨＬｓ 的ＣｙｃｌｉｎＤ１ 和ｐ３４ｃｄｃ２ 阳性率明显高于高分化ＮＨＬｓ（Ｐ＜ ０．０５）,而同免疫分型无关（ Ｐ＞０ ．０５） 。２ 个细胞周期调节因子的表达具有高度一致性（Ｐ＜０ ．０５）。提示２ 个细胞周期调节因子参与ＮＨＬｓ 的发生发展过程,其阳性表达率及表达强度同ＮＨＬｓ 恶性程度有密切关系,而同免疫分型无明显联系。ＣｙｃｌｉｎＤ１ 和ｐ３４ｃｄｃ２ 蛋白在部分ＮＨＬｓ 中共同起作用,使Ｇ１ →Ｓ期和Ｇ２ →Ｍ 期２ 个细胞检查点控制减弱。     

细胞周期蛋白D1和p21^WAF1／CIP1在喉癌癌变过程中表达？…

目的：研究喉癌变过程中细胞周期蛋白（ｃｙｃｌｉｎ）Ｄ１和ｐ２１＾ＷＡＦＩ／ＣＩＰ１表达及其临床病理学意义。方法：用免疫组化检测２０例正常黏膜、４０例不典型增生病变和６０例喉癌组织中ｃｙｃｌｉｎＤ１和ｐ２１＾ＷＡＦＩ／ＣＩＰ１的表达。结果：①ｃｙｃｌｉｎＤ和ｐ２１＾ＷＡＦＩ／ＣＩＰ１阳性表达定位于细胞核。②在喉癌癌变过程中,喉正常黏膜、不典型增生病变和喉癌中ｃｙｃｌｉｎＤ１阳性表达率分别为：５．０％     

细胞周期蛋白、细胞增殖核抗原在胸腺瘤中的表达及意义

目的：研究细胞周期蛋白（ｃｙｃｌｉｎＤ１）、细胞增殖核抗原（ＰＣＮＡ）在胸腺瘤中表达及意义。方法：用免疫组织化学方法（Ｓ－Ｐ）法,检测１８例良性胸腺瘤、２０例侵袭性胸腺瘤和１６例胸腺癌标本ｃｙｃｌｉｎＤ１、ＰＣＮＡ。结果：在３组胸腺肿瘤中ｃｙｃｌｉｎＤ１阳性表达分别为５／１８（２７．７８％）、１３／２０（６５．００％）、１４／１６（８７．５０％）（Ｐ〈０．０５）;ＰＣＮＡⅢ－Ⅳ指数分别为：５／１８     

p16,Cyclin D1在胃癌发生过程中的表达

研究ｐ１６，ＣｙｃｌｉｎＤ１在胃癌发生过程中的表达。方法：采用免疫组化ＡＢＣ法，检测胃癌、不典型增生、萎缩性胃炎及正常胃粘膜组织Ｐ１６和ＣｙｃｌｉｎＤ１的表达。结论：Ｐ１６和ＣｈｃｌｉｎＤ１在胃上皮癌变过程中起着重要作用，其在胃癌中的反向表达趋势提人才是可能存在相互抑制机制。     

细胞周期G1／S转换调控因子在喉癌癌变过程中的表达

目的：探讨喉癌癌变过程中ｐ２１＾ＷＡＦ１／ＣＩＰ１、ｐ５３和ｃｙｃｌｉｎＤ１表达的临床病理学意义。方法：用免疫组化检测２０例正常粘膜、４０例不典型增生病变和６０例喉癌组织中ｐ２１＾ＷＡＦ１／ＣＩＰ１、ｐ５３和ｃｙｃｌｉｎＤ１表达。结果：（１）ｐ２１＾ＷＡＦ１／ＣＩＰ１、ｐ５３和ｃｙｃｌｉｎＤ１阳性表达定位于细胞核；（２）在喉癌癌变过程中，喉正常粘膜、不典型增生病变和喉癌中ｐ２１ＷＡＦ１／ＣＩＰ１阳     

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.