肝癌组织中bcl—2和bax蛋白表达及与PCNA表达的关系

目的探讨ｂｃｌ－２和ｂａｘ与肝癌发生的关系。方法用免疫组化方法研究３４例肝癌组织中ｂｃｌ－２和ｂａｘ的表达及与ＰＣＮＡ的关系。结果显示３４例肝细胞癌中５例ｂｃｌ－２阳性,阳性率为１４．７％,８例癌旁组织阳性,阳性率为２３．５％。７例ｂａｘ阳性,阳性率为２０．６％,癌旁组织２２例阳性,阳性率为６４．７％。ｂｃｌ－２和ｂａｘ表达与ＰＣ－ＮＡ增殖指数间无明显关系（Ｐ＞０．０５）。结论ｂｃｌ－２和ｂａｘ的变化可能影响肝细胞的凋亡状态,在肝癌发生中可能起一定作用,而并不引起细胞的增殖。     

肝内胆管癌中丙型肝炎病毒感染及其与bcl—2基因异常的关系

目的 探讨肝内胆管癌中丙型肝炎病毒（ＨＣＶ）感染与ｂｃｌ－２基因异常的关系。方法采用半嵌套式原位聚合酶链反应和免疫组织化学方法对２９例原发性肝内胆管癌中ｂｃｌ－２／ＪＨ融合基因、ｂｃｌ－２蛋白及ＨＣＶ抗原（ＮＳ５抗原）进行原位观察。结果 ２９例胆管癌中ｂｃｌ－２／ＪＨ融合基因均阴性,２０例ｂｃｌ－２蛋白阳性,阳性率为６９．０％。ｂｃｌ－２蛋白表达与ｂｃｌ－２基因重排无相互对应关系。癌组织中ＮＳ５阳     

肝硬变和肝癌组织bcl-2及相关蛋白bax的表达及意义

为了探讨凋亡基因ｂｃｌ２及相关蛋白ｂａｘ与肝脏病变的关系，采用免疫组化ＳＰ法观察１５例肝硬变和４０例肝细胞癌组织中ｂｃｌ２及相关蛋白ｂａｘ的表达。结果发现肝硬变和正常肝组织中ｂｃｌ２表达较低，明显低于ｂａｘ的表达（Ｐ＜０．０５）；肝癌组织中ｂａｘ表达较正常肝组织、肝硬变及癌旁组织明显低（Ｐ＜０．０５），而ｂｃｌ２无明显变化，ｂｃｌ２和ｂａｘ阳性率无显著差异（Ｐ＞０．０５）。提示肝硬变至肝癌发展过程中ｂｃｌ２和ｂａｘ的比例发生了变化，这种变化可能影响了肝细胞的凋亡状态，在肝癌发生过程中可能起一定作用     

人胰腺癌bcl—2基因的过度表达：免疫组织化学和原位杂交研究

目的：应用地高辛标记ｂｃｌ－２ ｃＤＮＡ进行ｍＲＮＡ原位杂交和免疫组织化学分析胰腺癌中ｂｃｌ－２基因的ｍＲＮＡ转录和蛋白翻译，研究ｂｃｌ－２基因结构和功能表达的关系。方法：以胰腺癌病人癌组织（５０例）、胰腺癌转移灶组织（１５例）为研究对象，采用免疫组织化学（ＳＰ法）和分子原位杂交法检测ｂｃｌ－２在胰腺癌中的表达。对照组１０例为慢性胰腺炎组织。结果：ｂｃｌ－２蛋白在胰腺癌组明显高于胰腺癌转移灶组，Ｉ     

双歧杆菌对实验性大肠癌bcl—2及bax基因表达的影响

目的 通过观察大肠癌裸鼠移植瘤ｂｃｌ－２及ｂａｘ基因的蛋白表达水平，探讨双歧杆菌的抑瘤主机制。方法 采用免疫组化ＳＰ法检测了４０只裸鼠大肠癌移植瘤ｂｃｌ－２及ｂａｘ基因的蛋白表达率及表达强度。结果 双歧杆菌注射组大肠癌移植瘤ｂｃｌ－２蛋白表达率及阳性细胞密度均低于肿瘤对照组，ｂａｘ基因的表达情况则相反。结论 双歧杆菌可使大肠癌裸鼠移植瘤的ｂｃｌ－２基因表达下调，ｂａｘ基因表达增强，最终诱导肿瘤细胞     

bcl－2、bax基因产物表达与大肠癌术后化疗疗效关系初探

本文的目的是为探讨大肠癌ｂｃｌ—２／ｂａｘ基因产物表达与对化疗疗效的影响之间的关系。用免疫组化Ｓ—Ｐ技术检测２８例手术后随访５年以上的大肠癌标本中ｂｃｌ─２／ｂａｘ基因产物的表达。结果显示ｂｃｌ─２基因产物阳性表达者２３例，化疗后复发率５４．６％，５年生存率６９．５％。ｂｃｌ—２阴性表达者５例，复发率２５％，生存率８０％。ｂａｘ基因产物阳性表达者７例，复发率２０％，生存率８５．７％。ｂａｘ阴性表达者２１例，复发率５８．３％，生存率６６．７％。提示ｂｃｌ—２阳性表达对抗了化疗诱导的凋零，肿瘤复发率高于ｂｃｌ－２阴性者。ｂａｘ阳性表达促进了化疗诱导的凋零，肿瘤复发率低于ｂａｘ阴性者。监测ｂｃｌ—２／ｂａｘ表达有助于观察化疗疗效和预后。     

肝癌组织中人白细胞共同抗原和凋亡相关基因Fas,bcl—2及bax的表达 …

目的：探讨人白细胞抗的（ＨＬＡ－ＤＲ抗原）和凋亡相关基因Ｆａｓ、ｂｃｌ－２及ｂａｘ在肝癌中表达的意义。方法：应用免疫组化方法研究４０例肝癌组织中ＨＬＡ－ＤＲ、Ｆａｓ、ｂｃｌ－２及ｂａｘ的表达。结果：４０例肝细胞癌中１８例ＨＬＡ－ＤＲ阳性，阳性率４５％，癌旁肝细胞阴性。６例癌细胞Ｆａｓ阳性，阳性率为１５％，癌旁细胞２０例阳性，阳性率５０．０％，癌细胞ｂｃｌ－２阳性６例，阳性率为１５％，８例癌旁细胞阳     

胃原发癌和淋巴地转移癌细胞中bcl—2和c—myc基因蛋白表达的研究

为探讨ｂｃｌ－２、ｃ－ｍｙｃ基因蛋白在胃原发癌与转移癌中的表达特点，应用ＳＰ免疫组织化学方法，对８０例胃癌３６例相庆淋巴转移癌细胞进行ｂｃｌ－２、ｃ－ｍｙｃ基因蛋白的检测，并对２种基因的生物学和临床病理意义进行研究和探讨。结果发现ｂｃｌ－２、ｃ－ｍｙｃ基因蛋白的阳性表达率在３５例胃原发癌中分别为３１．４％、５７．１％，在淋巴结转移癌中分别为６８．６％、３１．４％，ｂｃｌ－２在淋巴结转移癌中的表达率     

Bcl—2,Bax在大肠癌组织的表达对术后化疗疗效的影响

为探讨凋亡抑制基因ｂｃｌ┐２和促进基因ｂａｘ在大肠癌组织中的表达及与术后化疗疗效的关系。方法采用免疫组化Ｓ┐Ｐ法，检测了４３例手术后随访５年以上的大肠癌组织中ｂｃｌ┐２、ｂａｘ基因产物的表达，统计术后化疗者与未化疗者的复发率和五年生存率。结果术后化疗者３１例，ｂｃｌ┐２阳性者复发率（３４．６％）明显高于ｂｃｌ┐２阴性者（２０．０％）（Ｐ＜０．０５）；ｂｃｌ┐２阳性者五年生存率（６９．２％）明显低于ｂｃｌ┐２阴性者（８０．０％）（Ｐ＜０．０５）。ｂａｘ阳性者复发率（７．１％）明显低于ｂａｘ阴性者（５２．９％）（Ｐ＜０．０５），而ｂａｘ阳性者五年生存率（９２．９％）明显高于ｂａｘ阴性者（５２．９％）（Ｐ＜０．０５）。未化疗组１２例，ｂｃｌ┐２、ｂａｘ阳性与阴性者的复发率，五年生存率均无显著差异。结论检测大肠癌组织中ｂｃｌ┐２、ｂａｘ表达有助于预测术后化疗疗效和预后。     

乳腺癌组织中CD44v6和MMP-2的表达及其与淋巴结转移的关系

目的：检测CD44v6、MMP-2在乳腺浸润性导管癌中的表达情况,探讨它们与淋巴结转移的关系。方法：采用免疫组化SP法检测100例乳腺浸润性导管癌中CD44v6、MMP-2的表达情况。结果：CD44v6蛋白在正常乳腺组织及乳腺浸润性导管癌中的阳性表达率分别为12．5％（5／40）、87％（87／100）,CD44v6在淋巴结转移组中的阳性表达率（56／60）明显高于无淋巴结转移组（P〈0．05）。MMP-2蛋白在正常乳腺组织及乳腺浸润性导管癌中的阳性表达率分别为0（0／40）、94％（94／100）,MMP-2在淋巴结转移组中的阳性表达率（59／60）明显高于无淋巴结转移组（P〈0．05）。结论：CD44v6、MMP-2蛋白在乳腺浸润性导管癌组织高表达,且均与淋巴结转移有关（P〈0．05）,联合检测CD44v6与MMP-2有助于综合判断乳腺浸润性导管癌的恶性程度和转移潜能。     

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.