bcl—xl,p53蛋白在上皮性久巢肿瘤中的表达及其临床意义

目的：探讨ｂｃｌ－ｘｌ蛋白和ｐ５３蛋白在上皮性卵巢癌中的表达及其相互关系。方法：应用免疫组织化学Ｓ－Ｐ法检测１０例正常卵巢、２１例良性上皮性卵巢肿瘤、１２例交界性肿瘤、７２例恶性肿瘤组织中ｂｃｌ－ｘｌ蛋白和ｐ５３蛋白表达情况，分析其表达与不同临床病理特征的关系。结果：ｂｃｌ－ｘｌ蛋白和ｐ５３蛋白在正常卵巢和良性上皮性卵巢肿瘤中均为阴性表达，在交界性肿瘤中阳性表达率分别为１６．６７％和８．３３％，恶     

RhoC蛋白在卵巢上皮性癌中的表达及临床意义

目的：探讨RhoC蛋白在正常卵巢组织、良性上皮性卵巢肿瘤、交界性上皮性卵巢肿瘤和卵巢上皮性癌组织中的表达，及其与卵巢上皮性癌发生、发展及生物学行为的相关性。方法：采用链霉菌抗生物素蛋白-过氧化酶（SP）免疫组织化学方法检测19例正常卵巢组织、20例卵巢良性上皮性肿瘤、27例卵巢交界性上皮性肿瘤及45例卵巢上皮性癌中RhoC蛋白的表达情况，并分析其与各临床病理特征的关系。结果：RhoC蛋白在正常卵巢组织及良性上皮性卵巢肿瘤中的表达均为阴性；RhoC蛋白在交界性上皮性卵巢肿瘤及卵巢上皮性癌中阳性表达率分别为25.93%和26.67%，与正常卵巢组织及卵巢良性上皮性肿瘤相比，差异有显著性（P〈0.05）；卵巢上皮性癌与交界性卵巢肿瘤表达比较，差异无显著性（P〉0.05）。RhoC蛋白的阳性表达率与临床分期及组织学分级有关（P〈0.05），与卵巢上皮性癌病理类型无关（P〉0.05）；卵巢上皮性癌临床分期越晚，组织学分级越高，分化越差，RhoC蛋白的表达水平越高。结论：RhoC蛋白在卵巢上皮性癌的发生、发展中起着重要的作用，可成为判断卵巢上皮性肿瘤由良性向恶性转化的标志，对其检测可用于判断卵巢肿瘤的恶性程度，并可用于判断预后。     

bcl-2、bax、c-myc和p53蛋白在卵巢上皮性肿瘤中的表达

目的：研究bcl-2、bax、c-myc和p53基因的蛋白产物在卵巢上皮性肿瘤中的表达，相互关系及其意义。方法；应用免疫组化方法，以抗bcl-2、bax、c-myc、p53的单克隆抗体为一抗，对86例卵巢上皮性肿瘤组织进行检测。同时选择12例正常卵巢组织作对照组。结果：bcl-2、bax、c-myc和p53在卵巢上皮良性、交界性、恶性肿瘤中的阳性表达率分别为6．25％、10．23%、39．28％；21．88%、50．00%、53．57％；6．25%、61．54%、64．28%和3．13%、53．85%、60．71％；而正常卵巢组织中均为阴性。结论：四个基因均以不同的作用方式参与了卵巢上皮性肿瘤的发生、发展过程，具有不同的生物学特性，并对该肿瘤的病情发展、疗效评价和预后估计均有一定意义。     

检测NFκB/p65蛋白在卵巢上皮癌表达的临床意义

目的探讨核转录因子（NFκB）家族蛋白在卵巢癌组织中的表达及其临床意义。方法通过免疫组化方法检测卵巢良性上皮性肿瘤、卵巢交界性上皮性肿瘤和卵巢癌中NFκB／p65的表达。结果NFκB／p65蛋白呈现棕黄色、细颗粒状物，在卵巢良性上皮性肿瘤、卵巢交界性上皮性肿瘤和卵巢癌中NFκB的阳性表达率分别为：26．7％、37．5％和72．5％；在卵巢癌中，p65核染色阳性与分化程度、淋巴结转移、临床分期及肿瘤大小明显相关（P〈0．05）。结论NFκB与分化程度、淋巴结转移、临床分期及肿瘤大小关系密切，可望和其他指标一起作为判断卵巢癌预后的标志物。     

bcl-xl、p53蛋白在上皮性卵巢肿瘤中的表达及其临床意义

目的　探讨bcl xl蛋白和p5 3蛋白在上皮性卵巢癌中的表达及其相互关系。方法　应用免疫组织化学S P法检测10例正常卵巢、2 1例良性上皮性卵巢肿瘤、12例交界性肿瘤、72例恶性肿瘤组织中bcl xl蛋白和 p5 3蛋白表达情况 ,分析其表达与不同临床病理特征的关系。结果　bcl xl蛋白和 p5 3蛋白在正常卵巢和良性上皮性卵巢肿瘤中均为阴性表达 ,在交界性肿瘤中阳性表达率分别为 16 .6 7%和 8.33 % ,在恶性肿瘤中分别为 48.6 1%和 5 1.39% ,两者都与肿瘤的临床分期有关。bcl xl蛋白在Ⅲ、Ⅳ期恶性肿瘤中的阳性率分别为 5 4.0 5 %、71.43 % ,Ⅰ、Ⅱ期为 12 .5 0 %、45 .0 0 % ;p5 3蛋白在Ⅲ、Ⅳ期恶性肿瘤中的阳性率分别为5 9 .46 %、71.43 % ,明显高于Ⅰ、Ⅱ期的 2 5 .0 0 %、40 .0 0 %。两者均与肿瘤的病理学类型和病理学分级无关 ,未发现两者有相关性(P >0 .0 5 )。结论　bcl xl蛋白和 p5 3蛋白参与了卵巢肿瘤的发生发展过程 ,可作为卵巢恶性肿瘤的生物学标志物之一。     

端粒酶与凋亡相关蛋白在卵巢交界性肿瘤中的表达

目的:探讨端粒酶蛋白亚单位(hTERT)与凋亡相关蛋白(bcl-2、caspase-3)在卵巢上皮性交界性肿瘤中的表达及临床意义.方法:选取天津市肿瘤医院病理科存档的卵巢上皮性交界性肿瘤41例,采用免疫组化SP法检测hTERT、bcl-2与caspase-3在肿瘤组织中的表达,与22例良性、30例恶性肿瘤进行比较,并探讨三者间表达的相关性.结果:1)hTERT在卵巢交界生肿瘤中阳性率为46.3%,而良性与恶性肿瘤分别为36.4%,73.3%,与交界性肿瘤相比,恶性肿瘤阳性率明显升高(P=0.023),而良性肿瘤与之的差异无统计学意义(P=0.446).2)bcl-2和caspase-3在卵巢交界性肿瘤中阳性率为58.5%和73.2%,良性与恶性肿瘤分别为59.1%、72.7%和86.7%、43.3%,其中bcl-2的阳性率在交界性肿瘤中明显低于恶性肿瘤(P=0.010),caspase-3反之(P=0.011);但它们在交界性肿瘤中的表达无相关性(r=-0.063,P＞0.05),且二者在交界性与良性肿瘤间的差异无统计学意义(P=0.966,0.970).3)对93例卵巢肿瘤研究发现,hTERT与bcl-2蛋白表达无相关性(r=0.037,P＞0.05);hTERT与caspase-3表达呈显著负相关(x2=4.8109,r=-0.227,P＜0.05)结论:hTERT蛋白表达可以反映端粒酶活性与hTERTmRNA水平,与凋亡相关蛋白(bcl-2、caspase-3)的联合检测可进一步判断卵巢交界性肿瘤良恶性,有望成为识别卵巢交界性肿瘤中高危人群的标志物.     

人类组织激肽释放酶6在卵巢上皮性癌中的表达及临床意义

[目的]研究人类组织激肽释放酶（kallikrein,KLK）6蛋白在卵巢上皮性癌组织及腹膜后淋巴结中的表达,探讨其在卵巢上皮性癌中的临床意义。[方法]回顾性分析卵巢肿瘤患者的临床病理资料,采用免疫组化检测72例卵巢癌、16例卵巢交界性肿瘤、20例良性卵巢上皮性肿瘤组织KLK6蛋白的表达;并采用配对设计研究KLK6蛋白在卵巢癌患者腹膜后淋巴结中的表达．探讨KLK6在卵巢上皮性癌发生、发展中的作用。[结果]KLK6在卵巢癌及交界性卵巢肿瘤中的阳性表达分别为52．8％（38／72）、25．O％（4／16）,均显著强于良性上皮性卵巢肿瘤15．0％（3／20）f19〈0．05）。KLK6阳性表达与卵巢癌的临床分期、组织学分级及淋巴结转移有关fP〈0．05）,与组织学类型无相关性（P〉0．05）;KLK6在卵巢癌原发灶与腹膜后转移淋巴结组织中的表达呈正相关（r=8．91,P=0．003）;KLK6阳性与阴性患者的平均生存时间分别为25．9个月和49．2个月（P〈O．051。[结论]KLK6高表达可能在卵巢上皮性癌的发生发展中起潜在作用,KLK6可能与卵巢上皮性癌的浸润、转移有关,KLK6是卵巢癌的不良预后因素之一。     

表皮生长因子受体在巢癌中的表达

目的：为研究表皮生长因子受体（ＥＧＦＲ）与卵巢癌发生发展的关系。方法：采用ＡＢＣ免疫组化、原位杂交方法研究了ＥＧＦＲ在６０例卵巢肿瘤（包括３８例卵巢癌，１０例良性卵巢肿瘤，１２例交界性卵巢肿瘤）及１２例正常卵巢组织中的表达。结果：ＥＧＦＲ在卵癌、良性卵巢肿瘤、交界性肿瘤及正交卵巢组织四组中的免疫组化检出率分别为７６．３２％、４０％、６６．６７％和４１．６７％，除交界性肿瘤组外，后三组与卵巢癌组相比     

人PTPRK基因在上皮性卵巢肿瘤中的表达及其意义

目的探讨受体型蛋白酪氨酸磷酸酶(PTPRK)基因在良性、交界性和恶性上皮性卵巢肿瘤及正常卵巢上皮组织中的表达规律及其与卵巢癌的关系.方法应用免疫组化间接法检测50例卵巢癌、13例良性上皮性卵巢肿瘤、14例交界性上皮性卵巢肿瘤及10例正常卵巢上皮组织中PTPRK基因的表达,采用Kaplan-Meier生存分析比较卵巢癌患者PTPRK蛋白表达与五年生存率的关系.结果(1)良性、交界性上皮性卵巢肿瘤和卵巢癌组中,PTPRK基因的阳性表达率分别为53.9%、57.1%、18.0%,显著低于正常卵巢上皮组的表达率100%(P均＜0.001).卵巢癌组中PTPRK基因的阳性表达率显著低于良性上皮性卵巢肿瘤组(P＜0.001)和交界性上皮性卵巢肿瘤组(P＜0.01).(2)卵巢癌高分化组中PTPRK基因的表达率为62.5%,显著高于中分化组(18.8%)和低分化组(6.3%)(P＜0.01).卵巢癌淋巴结无转移组PTPRK基因的表达率为27.3%,显著高于无阳性表达的淋巴结有转移组(P＜0.05).(3)PTPRK基因表达阳性组与表达阴性组的5年生存率分别为66.7%、46.7%,两组比较,差异无显著性(P＞0.05).结论PTPRK基因表达缺失发生在上皮性卵巢肿瘤组织中,肿瘤分化程度越低或者淋巴结已有转移则该基因表达缺失越明显.PTPRK基因可能是一种肿瘤抑制基因,其不同程度的表达缺失与上皮性卵巢肿瘤的发生和发展有关.     

PCNA及bcl-2与caspase-3在卵巢上皮性交界性肿瘤中的表达及意义

目的:探讨增殖细胞核抗原(PCNA)、bcl-2与caspase-3在卵巢上皮性交界性肿瘤中的表达及临床意义.方法:选取天津医科大学附属肿瘤医院病理科存档的卵巢上皮性交界性肿瘤40例,采用免疫组化SP法检测PCNA、bcl-2与caspase-3在肿瘤组织中的表达,并与良性、恶性肿瘤进行比较.结果:在卵巢交界性肿瘤中1)PCNA阳性率为72.5%,明显高于良性肿瘤(47.6%),低于恶性肿瘤(89.6%,P＜0.05);bcl-2与caspase-3的阳性率为60.0%和72.5%,而良性与恶性肿瘤分别为61.9%和76.2%、86.2%和44.8%,二者在恶性肿瘤中的表达与良性、交界性有显著差异(P＜0.05).2)PCNA与bcl-2的表达存在相关性,其协同表达率为52.5%,与良性(28.6%)、恶性肿瘤(75.9%),存在显著性差异(P＜0.05);PCNA、bcl-2与caspase-3的协同表达率为72.7%,良性与交界性肿瘤明显高于恶性肿瘤(P＜0.05).3)仅bcl-2与组织学类型有关,浆液性肿瘤的阳性率明显高于粘液性(P＜0.01);PCNA、caspase-3与临床病理参数无关.结论:PCNA与bcl-2任一高表达尤其协同表达,并伴caspase-3低表达是卵巢交界性肿瘤恶性潜能增加的标志,应密切随访.     

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.     

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.     

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.