非小细胞肺癌患者外周血CD44V6 mRNA表达与微转移的相关性研究

目的 探讨CD44V6 mRNA表达与非小细胞肺癌(NSCLC)外周血微转移的关系及临床意义,及其与CK19 mRNA在外周血中联合检测的临床意义.方法 应用免疫组化SP法检测56例NSCLC癌组织中CD44V6 mRNA的表达情况,应用逆转录聚合酶链反应(RT-PCR)技术检测外周血中CD44V6 mRNA与CK19 mRNA的表达情况.采集20例肺部良性病变患者正常肺组织和外周血作对照.结果 CD44V6 mRNA在NSCLC癌组织中表达明显高于良性病变正常肺组织(P<0.001),其阳性表达率在各病理分期间、有无淋巴结转移组间的差异具有统计学意义(P<0.05),而在各病理类型间差异无统计学意义(P>0.05).NSCLC患者外周血中CD44V6 mRNA阳性表达率高于对照组(P<0.05),其阳性表达率在各病理分期间、有无淋巴结转移间的差异具有统计学意义(P<0.05).CD44V6 mRNA在NSCLC组织中表达与外周血中表达呈正相关,NSCLC外周血中CD44V6 mRNA与CK19 mRNA表达呈正相关;CD44V6 mRNA与CK19 mRNA联合检测灵敏度为75.0%,优于单基因检测(P<0.05).结论 NSCLC外周血中CD44V6 mRNA的高表达与其侵袭转移有关,CD44V6 mRNA可作为检测NSCLC外周血微转移的分子肿瘤标志物,并有望成为判定NSCLC预后的分子标志物;CD44V6 mRNA与CK19 mRNA联合检测可提高NSCLC血行微转移诊断的敏感度.     

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。     

CD44v6在胃癌中的表达及其与幽门螺杆菌感染的关系

背景与目的:目前认为CD44v6在胃癌组织中有较高的表达率,并公认幽门螺杆菌(Helicobactor pylori,HP)感染为Ⅰ类胃癌致癌原,但迄今未见CD44v6与HP关系的文献报道。本文旨在探讨CD44v6在胃癌中的表达及其与HP感染的关系。方法:选取胃癌组织56例、癌旁非癌组织56例、非典型增生胃粘膜32例。CD44v6检测采用RT-PCR与Southern blot法;HP检测采用快速尿酶法与Warthin-Starry银染色;同时用ELISA测定56例胃癌患者血清中HP cagA抗体。结 果:胃粘膜HP阳性组中,转移性胃癌和非转移胃癌的CD44v6表达率分别达100％(12/12)和90.5％(19/21),明显高于癌旁非癌胃组织的48.6％(24/35)与非典型增生胃粘膜的23.6％(6/23);转移性胃癌与非转移胃癌的CD44v6表达率比较无显著差异(P>0.25),非典型增生胃粘膜与胃癌、癌旁非癌胃组织比较有非常显著性差异(P<0.005)。胃粘膜HP阴性组:在转移性胃癌、非转移胃癌、癌旁非癌组织和非典型增生CD44v6表达率分别是66.7％,51.4％,38.1％和18.1％,各组比较均无显著性差异。CD44v6表达与HP感染有密切关系(P<0.01)。肠型胃癌CD44v6表达与HP感染高于弥漫型胃癌(P>0.05)。胃癌患者血清HP cagA抗体阳性率高于胃癌组织HP感染率(P>0.05)。结论:CD44v6在胃癌中有较高的阳性率,与HP感染密切相关,可作为     

胃肠道癌外周血CEA-mRNA的表达及临床意义

目的　通过检测手术前、后胃肠道癌患者外周血癌胚抗原信使核糖核酸 (CEA mRNA)的表达 ,了解胃肠道癌血行播散转移情况及在围手术期综合治疗中的意义。方法　采用巢式逆转录 聚合酶链式反应 (Nest RT PCR)检测 6 2例胃肠道癌患者和 2 2例对照组外周血CEA mRNA的表达状况。结果　 6 2例癌患者样本中 ,术前 2 7例 (43.5 % )外周血CEA mRNA检测阳性 ,术后 2 6例阳性 (41.9% ) ,对照组 10例正常人及 12例良性胃肠病患者CEA mRNA测定均为阴性。Ⅰ、Ⅱ、Ⅲ、Ⅳ期患者外周血CEA mRNA阳性率依次为 37.5 %、2 7.3%、5 1.9%、80 .0 % ,各期间无显著性差异 (P >0 .0 5 )。Ⅰ +Ⅱ期与Ⅲ +Ⅳ期合并 ,两组患者间CEA mRNA的表达有显著性差异 (P <0 .0 5 )。胃肠道癌的分化程度及癌栓的形成与外周血CEA mRNA的表达无关。 35例伴局部淋巴结转移的患者的外周血CEA mRNA阳性率 (6 2 .9% )与 2 7例无淋巴结转移患者的阳性率 (18.5 % )有显著性差异 (P <0 .0 1)。手术前后外周血CEA mRNA阳性率差异无显著性 (P >0 .0 5 )。结论　外周血CEA mRNA检测可作为胃肠道癌复发、转移及预后的判断指标 ,对临床正确分期及综合治疗起指导作用。外周血CEA mRNA表达阳性的患者 ,应在围手术期辅以免疫治疗和 /或全身化疗 ,以遏止肿瘤复发、     

CD44V在口腔鳞状细胞癌患者外周血及癌组织表达的研究

目的:研究口腔鳞状细胞癌患者外周血可溶性CD44V的含量及口腔鳞癌组织中CD44v5、CD44v7的表达。方法:采用酶联免疫吸附试验检测39例口腔鳞状细胞癌患者术前外周血及30例健康成人外周血中可溶性CD44V含量;采用免疫组织化学方法测定同一口腔鳞状细胞癌患者口腔鳞癌组织中CD44v5、CD44v7的表达。结果:39例口腔鳞状细胞癌患者外周血可溶性CD44V的含量明显低于正常对照组,两者有统计学差异(P<0.05)。11例发生淋巴结转移的口腔鳞状细胞癌,其原发灶与转移灶(淋巴结)内CD44v5、CD44v7的表达水平均有统计学差异(P<0.05),且原发灶高于转移灶。同一口腔鳞状细胞癌患者术前外周血可溶性CD44V含量水平与口腔鳞癌组织中CD44v5、CD44v7的表达强度均未见相关性。结论:外周血中可溶性CD44V的含量水平对于口腔鳞状细胞癌的诊断可能具有参考价值;CD44v5、CD44v7的表达与口腔鳞状细胞癌的转移有一定的相关性。     

CD44v6 mRNA在原发性肝癌患者外周血中检测的临床意义

目的：检测原发性肝癌（primary hepatocellular neoplasms，PHC）患者外周血及组织中的CD44v6 mRNA表达，并探讨其临床意义。方法：采集60例PHC患者、40例肝良性疾病（10例肝血管瘤，10例肝囊肿，10例肝硬化，10例慢性肝炎）患者、30例健康志愿者的外周血，用RT—PCR方法检测外周血中CD44v6 mRNA的表达。同时RTPCR检测PHC患者的肝癌组织、癌旁及正常肝组织中CD44v6 mRNA的表达。结果：PHC患者外周血中CD44v6 mRNA检出率为53％（32／60），而肝癌组织中CD44v6 mRNA检出率为75％（27／36），癌旁组织中检出率为17％（6／36）。在肝癌组织中不表达CD44v6m RNA的肝癌病例，40倒肝良性疾病患者和健康志愿者外周血中，以及正常肝组织中均未检测出CD44v6 mRNA。PHC患者外周血中CD44v6 mRNA检出率与肿瘤大小、门静脉癌栓、血管浸润、肝内外转移密切相关（P〈0．05），而与肿瘤细胞分化程度及血清AFP水平无相关性（P〉0．05）。结论：外周血CD44v6 mRNA可能作为肝癌外周血微转移检测的特异性标志物。其检测结果有助于判断PHC患者的预后，监测其复发以及对PHC的鉴别诊断。     

非小细胞肺癌CD44v6的表达及其在患者预后判定中的作用

背景与目的CD44v6的过度表达与人类多种恶性肿瘤的发生、发展和转移密切相关。本研究旨在观察CD44v6在非小细胞肺癌中的表达及其在患者预后判定中的作用。方法采用RTPCR和免疫组化法,对52例非小细胞肺癌患者手术标本进行CD44v6检测,并随访。结果免疫组化法和RTPCR法测得52例肺癌组织中CD44v6阳性表达率分别为69.2%和75.0%。低分化肺癌组织中CD44v6阳性表达率显著高于高分化和中分化肺癌(P<0.05),有淋巴结转移者显著高于无淋巴结转移者(P<0.01),Ⅲ期显著高于Ⅰ期和Ⅱ期(P<0.05)。CD44v6阴性表达者生存率显著高于CD44v6阳性表达者(P=0.0115)。多元logistic回归分析显示,CD44v6阳性表达(P=0.048)和pTNM分期(P=0.035)对生存率有显著影响。结论肺癌中存在CD44v6过度表达,检测CD44v6的表达有助于预测肺癌患者的预后。     

黏附分子CD44的表达与大肠癌生物学特性间的关系

目的:探讨CD44s、CD44v6、CD44v3的表达水平与大肠癌生物学特性之间的关系及临床意义。方法:应用Envision TM免疫组化法,检测57例大肠癌组织标本和20例癌旁正常组织中CD44s、CD44v6、CD44v3的表达水平。结果:57例结直肠癌的组织标本中CD44s、CD44v6、CD44v3的阳性表达率为分别66.67%、63.16%、70.18%,而在20例正常组织中基本不表达,二者间具有统计学差异(P<0.01)。CD44s、CD44v6、CD44v3阳性表达与临床分期、肿瘤细胞分化程度显著性相关(P<0.05)。CD44v6、CD44v3阳性表达还与淋巴结转移显著相关。大肠癌组织中CD44s、CD44v6、CD44v3阳性,阴性表达的患者5年生存率分别为55.26%,78.95%;52.79%,80.95%;52.50%,88.24%,CD44s二者间差异无统计学意义(P>0.05);CD44v6、CD44v3二者间差异具有统计学意义(P<0.01)。生存率分析显示CD44s、CD44v6、CD44v3均是对生存有影响的因子。结论:黏附分子CD44s、CD44v6、CD44v3可能参与了大肠癌的发生与转移,检测其表达水平有助于预后判断。     

非小细胞肺癌患者外周血CEA mRNA表达及临床意义

 目的：检测非小细胞肺癌(NSCLC)患者外周血CEA表达情况,探讨其作为分子标志物检测 NSCLC微转移的可行性。方法：应用RT-PCR技术检测48例NSCLC患者,15例肺良性疾病(BLD)患者 和10例健康人外周血CEA mRNA的表达。结果：NSCLC患者CEA mRNA的阳性表达率明显高于BLD患 者和健康对照组(P<0.01)。Ⅰ~Ⅳ期NSCLC患者外周血中CEA mRNA阳性表达率分别为27.8%、 83.3%、61.5%和100%。NSCLC患者外周血CEA阳性表达与临床分期及淋巴结转移密切相关 (P<0.05),而与病理类型及分化程度无关(P>0.05)。结论：检测外周血CEA mRNA表达可作为诊 断NSCLC患者微转移的一个有价值的参考指标。     

单纯检测外周血CD44v6不宜作为筛选肿瘤转移的标志物

目的通过检测CD44v6剪接体在正常人外周血的表达情况,进而评价其作为肿瘤转移分子标志物的价值.方法提取50例健康志愿者的外周血单个核细胞,应用RT-PCR的办法检测CD44v6基因的表达,并对其产物进行DNA测序.结果在适当的对照控制条件下,50例外周血中有29例(58%)CD44v6 mRNA阳性.结论在普通人群外周血样本中应用RT-PCR的方法CD44v6检出率较高,因此单纯检测CD44v6不适宜作为筛选肿瘤转移的分子标记物.     

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.