CD44V6、EGFR在宫颈上皮内瘤变及宫颈鳞癌中的表达与意义

目的 探讨CD44V6、EGFR在正常宫颈组织、宫颈上皮内瘤变及宫颈鳞癌组织中的表达及其意义。方法 采用免疫组织化学方法检测20例正常宫颈组织、48例宫颈上皮内瘤变及128例宫颈鳞癌患者组织中的CD44V6、EGFR的表达。结果 CD44V6和EGFR的蛋白在宫颈鳞癌组织及宫颈上皮内瘤变中的阳性表达率分别为65．63％、35．42％和69．53％、56．25％。CD44V6和EGFR的蛋白表达与宫颈鳞癌的临床分期无关（P〉0．05），与病理组织学分级、淋巴结转移有关（P〈0．05、P〈0．01）。结论 CD44V6、EGFR可能是宫颈癌发生的相关基因，与肿瘤的发展和转移有关。联合检测CD44V6、EGFR表达可作为宫颈癌早期诊断、转移潜能和预后的判断。     

CD44v6 和MRP 在卵巢癌中的表达

 目的 探讨CD44v6和MRP在上皮性卵巢癌组织中表达与化疗疗效和预后的关系。方法 采用免疫组织化学S-P法，检测10例正常卵巢组织、20例卵巢良性肿瘤和50例卵巢恶性肿瘤上皮性组织中CD44v6和MRP的表达。结果 ①CD44v6和MRP在卵巢恶性肿瘤中的表达明显高于在良性及正常组织中的表达（P〈0．05）；②CD44v6和MRP强阳性率与卵巢癌的临床分期、组织学分级和淋巴结转移有关（P〈0．05）；③卵巢癌中CD44v6和MRP的表达呈正相关（r=0．557，P〈0．05）；④CD44v6和MRP阳性表达的病例，化疗疗效和预后差。结论 检测卵巢癌中的CD44v6和MRP表达可反映肿瘤细胞的化疗疗效及预测预后。     

EGFR、C—erbB-2和VEGF在胃癌中的表达及临床意义

目的检测EGFR、C—erbB-2和VEGF在胃癌及正常组织中的表达,探讨它们的一致性及与临床病理特征的关系。方法选择临床病理资料齐全的胃癌蜡块标本120例为实验组,正常胃黏膜标本30例为对照组,采用免疫组织化学S—P法检测EGFR、C—erbB-2和VEGF在其中的表达。结果EGFR、C—erbB-2和VEGF在胃癌中的阳性表达率（40．00％、26．70％和52．50％）明显高于正常组织（7．14％、3．43％和7．14％）。EGFR、C-erbB-2和VEGF蛋白表达与患者年龄、性别、肿瘤大小、分化程度均无显著性差异（P〉0．05）;EGFR、C—erbB-2和VEGF蛋白表达与肿瘤浸润深度、淋巴结转移、临床分期及远处转移相关（P〈0．05）。胃癌中EGFR、C—erbB-2和VEGF蛋白表达具有一致性（Kappa〉0．4,P〈0．05）。结论EGFR、C—erbB-2和VEGF可作为临床判定胃癌恶性程度及评估预后的指标,对指导靶向治疗具有一定的意义。     

细胞外信号调节激酶在卵巢肿瘤的表达

[目的]探讨细胞外信号调节激酶(ERK)在卵巢上皮性肿瘤组织中的表达及其意义。[方法]应用免疫组织化学技术,检测49例卵巢上皮性癌组织、26例卵巢上皮性良性肿瘤组织及10例正常卵巢组织中ERK1/2蛋白和活性ERK1/2蛋白表达。[结果]ERK1/2在卵巢上皮性癌组织中的表达阳性率为63%,显著高于正常卵巢组织(阴性)和卵巢良性肿瘤组织(27%)(P<0.01)。活性ERK1/2在卵巢上皮性癌中的阳性表达率为65%,明显高于卵巢良性肿瘤组织中的阳性表达率19%(P<0.01)。Ⅲ~Ⅳ期卵巢癌组织中ERK1/2及活性ERK1/2表达水平高于Ⅰ~Ⅱ期,差异有显著性(P<0.05,P<0.01)。病情进展患者活性ERK1/2表达阳性率为82%,较病情未进展者(43%),差异有显著性(P<0.01)。[结论]ERK蛋白的过表达在卵巢上皮性癌患者的发生、发展中可能起重要促进作用,可判断卵巢上皮性癌的病情进展情况。     

存活素和CD44V6在甲状腺癌组织中的表达及意义

目的探讨细胞凋亡抑制因子存活素（survivin）和黏附分子CD44V6在甲状腺癌中的表达及其与甲状腺癌侵袭转移的关系。方法采用S-P免疫组织化学染色法，检测100例甲状腺癌和10例正常甲状腺组织中Survivin、CD44V6表达情况。结果Survivin在正常甲状腺组织中无表达，在70例甲状腺乳头状癌（PTC）及30例甲状腺滤泡癌（FTC）中阳性表达率分别为45．7％（32／70）、53．3％（16／30）；CD44V6在70例甲状腺乳头状癌及30例甲状腺滤泡癌中阳性表达率分别为50．0％（35／70）、66．7％（20／30），显著高于正常甲状腺组织；在甲状腺癌组织中Survivin表达与CD44V6表达具有显著相关性（7=0．386，P〈0．05），且两者表达与甲状腺癌的临床分期及有、无淋巴结转移显著相关。结论Survivin和CD44V6表达与甲状腺癌侵袭转移密切相关，且呈协同效应。     

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。     

HMGA1在卵巢上皮性癌组织中的表达及临床意义

[目的1探讨高迁移率族蛋白A1（HMGAl）在卵巢上皮性癌中的表达及其临床茬义。[方法]应用RT—PCR技术和免疫组化法检测38例卵巢上皮性癌组织中及44例正伴卵巢组织中HMGAlmRNA和蛋白的表达情况。[结果]HMGAImRNA和蛋自在卵巢上咸性癌组织中的阳性表达率均明显高于正常卵巢组织（P〈0．01）。HMGAI蛋白在组织学分纫G3癌组织中的阳性表达率高于在G1、G2级（P〈0．05）,在有淋巴结转移、脉管浸润的癌组够中的阳性表达率高于无淋巴结转移、脉管浸润的癌组织（P〈0．05）。[结论]HMGAl在卯葬癌组织中呈高表达．高水平HMGA1表达与肿瘤组织学分级、淋巴结转移、脉管浸润等一署列导致较差预后的临床病理因素相关．提示HMGA1的表达不仅有助于卵巢癌的诊断,也有助于预后的判断。     

Kilon基因在卵巢上皮性肿瘤中的表达状况的探讨

目的 探讨Kilon基因在卵巢上皮性癌中的表达状态及其与基因启动子CpG岛甲基化的关系。方法 采用RTPCR的方法检测20例卵巢正常组织，17例良性上皮性肿瘤，72例卵巢上皮性癌组织和SKOV3、3AO、CaoV3卵巢癌细胞株Kilon基因mRNA的表达并用限制性内切酶一PCR的方法检测基因启动子中CpG岛甲基化的状况。结果 在卵巢上皮性癌组织中KilonmRNA的表达率（33．3％），显著低于正常卵巢组织和卵巢良性上皮性肿瘤组织的表达率分别为60．0％，76．5％。SKOV3、ca0V3和3AO均未见KilonmRNA表达。启动子甲基化在3种组织中的阳性率分别为0，11．8％和5．6％，卵巢癌与卵巢正常组织和良性肿瘤无显著差异。卵巢癌Kilon启动子HapII内切酶位点甲基化与mRNA失表达无相关性。SKOV-3、CAOV3和3AO均未发现甲基化。结论 卵巢上皮性癌细胞存在Kilon基因表达缺失。基因启动子CpG岛HapII酶切位点的甲基化与Kilon基因低表达无相关性。     

EGFR／HER1和C—erbB-2／HER2在乳腺癌表达的意义及其相关性

目的：探讨乳腺癌中EGFR和C—erbB-2基因蛋白表达的临床意义。方法：乳腺癌86例，乳腺腺瘤36例，采用免疫组织化学方法，检测EGFR／HER。和C—erbB-2／HER：阳性率，分析它们的相关性。结果：EGFR和C—erbB-2在乳腺癌中的表达高度正相关（r=0、73）。它们在乳腺癌中的阳性率明显高于腺瘤（P〈0．001）。在乳腺癌中EGFR和C—erbB-2的阳性率分别为56．98％（49／86）和70．93％（61／86），差异无显著性（P〉0．05）。在浸润癌和有淋巴结转移组阳性率高于非浸润组和无淋巴结转移组（P〈0．001）。结论：EGFR和C—erbB-2在乳腺癌发生中有协同作用，是预后不良的指标。     

CD44v6和LYVE-1蛋白在卵巢上皮性肿瘤中的表达及意义

目的探讨CD44v6和LYVE-1蛋白在卵巢上皮性肿瘤中的表达及意义。方法应用免疫组化链霉菌抗生物素蛋白-过氧化物酶连接(SP)法检测CD44v6、和LYVE-1在63例卵巢上皮性癌、5例卵巢良性上皮性肿瘤和4例正常卵巢组织中的表达情况。结果正常卵巢组织、卵巢良性上皮性肿瘤和卵巢上皮性癌中CD44v6和LYVE-1蛋白的表达具有显著差异;CD44v6表达强度与卵巢癌临床分期和组织学分级呈正相关,LYVE-1的表达和卵巢癌的临床分期正相关,而不同组织学分级间差异无显著性;CD44v6和LYVE-1的表达强度与淋巴结有无转移显著相关;CD44v6和LYVE-1在卵巢癌中协同表达。结论CD44v6和LYVE-1在卵巢癌发生发展、和淋巴转移中起不同程度的作用,其检测可为卵巢肿瘤生物学行为判定提供参考依据。     

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.     

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.     

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.     

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.     

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。     

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。     

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.