经尿道前列腺电汽化术治疗晚期前列腺癌后尿道梗阻26例

[目的]探讨经尿道前列腺电汽化术(TUVP)对晚期前列腺癌致后尿道梗阻的治疗作用.[方法]对26例晚期前列腺癌致后尿道梗阻患者采用TUVP加双侧睾丸切除术和术后缓退瘤口服治疗.[结果]TUVP切除前列腺组织10g～45g,平均23.23±6.90g.术后均一次性解除后尿道梗阻,最大尿流率从术前6.38±2.04ml/s升至14.15±1.95ml/s,残余尿从术前平均125ml减少至20ml.国际前列腺症状评分(Ⅰ-PSS)从术前29.54±3.19分降至8.54±1.58分.生活质量评分从术前5.35±0.63分降至1.15±0.37分.术前后各参数值比较,P＜0.05.[结论]晚期前列腺癌致后尿道梗阻,在雄激素阻断治疗的同时,加用TUVP治疗,可有效、迅速改善后尿道梗阻症状,对提高患者生活质量有明显作用.     

经尿道前列腺等离子体双极电切联合去势术治疗晚期前列腺癌并膀胱出口梗阻(附25例报告)

目的:探讨经尿道前列腺等离子体双极电切联合去势术治疗晚期前列腺癌所致膀胱出口梗阻(BOO)的效果.方法:对25例晚期前列腺癌合并膀胱出口梗阻患者行经尿道前列腺等离子体双极电切术(TUPKVP)联合去势术治疗.结果:切除前列腺组织21g～103g,平均(42.6±12.8)g,国际前列腺症状评分(IPSS)由术前平均(24.3±3.2)分降至术后平均(8.3±3.7)分(P＜0.01),最大尿流率(Qmax)由术前平均(4.3±2.3)ml/s升至术后平均(19.9±2.1)ml/s(P＜0.01),剩余尿量由术前平均(165.5±51.3)ml降至术后平均(33±12ml),生活质量评分(QOL)由术前平均(5.1±2.0)分降至术后平均(1.8±0.5)分.术后22例平均随访1.5年,1例因尿潴留需再次手术治疗,2例因肿瘤复发转移死亡.结论:TUPKVP安全性高,可有效减轻临床症状,提高生活质量.     

等离子电切术联合抗雄激素治疗伴膀胱出口梗阻的晚期前列腺癌的疗效观察

目的探析等离子电切术与抗雄激素联合治疗晚期前列腺癌且伴膀胱出口梗阻的临床疗效。方法入选104例伴膀胱出口梗阻的晚期前列腺癌患者,根据入院先后顺序分为2组,观察组54例采用等离子电切术与间断雄激素药物联合治疗,对照组50例仅采用等离子电切术治疗,观察并对比2组治疗前后前列腺体积、前列腺特异性抗原(PSA)、国际前列腺症状(IPSS)评分、残余尿量(RU)、最大尿流率(Qmax)及生活质量评分(QOL)的改变。结果经治疗,观察组前列腺体积(46.5±13.4)cm3显著小于对照组(57.6±13.9)cm3,PSA(1.8±0.6)μg/L显著低于对照组(2.6±0.9)μg/L,IPSS评分(12.8±3.4)分显著低于对照组(15.3±3.5)分,RU(29.6±16.4)ml显著低于对照组(46.2±18.3)ml,Qmax(19.2±4.0)ml/s显著高于对照组(16.3±3.8)ml/s,QOL评分(2.2±1.3)分显著低于对照组(2.8±1.4)分,差异均具有统计学意义(P均<0.05)。结论等离子电切术与抗雄激素联合治疗有助于提高伴膀胱出口梗阻的晚期前列腺癌的临床疗效。     

高危前列腺癌合并膀胱出口梗阻的治疗

背景与目的:近年前列腺癌的发病率和检出率明显增加,尤其是高龄合并多种老年性疾病的患者增加,且常伴有严重的膀胱出口梗阻症状,患者生活质量大受影响。本文探讨高危前列腺癌合并膀胱出口梗阻患者的适宜治疗方案。方法:对80例高危前列腺癌合并膀胱出口梗阻的患者采取经尿道前列腺电汽化术 双侧睾丸切除术 抗雄激素内分泌治疗。术前对每个患者进行个体化准备,围手术期加强监护。术前及术后均对患者进行国际前列腺症状评分(internationalprosteticsymptomscore,IPSS),并测定最大尿流率(maximumofflow,Qmax)、血PSA及行B超检查以确定疗效。结果:80例患者均顺利手术。无尿潴留者术前、术后3个月IPSS分别为31±2、11±3,Qmax分别为(8.9±3.4)ml/s、(19.4±2.7)ml/s;尿潴留者术前、术后3个月IPSS分别为31±2、13±3,术后3个月Qmax为(19.0±3.3)ml/s。术前、术后IPSS、Qmax测定比较有显著性差异(P<0.01)。术后血PSA迅速下降,B超检查显示前列腺体积明显缩小。结论:经尿道前列腺电汽化术 双侧睾丸切除术 抗雄激素内分泌治疗对高危前列腺癌合并膀胱出口梗阻患者是一种安全有效的治疗方法。     

三种前列腺电切术对老年前列腺癌致膀胱梗阻患者超敏C反应蛋白和肌钙蛋白Ⅰ的影响

目的 比较经尿道前列腺电切(TURP)、经尿道前列腺汽化电切(TUVP)、经尿道前列腺等离子电切(PKRP)对老年晚期前列腺癌致膀胱梗阻患者超敏C反应蛋白(hs-CRP)、心肌肌钙蛋白Ⅰ(CTn-I)的影响.方法 收集83例年龄＞65岁前列腺癌致膀胱梗阻患者的临床资料,按手术方式不同分为TURP组、TUVP组和PKRP组,术前详细采集相关临床资料及超敏C反应蛋白、心肌肌钙蛋白Ⅰ,术后2～4h复查.结果 TURP组晚期前列腺癌致膀胱梗阻患者超敏C反应蛋白、心肌肌钙蛋白Ⅰ有不同程度的增高,TUVP组和PKRP组无改变.结论 TURP会对患者心脏造成损害,TUVP和PKRP则相对安全.     

TVP联合雄激素阻断治疗晚期前列腺癌合并膀胱出口梗阻的临床观察

前列腺癌晚期患者常伴有严重的膀胱出口梗阻(BOO)症状.我院对此类患者采取经尿道前列腺电汽化术(transufe-thral electrovaporization of the prostatet TVP)+双侧睾丸切除术+抗雄激素内分泌治疗,疗效满意,总结报道如下.     

前列腺癌雄激素依赖转化后雄激素受体基因表达变化的研究

背景与目的:前列腺癌雄激素依赖性转化的机制目前尚不完全清楚,多数认为雄激素受体(androgen receptor,AR)基因的变化可能起重要作用,本研究主要探讨AR基因表达变化在前列腺癌雄激素依赖转化过程中的作用.方法:通过对33例晚期前列腺癌患者进行雄激素阻断治疗并长时间的随访,期间有18例患者发生了雄激素依赖转化,15例患者未发生雄激素依赖转化.采用RT-PCR法测定18例患者雄激素依赖转化前后及15例患者雄激素阻断治疗前后癌细胞内AR基因的表达情况.结果:18例患者雄激素依赖转化前后AR基因的表达分别为[(28.4±3.4) Ct vs (36.7±1.8)Ct],两者之间差异有统计学意义(t=14.43,P<0.001),15例患者雄激素阻断治疗前后AR基因的表达分别为[(29.5±3.1)Ct vs (29.1±3.2)Ct],两者之间差异无统计学意义(t=0.409,P>0.05).结论:AR基因表达增强是前列腺癌雄激素依赖转化的原因之一.     

TVP联合内分泌治疗晚期前列腺癌伴膀胱出口梗阻的近期疗效

目的观察经尿道前列腺电气化术（transurethralelectrov印orizationoftheprostate，TVP）联合内分泌治疗晚期前列腺癌伴膀胱出口梗阻的近期疗效。方法回顾分析采用TVP联合内分泌治疗的48例晚期前列腺癌合并膀胱出口梗阻的临床资料。结果48例晚期前列腺癌均行TVP手术。其中27例术中行睾丸切除，术后予抗雄药物康士得、福至尔或扶他胺治疗。21例未行睾丸切除者，常规应用药物去势（诺雷德、抑那通）联合抗雄药物（康士德、福至尔或扶他胺）。术后3个月复查，所有患者下尿路梗阻症状均有不同程度改善。PSA明显下降，骨转移患者骨痛症状减轻，转移灶稳定。结论TVP联合内分泌治疗伴膀胱出口梗阻的晚期前列腺癌近期疗效满意，是一种有效、安全、可行的治疗方法。     

前列腺、精囊

腹腔镜经腹途径前列腺癌根治术（附2例报告）；人前列腺癌多药耐药细胞系的建立；前列腺增生合并慢性前列腺炎临床分析；经尿道汽化切除治疗伴膀胱出口梗阻的晚期前列腺癌；经直肠内线圈三维氢质子磁共振波谱诊断前列腺癌的临床价值;     

经尿道前列腺电切术联合间歇性雄激素阻断治疗晚期前列腺癌

目的探讨经尿道前列腺电切术联合间歇性雄激素阻断治疗晚期前列腺癌的临床效果。方法回顾性总结盐城市中医医院2006年1月至2012年1月行前列腺电切加雄激素阻断治疗晚期前列腺癌并得到有效随访的36例临床资料。结果 36例患者均顺利完成手术。术后3个月检查睾酮水平、前列腺特异抗原、最大尿流率、残余尿量、前列腺症状评分,较术前均显著改善。随访12~36个月,26例患者带瘤生存,排尿无明显异常。结论前列腺电切术联合间歇性雄激素阻断治疗晚期前列腺癌近期疗效肯定,可以明显的改善患者症状,减轻药物毒副作用,提高患者生活质量。     

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.