胃、结直肠癌术后良、恶性肠梗阻病因分析

目的:探讨胃癌、结直肠癌手术后肠梗阻的原因。方法:对手术探查的68例胃癌、结直肠癌术后肠梗阻的病例进行回顾性分析,探讨良、恶性原因所致肠梗阻在发生时间、病理、临床表现及癌胚抗原(CEA)的特点。结果:良、恶性肠梗阻分别占55.9%(38/68)和44.1%(30/68)。76.3%(29/38)的良性肠梗阻发生在术后6个月以内,恶性肠梗阻83.3%(25/30)出现在术后6个月以后,差异有统计学意义(P<0.01)。原发肿瘤分化较差、分期较晚者更多发生恶性肠梗阻(P<0.05);良性肠梗阻更多表现为完全性肠梗阻,且血清CEA平均水平和阳性率较恶性肠梗阻低(P<0.05)。结论:胃癌、结直肠癌术后发生肠梗阻可根据初次手术时间结合临床特点、原发肿瘤病理及CEA大致判断为良、恶性原因所致。     

胃癌患者外周血CEA mRNA表达相关病理因素分析

目的 探讨胃癌患者外周血CEA mRNA表达的相关病理因素.方法 对2004年1月至2004年6月手术治疗的38例胃癌患者外周血CEA mRNA表达进行检测,并回顾性分析胃癌患者年龄、性别、胃癌原发部位、大体类型、组织学类型、淋巴结转移以及胃癌组织p53和CerbB-2表达等临床病理因素与胃癌患者外周血CEA mRNA表达的关系.结果 胃癌患者外周血CEA mRNA表达的阳性率为60.5%（23/38）.单因素分析显示：胃癌患者外周血CEA mRNA表达与胃癌原发病灶部位（P〈0.05）、组织学类型（P〈0.05）及淋巴结转移（P〈0.05）相关;多因素Logistic回归分析表明：胃癌淋巴结转移、胃癌原发病灶部位为影响胃癌患者外周血CEA mRNA表达的独立因素.结论 胃癌血道转移的高危因素为胃窦癌和淋巴结转移.     

结直肠癌术后急性肠梗阻的危险因素分析

目的:探讨结直肠癌术后急性肠梗阻的危险因素。方法:回顾性分析我院248例行择期结直肠癌根治术的结直肠癌患者临床资料,根据术后1个月内是否发生急性肠梗阻分为急性肠梗阻组和非急性肠梗阻组,对两组相关因素进行单因素和多因素Logistic回归分析。结果:248例行择期结直肠癌根治术的结直肠癌患者中,35例（14.11%）发生急性肠梗阻（急性肠梗阻组）,213例（85.89%）未发生急性肠梗阻（非急性肠梗阻组）。两组性别、肿瘤直径、胃肠手术史、手术方法、手术时间比较,差异无统计学意义（P＞0.05）;急性肠梗阻组年龄＞60岁、肿瘤分期偏高、开腹手术发生率均高于非急性肠梗阻组（P＜0.05）,而术后生长抑素使用率低于非急性肠梗阻组（P＜0.05）;其中年龄＞60岁、肿瘤分期偏高、开腹手术为影响结直肠癌根治术后急性肠梗阻发生的独立危险因素（OR=3.564、3.149、2.895,P＜0.05）,而术后使用生长抑素为影响结直肠癌根治术后急性肠梗阻发生的独立保护因素（OR=0.271,P＜0.05）。结论:对年龄＞60岁、肿瘤分期偏高、开腹手术治疗等术后急性肠梗阻高危的结直肠癌患者,应在术后予以生长抑素等防治措施,以减少急性肠梗阻等并发症发生,促进患者术后康复。     

结直肠癌组织MMP-7、MMP-9表达与腹腔微转移的相关性研究

目的：探讨MMP-7、MMP-9在结直肠癌腹腔微转移中的作用以及相关性。方法：收集98例结直肠癌患者手术中腹腔冲洗液,进行CEA、CK20免疫细胞化学染色确定腹腔微转移。使用组织阵列仪制作组织芯片,进行免疫组化染色（SP）,检测MMP-7、MMP-9在结直肠癌组织中的表达情况,分析其与腹腔微转移的关系。结果：CEA、CK20联合检测腹腔微转移率为32.7%（32/98）。MMP-7、MMP-9在伴有腹腔微转移的结直肠癌中阳性表达率分别为93.75%和96.88%,明显高于无腹腔微转移结直肠癌表达率72.73%和68.18%（P〈0.05,P〈0.01）。结论：MMP-7、MMP-9可能在结直肠癌腹腔微转移的发生过程中起重要作用。     

CEA E-cadherin表达与结直肠癌术后肝转移关系

目的：探讨血清CEA和上皮粘附分子E-cadherin在结直肠癌的表达及其对肝转移的预测作用。方法：采用化学发光法动态检测60例结直肠癌患者术后血清CEA水平,采用免疫组化法检测60例结直肠癌术后标本E-cadherin表达。结果：在26例肝转移组中24例（92.3%）患者出现不同程度CEA升高,在34例非肝转移组中共有9例（26.5%）患者出现CEA升高（P=0.004）。结直肠癌原发灶分化程度不同E-cadherin表达也有差异。但是不同T分期和N分期同E-cadherin表达无明显联系。E-cadherin表达阳性肝转移率明显低于阴性肝转移率,生存分析显示不同表达状态其肝转移出现时间差异有统计学意义（P〈0.05）。结论：血清CEA水平检测同结直肠癌术后肝转移相关;组织E-cadherin表达同结直肠癌肿瘤细胞分化程度和术后肝转移发生相关。     

腹腔镜与开腹结直肠癌根治术围手术期并发症对比及原因分析

目的对腹腔镜下结直肠癌根治术与开腹手术的围手术期并发症发生率进行对比,并探讨并发症常见原因,为临床减少、预防并发症提供依据。方法回顾性分析开封市中心医院普外科2012年10月至2014年12月由同一组医师实施的68例腹腔镜结直肠癌根治术与70例开腹结直肠癌根治术的临床资料,比较其围手术期并发症的差异。结果腹腔镜组与开腹组围手术期总并发症发生率分别为26.47%(18/68)和41.43%(29/70),术中出血发生率分别为5.88%(4/68)和4.28%(3/70),术后吻合口瘘发生率分别为5.88%(4/68)和7.14%,术后吻合口出血发生率分别为1.47%(1/68)和2.86%(2/70),差异均无统计学意义(P0.05)。腹膜后气肿发生率分别为7.35(5/38)和0,肠梗阻发生率分别为2.94%(2/68)和12.86%(9/70),切口感染发生率分别为2.94%(2/68)和14.29%(10/70),差异均有统计学意义(P0.05)。结论腹腔镜下结直肠癌根治术与开腹手术相比具有腹部切口小、术中出血少,手术后疼痛轻、术后恢复快等优点。两组围手术期总体并发症发生率无差异,术中出血、术后吻合口瘘、吻合口出血等发生率均无差异,但术后肠梗阻及切口感染发生率腹腔镜组明显低于开腹组。     

TPS、CA199和CEA在结直肠癌患者血清中的表达及其临床意义

[目的]研究结直肠癌患者血清中组织多肽特异性抗原（TPS）、CA199和CEA水平及结直肠癌患者根治术前后两者水平的变化,为结直肠癌的临床诊断、预后提供参考。[方法]用ELISA法检测血清TPS水平：用ECL法检测血清CA199和CEA水平。[结果]结直肠癌患者的血清TPS、CA199和CEA水平与结直肠良性疾病和正常人比较有显著性差异（P〈0.001），且随TNM分期增加而升高。手术治疗后三种肿瘤标志物水平明显下降,而术后复发患者的水平则明显升高。各种组合检测中，以TPS＋CA199＋CEA组合的敏感性和约登指数最高。[结论]血清TPS、CA199和CEA均可作为结直肠癌诊断、预后的临床指标,三者联合检测可提高结直肠癌的临床应用价值。     

血清CA199与CEA检测对结直肠癌的诊断价值

目的：研究肿瘤相关糖类抗原199（CA199）与癌胚抗原（CEA）检测对结直肠癌的诊断价值。方法：采用电化学发光方法检测44例结直肠癌患者与19例正常人血清中CA199与CEA的水平并进行统计学分析。结果：结直肠癌患者血清中CA199和CEA水平明显高于正常对照组良性对照组（P〈0．05）;治疗后CA199与CEA含量与治疗前相比显著降低（P〈0．05）。结论：CA199与CEA检测结对结直肠癌临床诊断与疗效评价有一定的意义。     

腹腔镜结直肠癌术后非计划再次手术原因及危险因素分析

目的：探讨腹腔镜结直肠癌手术后非计划再次手术发生的现状、原因及相关危险因素。方法：回顾性分析2017 年至 2020 年四川省肿瘤医院大肠外科中心腹腔镜下结直肠癌手术 2 241 例，术后发生非计划再次手术 55 例， 对其发生原因及危险因素进行单因素和多因素分析并建立风险预测模型。结果：腹腔镜结直肠癌术后非计划再次 手术发生率为 2.45%，发生非计划再次手术的原因主要是吻合口瘘（45.46%）、肠梗阻（40.00%），其余原因包括出血（5.45%）、感染（5.45%）、切口裂开（1.82%）和腹腔引流管嵌顿（1.82%）。单因素和多因素分析显示，男性（OR = 4.608 ；95％ CI = 2.116 ~ 10.035）、合并心脑血管疾病（OR = 11.769； 95％ CI = 6.106 ~ 22.684）、低蛋白血症（OR = 2.312； 95％CI = 1.121 ~ 4.768）和既往有腹部手术史（OR = 1.907； 95％ CI = 1.005 ~ 3.619）是腹腔镜下结直肠癌术后非计划再次手术的独立危险因素。通过独立危险因素构建风险预测模型，校准曲线拟合良好，ROC 下面积为 0.781。说明该模型具有良好的预测价值。结论：腹腔镜下结直肠癌术后非计划再次手术发生最常见的原因为吻合口瘘和肠梗阻，对男性、合并心脑血管疾病患者、低蛋白血症及既往有腹部手术史的患者应注意加强防范非计划再次手术的发生。根据危险因素构建的风险预测模型能帮助识别腹腔镜结直肠癌术后发生非计划再次手术的高危人群。     

β-七叶皂苷钠注射液预防结直肠癌术后粘连性肠梗阻及对血清分子标志物的影响

目的:观察β-七叶皂苷钠注射液预防结直肠癌术后粘连性肠梗阻作用及对患者胃肠功能恢复、血清癌胚抗原（CEA）、糖类抗原199（CA199）、糖类抗原724（CA724）水平的影响。方法:选取112例结直肠癌患者作为观察对象,所有患者均接受手术治疗,随机分为对照组和观察组,每组各56例。术后,对照组给予常规治疗,观察组在对照组基础上给予β-七叶皂苷钠注射液治疗。比较对照组和观察组患者术后粘连性肠梗阻发生率、胃肠功能恢复指标、手术前后血清CEA、CA199、CA724水平。结果:随访3个月,观察组患者粘连性肠梗阻发生率低于对照组（3.6% vs 14.3%,P<0.05）。术后胃肠功能恢复指标显示,与对照组相比,观察组患者肠鸣音恢复时间、肛门首次排气时间及首次进食时间缩短,组间比较均有统计学差异（P均<0.05）。术后3个月,与对照组相比,观察组患者血清CEA、CA199、CA724水平降低,组间比较均有统计学差异（P均<0.05）。结论:β-七叶皂苷钠注射液能够有效预防结直肠癌术后粘连性肠梗阻发生,并且能够促进胃肠功能恢复,降低血清CEA、CA199、CA724水平,临床上值得应用。     

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.     

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.     

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。     

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.     

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。     

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.