肥胖与结直肠癌预后关系的研究进展

结直肠癌(colorectal cancer,CRC)是世界范围内最常见的癌症之一.近年来,随着人们生活方式及饮食结构的改变,肥胖人群的比例越来越多,大量流行病学研究发现,结肠癌的发生风险跟肥胖密切相关.但是,对于肥胖是否影响CRC的预后,研究结果各不相同.文章就肥胖与CRC患者预后的相关性进行阐述,目前临床上对这一问题存在正反两种观点,多数研究结果显示肥胖在很大程度上影响CRC的预后;对肥胖影响CRC预后的可能作用机制进行分析,包括肥胖的胰岛素抵抗/高胰岛素血症、肥胖引起慢性炎症及脂肪酸合成酶(fatty acid synthase,FASN)表达过度.总之,肥胖作为CRC的主要危险因素及不良预后因素,在一定程度上影响CRC病死及复发.     

瘦素与儿童肥胖

瘦素(leptin)可影响机体的摄食和能耗。肥胖患者多有高瘦素血症,存在瘦素抵抗[1]。为了解血清瘦素水平与儿童肥胖的关系,本文研究了儿童肥胖患者瘦素含量变化,现报道如下。对象与方法1对象儿童肥胖患者193例,年龄6～12岁,平均年龄9.6±3.5岁。正常儿童122名,年龄7～12岁,平均年     

STAT3与结直肠癌的研究进展

STAT3是信号转导和转录因子家族（STAT）的重要成员,经细胞外细胞因子、生长因子等多种刺激信号激活,作用于细胞核内特异的DNA片段,调控靶基因的转录。近年来研究表明,STAT3在结直肠癌的发生、发展中起重要的作用。通过调控STAT3可能成为结直肠癌分子治疗的新靶点。     

COX-2与结直肠癌早期发病的关系

环氧合酶(cyclooxygenase，COX)又称为环氧化酶和PG内过氧化物合成酶。COX的主要功能是将花生四烯酸转变成前列腺素(PG)。COX家族主要有两个亚型，分别是环氧合酶1(cycl00xygenase-1，COX-1)和环氧合酶2(cyclooxy-genase-2，COX-2)。PG参与体内的许多生理和病理过程，高水平的PG特别是PGE2对多种癌细胞的增殖、侵袭、转移具有促进作用。因此，作为合成PGE2过程中主要的限速酶，COX家族对肿瘤的发生和发展具有重要的调节作用。     

肥胖与瘦素

肥胖的病因和发病机制尚未完全明了.其病因相当复杂,主要有环境因素和遗传因素.而近7年来对瘦素在调节体脂方面作用的研究,为认识肥胖提供更多的依据.本文对瘦素、瘦素受体以及瘦素的节律性分泌与肥胖的关系进行简要的综述,同时对运用瘦素治疗肥胖的意义前景做了展望.     

腹腔镜与传统开腹结直肠癌根治术手术效果对比

目的 分析腹腔镜结直肠癌根治术的微创优势。方法 选取 2015 年4月~2017年2月我院收治的 80 例结直肠癌患者作为研究对象,根据随机数字表法分为对照组和试验组,每组40例。对照组采用开腹结直肠癌根治术治疗,试验组采用腹腔镜结直肠癌根治术治疗,比较两组患者的切口长度、术中出血量、手术时间、肛门排气时间、住院时间以及术后肺部感染、尿路感染、异常出血、吻合口瘘、切口愈合不良并发症发生率。结果 试验组切口长度小于对照组[（6.30±1.24）cm vs （14.80±3.80）cm]、术中出血量少于对照组[（68.45±29.65）ml vs （134.68±35.49）ml]、肛门排气时间[（2.89±1.32）d vs （3.82±1.45）d]、住院时间[（11.47±3.04）d vs （18.62±2.67）d]更短,差异具有统计学意义（P＜0.05）;两组手术时间比较,差异无统计学意义（P＞0.05）;对照组患者并发症总发生人次高于试验组（19 vs 4）,试验组切口愈合不良发生率更低（0/37 vs 7/39）,差异有统计学意义（P＜0.05）。结论 腹腔镜结直肠癌根治术短期疗效确切,具有创伤小,术中出血量少,术后胃肠道功能恢复快,术后并发症少等优势。     

JC病毒与人结直肠癌关系的研究进展

JC病毒((JC virus,JCV)是人类多瘤病毒的一种,在人群中广泛存在.JCV感染发生在人的童年时期,没有明显的症状,但对于免疫力缺陷和长期服用免疫抑制药物的患者,能够引起致命的进行性多灶性白质脑病(Progressive Multifocal Leukoencepha|opathy,PML).由于JCV属无症状感染,其具体感染途径至今不清楚.自1971年首次报道了JCV以来,随着研究的不断深入,大量实验结果显示JCV与人类结直肠癌(Colorectal Cancer,CRC)相关,其编码产物大T抗原(large tumor anti-gen,T-Ag)在致癌过程中起重要作用.     

瘦素与前列腺癌

瘦素主要是由脂肪细胞分泌的调节能量平衡和脂肪代谢的重要激素.近年研究发现瘦素与人类多种恶性肿瘤相关.本文就瘦素及其在前列腺癌发生发展过程中作用的研究进展展开综述.     

乳腺癌并发肥胖症患者血浆瘦素水平与乳腺癌组织中瘦素mRNA的表达及临床病理的关系

目的:检测乳腺癌并发肥胖症患者乳腺癌组织中瘦素(leptin)mRNA的表达情况和血浆leptin水平,并探讨两者之间及其与临床病理之间的关系。方法:对124例居住在武汉检查者同时采集病史、进行体格检查并留取血浆,测定其leptin水平。采用半定量逆转录-聚合酶链反应(RT-PCR)检测瘦素mRNA的表达。结果:乳腺癌并发肥胖组血浆leptin水平(12.02μg.L-1±1.23μg.L-1)显著高于乳腺良性病变并发肥胖组(9.84μg.L-1±0.98μg.L-1)及单纯肥胖组(9.79μg.L-1±1.16μg.L-1)(P<0.05)。瘦素mRNA在乳腺癌并发肥胖组中的表达水平(0.71±0.32)明显高于乳腺良性病变并发肥胖组(0.41±0.26)(P<0.05)。血浆lep-tin水平与乳腺组织中瘦素mRNA表达水平显著正相关(r=0.4220,P=0.0180)。血浆leptin和瘦素mRNA的表达与腋窝淋巴结转移、绝经、TNM分期及病理类型均无显著相关性。结论:leptin可能参与了乳腺癌的发生。     

乳腺癌患者血清瘦素及可溶性瘦素受体的作用分析

目的：分析瘦素（leptin,Lp）及可溶性瘦素受体（soluble leptin receptor,sLR）水平在乳腺癌患者血清中的变化。方法：用放射免疫分析测定68例乳腺癌患者血清瘦素水平,并同步测量体重指数（MBI）和用酶联免疫吸附试验法检测可溶性瘦素受体水平,与31例良性乳腺疾病和40例健康体检者进行对照比较。结果：乳腺癌组血清瘦素水平显著高于健康对照组（P〈0．01）,消除体重指数的影响后,这种显著性差异依然存在;可溶性瘦素受体水平与对照组比水平下降（P〈0．05）,消除体重指数的影响后,这种显著性差异消失（P〉0．05）;良性乳腺疾病对照和健康对照之间均无显著性差异。结论：乳腺癌患者瘦素呈现过表达现象,瘦素与瘦素受体结合,促进肿瘤生长,瘦素可作为乳腺癌的潜在检测指标,其对于研究乳腺癌的发生发展、与肥胖的关系、辅助诊断乳腺癌都具有重要意义。     

Genetic susceptibility to non-polyposis colorectal cancer

Familial colorectal cancer (CRC) is a major public health problem by virtue of its relatively high frequency. Some 15-20% of all CRCs are familial. Among these, familial adenomatous polyposis (FAP), caused by germline mutations in the APC gene, accounts for less than 1%. Hereditary non-polyposis colorectal cancer (HNPCC), also called Lynch syndrome, accounts for approximately 5-8% of all CRC patients. Among these, some 3% are mutation positive, that is, caused by germline mutations in the DNA mismatch repair genes that have so far been implicated (MLH1, MSH2, MSH6, PMS1, and PMS2). Most of the remaining patients belonging to HNPCC or HNPCC-like families are still molecularly unexplained. Among the remaining familial CRCs, a large proportion is probably caused by gene mutations and polymorphisms of low penetrance, of which the I1307K polymorphism in the APC gene is a prime example.Molecular genetic findings have enabled hereditary CRC to be divided into two groups: (1) tumours that show microsatellite instability (MSI), occur more frequently in the right colon, have diploid DNA, harbour characteristic mutations such as transforming growth factor beta type II receptor and BAX, and behave indolently, of which HNPCC is an example; and (2) tumours with chromosomal instability (CIN), which tend to be left sided, show aneuploid DNA, harbour characteristic mutations such as K-ras, APC, and p53, and behave aggressively, of which FAP is an example. This review focuses most heavily on the clinical features, pathology, molecular genetics, surveillance, and management including prophylactic surgery in HNPCC. Because of the difficulty in diagnosing HNPCC, a detailed differential diagnosis of the several hereditary CRC variants is provided. The extant genetic and phenotypic heterogeneity in CRC leads to the conclusion that it is no longer appropriate to discuss the genetics of CRC without defining the specific hereditary CRC syndrome of concern. Therefore, it is important to ascertain cancer of all anatomical sites, as well as non-cancer phenotypic stigmata (such as the perioral and mucosal pigmentations in Peutz-Jeghers syndrome), when taking a family cancer history.     

Polyp pT1 colorectal cancer

With the introduction of NHS Bowel Cancer Screening Programme, coupled with advances made in endoscopic equipment and techniques, there is a higher detection rate for early pT1 polyp colorectal cancers (CRC). The current clinical trend is towards a conservative approach without surgical resection, if felt that there is successful endoscopic excision and without unfavourable histology parameters. Nonetheless, the further management of malignant polyps, observation or resection, remains controversial.     

Leptin in human reproduction.

The recent discovery of the obese (ob) gene has provided new insight into the mechanism which controls body fat mass. Leptin, a product of the ob gene, serves as the link between fat and the brain. This protein, by acting at the level of the hypothalamus, decreases food intake and increases energy expenditure. Animals that lack leptin (ob/ob mice) develop profound obesity and become infertile. Treatment of these animals with leptin reduces food intake and restores normal fertility. Although leptin is important for the control of fat stores in certain species, the role of this substance in the development of human obesity remains obscure. However, it has been speculated that, in humans, obesity is related to leptin resistance. The relationship between fat and reproduction has been recognized for >20 years. This article discusses the relationship between leptin and human reproduction. In particular, recent knowledge about the possible role of leptin in various conditions such as puberty, polycystic ovary syndrome and pregnancy is reviewed. Also, the article discusses the possible role of leptin in ovarian function and the relationship of this protein with gonadal steroids. It is expected that future research will clarify the physiological importance of leptin in human reproductive function.     

长链非编码RNA与结直肠癌

长链非编码RNA(lncRNA)是一类长度大于200 nt的非蛋白编码RNA分子,能同时与DNA、RNA和蛋白质分子相互作用,通过转录和转录后调控等多种作用机制在结直肠癌中发挥促癌或抑癌的双重作用。lncRNA表达异常或突变在结直肠癌的发生、发展、侵袭和转移过程中扮演着重要角色,且与患者预后密切相关。lncRNA有望为成为结直肠癌新的诊断和治疗靶点。     

癌胚抗原阴性的结、直肠癌检测和结直肠癌预后相关生物标记

目的探讨结直肠癌的发生、发展过程中患者血清质谱多肽蛋白图谱的变化,筛选与结直肠癌预后及癌胚抗原(CEA)阴性检测相关的肿瘤标记分子。方法用蛋白指纹图谱技术检测结直肠癌,结直肠管状腺瘤患者和健康者血清质谱多肽蛋白图谱。结果初步筛选出对结直肠癌有代表性的7个差异蛋白;2个与其淋巴结转移相关的差异蛋白;4个与其远处转移相关的差异蛋白;3个在其根治性切除后表达下降的差异蛋白;而由3398·3u、5477·1u和8453·9u组成的诊断模型对CEA阴性表达结直肠癌的阳性检测率为100%。结论蛋白指纹图谱技术可筛选出有意义的生物标记差异蛋白,这对结直肠癌预后判断、CEA阴性的结直肠癌检测和改变结直肠癌的进程具有重要意义。     

Epigenetics of colorectal cancer

Colorectal cancer (CRC) develops through a multistep process that results from the progressive accumulation of mutations and epigenetic alterations in tumor suppressor genes and oncogenes. Epigenetic modifications, that have a fundamental role in the regulation of gene expression, involve DNA methylation, specific histone modifications and non-coding RNAs (ncRNAs) interventions. Many genes have been until now studied to detect their methylation status during CRC carcinogenesis; and the functions of many of these genes in cancer initiation and progression are being clarified. Less is known about the patterns of histone modification alterations in CRC. Epigenetic deregulation of the ncRNAs or the genes involved in their biogenesis have been described in tumor progression and some examples of dysregulated microRNA were found also in CRC cells. Diet has an important role in the etiology of colon cancer. Folate is involved via 5-methyltetrahydrofolate in the conversion of homocysteine to methionine, which is then used to form the main DNA methylating agent S-adenosylmethionine. However, the role of folate in protecting from or in promoting CRC, depending on conditions, is still debated. The study of epigenetic marks to better characterize CRC and to identify new tools for diagnosis and prognosis as well as for therapeutic interventions is extremely promising.