食管癌(英文版)

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英语常见疾病英文 (1).docx

英语常见疾病英文 (1).docx

常见疾病Common Diseases1.癌症cancer2.肠癌cancer of the intestine3.肺癌lung cancer4.肝癌liver cancer5.食管癌cancer of esophagus6.胃癌gastric carcinoma7.胰腺癌cancer of the pancreas8.子宫颈癌cancer of the cervix9.鼻炎rhinitis10.鼻窦炎sinusitis11.扁桃体炎tonsillitis12.病毒性心肌炎viral myocarditis13.肠胃炎enterogastritis14.胆囊炎cholecystitis15.蜂窝组织炎cellulitis16.风湿性关节炎rheumarthritis17.腹膜炎peritonitis18.关节炎arthritis19.肺炎pneumonia20.睾丸炎orchitis21.宫颈炎cervicitis22.巩膜炎scleritis23.过敏性鼻炎allergic rhinitis24.喉炎laryngitis25.急性胃炎acute gastritis26.脊髓灰质炎poliomyelitis/ infantile paralysis27.甲沟炎paronychia28.角膜炎keratitis29.腱鞘炎tenosynovitis30.接触性皮炎dermatitis31.结肠炎colitis32.结膜炎conjunctivitis33.口角炎angular stomatitis34.泪腺炎dacryoadenitis35.流行性脑膜炎epidemic encephalitis36.流行性腮腺炎mumps37.流行性乙型肝炎epidemic hepatitis B38.阑尾炎appendicitis39.卵巢炎oophoritis40.面神经炎facial neuritis41.脑膜炎cerebral meningitis42.黏膜炎catarrh43.尿道炎urethritis44.膀胱炎urocystitis45.盆腔炎pelvic inflammatory disease46.皮炎dermatitis47.气管炎tracheitis48.前列腺炎prostatitis49.乳腺炎mastitis50.腮腺炎parotiditis51.神经炎neuritis52.神经性皮炎neurodermatitis53.肾炎nephritis54.肾盂肾炎pyelonephritis55.食管炎esophagus56.输卵管炎salpingitis57.外耳炎otitis externa58.胃炎gastritis59.牙髓炎pulpitis60.牙周炎periodontitis61.牙龈炎gingivitis62.咽炎pharyngitis63.阴道炎vaginitis64.支气管炎bronchitis65.中耳炎otitis media66.艾滋病AIDS67.白化病albinism68.白血病leukemia69.败血病septicemia70.风湿病rheumatism71.疯牛病mad cow disease72.高血压hypertension73.冠心病coronary heart disease74.黑死病black death75.黄热病yellow fever76.蛔虫病ascariasis77.结核病tuberculosis78.精神病insanity79.佝偻病richets/ rickets80.狂犬病rabies81.痨病phtisis82.淋病gonorrhoea83.慢性肺源性心脏病chronic cor pulmonale84.皮肤真菌病dermatomycosis85.伤科病disease of the traumatology86.糖尿病diabetes87.外科病surgical diseases88.胃病gastropathy89.心脏病heart disease90.性病veneral disease91.癔症hysteria92.硬皮病scleroderma93.偏头痛migraine/ splitting headache94.三叉神经痛trigeminal95.神经痛neuralgia96.头痛headache97.心绞痛angina pectoris98.坐骨神经痛sciatica99.流产abortion100.习惯性流产habitual abortion 101.先兆流产threatened abortion 102.自然流产miscarriage103.恶性肿瘤malignant tumor 104.骨瘤osteoma105.良性肿瘤benign tumor106.神经瘤neuroma107.脂肪瘤lipoma/ adipoma108.肿瘤tumor109.胆石症cholelithiasis110.肥胖症obesity111.精神分裂症schizophrenia112.神经过敏症neuroticism113.厌食症anorexia114.抑郁症depression115.营养不良症malnutrition116.中风后遗症sequela of wind stroke 117.白喉diphtheria118.白癜风vitiligo119.白内障cataract120.百日咳whooping cough121.斑疹伤寒typhus122.鼻子过敏nasal allergy123.扁桃体肥大hypertrophy of tonsils 124.便秘constipation125.不孕sterility126.痤疮acne127.带状疱疹zona128.丹毒erysipelas129.单纯性肥胖simple obesity 130.癫痫epilepsy131.冻伤frostbite132.非典SARS/ Severe Acute Respiratory Syndrome 133.痱子prickly heat/ sudamen134.肺结核pulmonary tuberculosis135.肺脓肿pulmonary136.肺气肿pulmonary emphysema137.粉碎性骨折comminuted fracture138.风湿热rheumatic fever139.风疹German measles140.肝硬化cirrhosis141.肝肿大hepatomegaly142.感冒,伤风,着凉cold143.肛裂anal fissure144.肛瘘anal fistula145.高脂血症hyperlipidemia146.鼓膜穿孔performation of the tympanic membrane 147.骨折fracture148.红斑狼疮lupus erythematosus149.坏疽gangrene150.黄疸jaundice151.黄褐斑chloasma152.霍乱cholera153.晕厥syncope154.甲状腺功能亢进hyperthyroidosis155.甲状腺肿goitre156.疥疮scabies157.精神错乱mental disorder158.近视near sight159.开放性骨折open fracture/ compound fracture 160.咳嗽cough161.口疮aphtha162.流感influenza/ flu163.痢疾dysentery164.麻痹paralysis165.麻疹measles166.马耳他热Malta fever167.麦粒肿sty168.慢性菌痢chronic bacillary dysentery169.梅毒syphilis170.面瘫facial paralysis171.尿崩症diabetes insipidus172.牛皮藓psoriasis173.疟疾malaria174.偏瘫hemiplegia175.皮肤过敏allergic skin reaction176.贫血anemia/ anaemia177.葡萄胎hydatidiform mole178.破伤风tetanus179.青光眼glaucoma180.禽流感bird flu/ avian influenza181.褥疮bedsore/ pressure score182.沙眼trachoma183.烧伤burn184.上呼吸道感染upper respiratory infection 185.神经衰弱neurasthenia186.肾结石kidney stone187.湿疹eczema188.水痘chicken pox, varicella189.天花smallpox190.痛风gout191.胃溃疡gastric ulcer192.胃下垂gastroptosis193.消化不良indigestion194.小儿肌性斜颈infantile myogenic torticollis 195.哮喘asthma196.斜颈torticollis/ wryneck197.心肌梗死miocardial infarction198.心律不齐arrhythmia199.猩红热scarlet fever200.夏季热summer heat201.血栓形成thrombosis202.荨麻疹urticaria203.癣tinea/ ringworm204.阳痿impotence205.羊水过多hydramnios206.遗精emission207.遗尿enuresis208.婴儿腹泻infantile diarrhea209.营养不良malnutrition210.再生障碍性贫血aplastic anemia211.早产premature labor212.沼地热swamp fever213.支气管哮喘bronchitic asthma214.重症肌无力myasthenia gravis215.子宫出血metrorrhagia216.子痫eclampsia217.痔疮hemorrhoid。

医学常用肿瘤名称中英文翻译

医学常用肿瘤名称中英文翻译

医学常用肿瘤名称中英文翻译肿瘤在医学中是一个常见的概念,它指的是异常增生的细胞群体。

肿瘤可以分为良性和恶性两种类型,其中恶性肿瘤常被称为癌症。

在医学领域中,有许多常用的肿瘤名称需要中英文翻译,以便于国际间的交流与合作。

以下是一些常见肿瘤名称及其中英文对照:1. 食管癌 (Esophageal cancer)2. 胃癌 (Gastric cancer)3. 肝癌 (Liver cancer)4. 胰腺癌 (Pancreatic cancer)5. 大肠癌 (Colorectal cancer)6. 肺癌 (Lung cancer)7. 乳腺癌 (Breast cancer)8. 卵巢癌 (Ovarian cancer)9. 子宫颈癌 (Cervical cancer)10. 头颈部肿瘤 (Head and neck tumors)11. 前列腺癌 (Prostate cancer)12. 脑瘤 (Brain tumor)13. 黑色素瘤 (Melanoma)14. 骨肿瘤 (Bone tumors)15. 乳腺瘤 (Breast tumor)16. 十二指肠癌 (Duodenal cancer)17. 胆囊癌 (Gallbladder cancer)18. 肾癌 (Renal cell carcinoma)以上仅为一部分常见肿瘤的中英文对照,实际上在医学名词中有更多肿瘤名称需要进行翻译和对照。

这些肿瘤名称的中英文对照的准确性对于医学领域的研究和诊断具有重要意义。

医学翻译是一项专业性很高的工作,它要求译者具备扎实的医学知识、语言能力和翻译技巧。

在进行肿瘤名称的翻译时,需要注意以下几点:首先,要了解肿瘤的类型、部位和特点,以便准确理解其名称的含义。

肿瘤名称中的每个词汇都具备一定的医学意义,因此译者必须对其进行正确的翻译。

其次,在进行中英文对照时,要确保语义的准确、明确和一致。

翻译过程中需要考虑两种语言的语法结构和表达习惯,以便将原文的意思准确传达到译文中。

常见肿瘤英文名

常见肿瘤英文名

常见肿瘤英文名1.乳腺癌: breast cancer2.非霍奇金淋巴瘤: non-hodgkin lymphoma3.霍奇金淋巴瘤: hodgkin lymphoma4.奥沙利铂: Oxaliplatin5.吉西他滨:Gemcitabine6.多发性骨髓瘤: multiple myeloma7.胸膜间皮瘤: pleural mesothetioma8.贲门癌: cancinoma of gastric cardia9.阴茎癌: penis cancer10.氟尿嘧啶: Fluorouracil11.洛铂: Lobaplatin12.培美曲塞: pemetrexed13.胰腺癌: pancreatic cancer14.前列腺癌: prostatic cancer15.卵巢癌: ovarian cancer16.食管癌: esophageal cancer17.绒毛膜癌: chorioblastoma18.宫颈癌: cervical cancer19.胃癌: gastric cancer20.肝癌:liver cancer21.结肠癌: colonic cancer22.直肠癌:rectal cancer23.肺癌:lung cancer24.子宫内膜癌:cancer of endometrium25.肾癌:renal cancinoma26.膀胱癌:bladder cancer27.鼻咽癌:nasopharyngeal cancinoma28.上颌窦癌:cancinoma of maxillary sinus29.喉癌:cancinoma of larynx30.下咽癌:Hypopharyngeal cancer31.睾丸肿瘤:tumor of testis32.恶性黑色素瘤:chromoma;malignant melanoma33.皮肤癌:skin cancer34.胆管癌:cancinoma of bile duct35.甲状腺癌:thyroid cancer36.脑恶性肿瘤:malignant brain tumor37.垂体瘤:pituitary tumors38.急性白血病:acute leukemia (AL)39.慢性粒细胞性白血病: chronic myelocytic leukemia (CML)40.慢性淋巴细胞性白血病: chronic lymphocytic leukemia (CLL)41.多毛细胞性白血病: hairy cell leukemia (HCL)42. malignant neoplasm of spermatic cord(精索恶性肿瘤)43.prolactinoma(泌乳素瘤)44.Hypopituitarism(垂体功能减退症)。

食管癌esophageal cancerPPT精品课程课件讲义

食管癌esophageal cancerPPT精品课程课件讲义

60% 4% 41% 16.8m 43%
54% 0% 42% 13.3m 34%
随机对照术前放化疗对术前化疗(N=40例) 放化疗组 N=17 ——————— 病理CR率 17.6% 住院死亡率 0 1年生存率 80.2% 3年生存率 53.5% 化疗组N=23 ——————— 0% 4.3%(1) 56.5% 30.4%
随机对照术前放化疗对单独手术(N=100例) 单独手术组 ______________ 放化疗组 _____________
中位生存期
3年生存率
17.6m
16%
16.9m
30%(P=0.15)
化学治疗
• 分为姑息性化疗、新辅助化疗(术 前)、辅助化疗(术后)。 • 原则: • 必须掌握临床适应证。 • 必须强调治疗方案的规范化和个体 化。
鉴别诊断
• 中晚期有吞咽困难者: ①贲门失弛症 ②食管良性狭窄 ③食管良性肿瘤
鉴别诊断
• 贲门失弛症:
1.年轻(青壮年)、女性多见 2.病程长,间歇性吞咽困难 3.食管吞钡X线检查:可见食管下端 呈光滑鸟嘴状狭窄 4.食管镜检查
鉴别诊断
• 食管良性狭窄
1.化学灼伤史
2.钡餐X线不规则细线状 狭窄
• M1a 没有应用 • M1b 非区域淋巴结发生转移,和(或)其它远处转移
• M1a 腹腔动脉淋巴结转移 • M1b 其它远处转移
食管癌TNM分期标准
局部进展期食管癌的综合治疗: 局部进展期(IIB期、III期)食管癌的治疗还有争议,以下结论 源于随机III期临床对比研究的结果: (1)单纯放疗效果不明显,对临床上可手术切除的食管癌患者仍需 选择手术切除。 (2)术前同步化放疗,再做手术切除比单纯手术有明显的生存优势。 (3)同步化放疗中化疗的最佳方案、剂量和给药方法尚不清楚,但 含DDP的联合方案优于单药DDP。 目前推荐: DDP:75mg/m2,d1+5-Fu1000mg/m2,连续静注,d1~4,每4周重复, 2周期化疗,同时放疗50Gy/5周。 含紫衫类或伊立替康的方案在研究中,是否优于DDP和5-Fu的方 案还没有结论。

食管癌英文版

食管癌英文版
手术方式
包括开胸手术、胸腹腔镜联合手术和机器人辅 助手术等,其中开胸手术最为常见。
3
术后恢复
手术后患者需要逐步恢复身体状况,包括呼吸 功能、心肺功能和消化功能等。
放疗和化疗
放疗
放疗可以杀死癌细胞并缓解患者的症状,对于不能手术的患 者,放疗是常用的治疗方法。
化疗
化疗可以通过药物杀死癌细胞,通常与放疗联合应用,对于 晚期食管癌患者,化疗可以提高生活质量并延长生存期。
内镜治疗
01
02
03
适应症
内镜治疗适用于早期食管 癌,尤其是Tis和T1期肿 瘤。
治疗方式
包括内镜下黏膜切除术 (ESD)、内镜下黏膜剥离 术(EMD)和激光治疗等。
优点
内镜治疗对患者损伤较小 ,术后恢复较快,对于早 期食管癌患者,其效果与 手术治疗相似。
04
食管癌的预防
改变生活习惯
健康饮食
增加蔬菜、水果、全谷类 和富含蛋白质食物的摄入 ,减少高盐、高脂、油炸 、霉变食物的摄入。
02
食管癌的诊断
食管癌的症状
早期症状
包括吞咽困难、胸骨后疼痛、烧心等。
中晚期症状
包括体重减轻、乏力、贫血、持续性胸痛等。
食管癌的诊断方法
内镜检查
包括普通白光内镜和色素内镜,可以观察到食管黏膜的病变情况 。
X线钡餐检查
通过吞食含有钡剂的钡条,在X线下观察钡剂通过食管的情况, 可以间接观察食管黏膜的病变情况。
食管癌的发病率和死亡率
食管癌在全球范围内的发病率逐渐上升,尤 其在发展中国家,发病率较高。
食管癌的死亡率也较高,主要与发现时已处 于晚期、治疗不彻底、复发和转移等因素有
关。
食管癌的发病原因和风险因素

dis-base-胸外科-食管癌

dis-base-胸外科-食管癌

【疾病名】食管癌【英文名】esophageal carcinoma【缩写】【别名】膈症;食道癌;噎膈;carcinoma of esophagus【ICD号】C15.9【概述】食管癌是(esophageal carcinoma)人类常见的恶性肿瘤,占食管肿瘤的90%以上,在全部恶性肿瘤死亡回顾调查中仅次于胃癌而居第2位。

据估计全世界每年大约有20万人死于食管癌,是对人民的生命和健康危害极大的最常见的恶性肿瘤之一。

据史书记载,我国早在2000年前即对本病有所描述,称为“噎膈”或“膈症”,并提出多饮酒、饮热酒及高龄等为可能之病因。

域外2世纪时,Calen 医师描述过阻塞食管之新生物。

Czerny于1877年首次成功切除一女性颈部食管癌,食管远端造瘘进食,存活15个月。

随着麻醉技术的发展,Torek于1913年成功地经胸切除中段食管癌。

同年Zaaijer切除下段食管癌,上段食管造瘘,用胶管连接腹部的胃造瘘口进食。

Kummell(1922)和Turner(1933)不开胸经纵隔钝性盲目分离切除食管,用胃上提至颈部行食管胃吻合术。

Lewis(1946)和Tanner(1947)分别报告了经右胸和腹径路切除中三分之一处的食管癌。

1940年吴英恺等在我国首次成功地为一病人切除食管癌并行胸内食管胃吻合术。

新中国成立后,近50年来在我国广大医务人员的积极努力工作下,食管癌的外科治疗工作取得了巨大的进展,县市级医院都能胜任切除手术,高发区少数乡镇医院每年也能手术治疗大量食管癌病人。

术式多样化,食管代用器官以胃为主,少数作者也有习惯用结肠或空肠移植的。

手术适应证逐渐扩大,手术并发症逐渐减少,肿瘤切除率也明显提高,手术死亡率从当年吴英恺创业时的30%以上,下降到目前的3%~4%。

【流行病学】我国是世界上食管癌的高发地区,其死亡率一直位居世界首位。

根据1997年卫生部和全国肿瘤防治研究办公室公布的全国27省、市抽样地区10种常见恶性肿瘤死亡率构成及位次统计资料,中国食管癌世界调整死亡率为20.4/10万,在胃癌、肝癌和肺癌之后居第四位。

食管癌英文版

食管癌英文版
家族聚集性
吸烟
吸烟是食管癌发病的重要环境因素之一,吸烟者的发病风险高于非吸烟者
饮酒
长期大量饮酒可能导致食管黏膜损伤,增加食管癌的发病风险
环境因素
摄入过多热食、硬食、快食等习惯可能增加食管癌的发病风险
饮食习惯
缺乏体育锻炼或运动导致肥胖和消化不良,这些也是食管癌的发病因素之一
运动不足
生活方式因素
营养失衡
放疗
01
放疗是利用放射线治疗食管癌的一种方法,可单独使用或与化疗联合使用。放疗能够缩小肿瘤、缓解症状、延长生存期。
放疗和化疗
化疗
02
化疗是使用化学药物进行治疗的方法,可单独使用或与手术、放疗联合使用。化疗能够有效杀死癌细胞,防止复发,提高患者的生活质量。
放疗和化疗的副作用
03
放疗和化疗在杀死癌细胞的同时也会对正常细胞造成损伤,因此会引起一些副作用,如恶心、呕吐、乏力、骨髓抑制等。
食管癌定义
根据病理学分类,食管癌主要分为鳞状细胞癌和腺癌两种类型。
鳞状细胞癌是食管癌的主要类型,占90%以上,多发生在中老年患者,与吸烟、饮酒、长期食用热食等不良生活习惯密切相关。
腺癌则相对较少见,多发生在食管下段,与胃食管反流、Barrett食管等有关。
食管癌类型
食管癌发病率和死亡率
在我国,食管癌的发病率和死亡率均居恶性肿瘤前列,且呈逐年上升趋势,主要集中在我国东部地区和农村地区。
2023
食管癌英文版
食管癌简介食管癌病因食管癌筛查和预防食管癌治疗食管癌护理和康复食管癌研究展望
contents
目录
01
食管癌简介
食管癌是指发生在食管黏膜上皮的恶性肿瘤,主要与饮食、环境、遗传等多种因素有关。

食管癌

食管癌

Send Orders of Reprints at bspsaif@.ae1292Current Pharmaceutical Design, 2013, 19, 1292-1300MicroRNA in the Pathogenesis and Prognosis of Esophageal CancerJian Gu, Yan Wang and Xifeng Wu*Department of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USAAbstract: Esophageal cancer (EC) is a deadly disease. EC usually occurs as either adenocarcinoma (EAC) or squamous cell carcinomas (ESCC). The development of EAC generally follows the metaplasia-dysplasia-carcinoma sequence. Barrett’s esophagus (BE) is a metas-plastic precursor of E AC. Multiple global miRNA expression profiling and candidate gene studies have been performed in E AC and ESCC that clearly support the important roles of miRNAs in the pathogenesis of EAC and ESCC. A number of consistently dysregulated miRNAs have been identified in E AC and/or E SCC, including upregulation of miR-21, miR-192, miR-194, miR-106-25 polycistron (miR-25, miR-93, and miR-106b), miR-10b, miR-151, and miR-93, and downregulation of miR-375, miR-203, miR-205, miR-145, miR-27b, miR-100, miR-125b, let-7c, etc. Most of these miRNAs are also dysregulated in other cancer types and their target genes have been extensively studied in different cancers. The prognostic value of miR-21 and miR-375 has been replicated in independent studies. Circu-lating miRNAs as potential biomarkers for early detection, prognosis, and treatment response have only been scarcely studied in EC. The association of genetic variations in miRNA regulatory pathway with EC risk or outcome is a largely uncharted territory. Future studies should be focused on the role of miRNAs in the prognosis of EC, the identification of circulating miRNAs and miRNA-related genetic variations as biomarkers in EC, and the biological mechanisms underlying the contribution of miRNA dysreguation to EC. A better un-derstanding of roles of miRNA in EC developemnt may provide new avenues for the early detection, diagnosis, prognosis, and therapy of this deadly disease.Keywords: microRNA, esophageal cancer, Barrett's esophagus, early detection, prognosis, circulating biomarker.INTRODUCTIONEsophageal cancer (EC) is the sixth most common cancer and the fifth leading cause of cancer death in men worldwide [1]. There was an estimated 482,300 new E C cases and 406,800 E C-caused deaths in 2008 worldwide [1]. The majority of EC patients are di-agnosed at advanced stages when current therapies are largely inef-fective, leading to an overall five-year survival rate of 16.8% [2]. This dismal prognosis highlights the need for early detection, better prediction of prognosis and treatment response, and novel therapies of EC. EC usually occurs as either ESCC or EAC. ESCC forms in squamous cells and mostly occurs in the upper third of the esopha-gus. EAC begins in glandular cells and usually forms in the lower one third of the esophagus near the stomach. There is a striking geographic differences in the incidences of these two histologies [3]. Once a rare tumor representing about 5% of E C in the U.S., EAC is the fastest growing cancer in the past few decades and cur-rently accounts for over 80% of new EC cases in the U.S. [4]. The incidence of E AC remains rare in Asian and African countries where ESCC still dominates. The etiology of these two subtypes is very different. Smoking and alcohol drinking are the predominant risk factors for E SCC, whereas E AC is associated with Barrett's esophagus (BE), gastro-esophageal reflux disease (GE RD) and obesity [4]. Smoking also contributes to an increased risk of EAC but its effect is much weaker on EAC than on ESCC, while alcohol drinking is not associated with EAC [3,4].MicroRNAs (miRNAs) are a class of small non-coding endoge-nous RNAs of 18-25 nucleotides highly conserved among a wide variety of species [5,6]. MiRNAs are capable of simultaneous regu-lation of hundreds of genes through binding to the 3'-untranslated region (3’-UTR) of target mRNAs resulting in either mRNA degra-dation or translation inhibition [7,8]. It was estimated that miRNAs may regulate one third to as many as two thirds of human and mammalian genes [9,10]. More than half of miRNA genes are *Address correspondence to this author at the Department of Epidemiology, The University of Texas MD Anderson Cancer Center, 1515 Pressler Blvd., Houston, TX 77030, USA; Tel: 713-745-2485;E-mail: xwu@ located in cancer-associated genomic regions or in fragile sites in human genome [11]. Overexpressed miRNAs in cancers, such as miR-21 and miR-17 92 cluster, may function as oncogenes and promote cancer development by negatively regulating tumor sup-pressor genes, whereas underexpressed miRNAs, such as let-7 fam-ily and miR-34 family miRNAs, may function as tumor suppressor genes by regulating oncogenes [12]. Identification of miRNAs that are altered during the initiation, development, progression, metasta-sis, and treatment of cancer may not only elucidate the mechanisms of carcinogenesis, but also identify biomarkers of early detection, prognosis and treatment response, and as potential targets for pre-vention and therapy. There are a number of advantage for using miRNA as biomarkers: first, a single miRNA may regulate hun-dreds of mRNAs and therefore an array of a few hundreds of miR-NAs may contain much higher information than an array of tens of thousands of mRNAs [13]; second, the total number of miRNAs are much smaller than mRNAs and it is easier to screen and validate biomarkers from a pool of hundreds of miRNAs than thousands of mRNA transcripts; third, miRNAs are small in size, contain stem-loop structure, and are more stable than mRNAs, which makes it special attractive biomarkers formalin-fixed paraffin-embedded (FFPE) tissues and bodily fluids.Many studies using either candidate miRNAs or global profil-ing have been conducted to investigate dysregulation of miRNAs in E C pathogenesis and prognosis and to explore the utilization of miRNAs as biomarkers for E C [14-20]. In this review, we will summarize current literature regarding the multi-faceted roles of miRNAs in EC.MiRNAs IN THE PATHOGENESIS OF ECDysregulation of miRNAs in EAC and its Precursor BE Most EAC cases arise from BE, a precursor lesion in which the squamous epithelium of the esophagus is replaced by a metaplastic columnar epithelium. BE is estimated to be present in 1% to 2% of the general population and confers a 30-fold increased risk of de-veloping EAC. The malignant progression of BE generally follows the sequence of metaplasia, low-grade dysplasia (LGD), high-grade dysplasia (HGD), and adenocarcinoma [21,22]. Clinically, the man-1873-4286/13 $58.00+.00 © 2013 Bentham Science PublishersMicroRNA in the Pathogenesis and Prognosis of Esophageal Cancer Current Pharmaceutical Design, 2013, Vol. 19, No. 7 1293agement of BE is completely dependent on the grading of dysplasia, which is subjective with substantial inter-observer variations. Inde-pendent objective biomarkers may improve the prediction of pro-gression from BE to E AC beyond relying solely on histology. MiRNA is among the most promising biomarkers for this purpose.There have been six miRNA expression profiling of E AC tis-sues and paired normal tissues, most of which also included BE tissues as a comparison (Table 1).Feberet al. [23] compared the expression of 328 human miR-NAs in 10 EAC, 10 ESCC, 5 BE, 1 HGD, and 9 normal squamous epithelium (NSE) tissues. Unsupervised hierarchic clustering showed that miRNA expression profiles could clearly separated disease tissues from NSE tissues. BE and EAC miRNA expression profiles were similar. The single HGD specimen had a miRNA expression profile similar to EAC samples. Thirteen miRNAs were significantly altered in E AC tissues compared to NSE, such as upregulation of miR-21, miR-192, mir-194 and miR-93 and down-regulation of miR-203, miR-205, miR-27b, miR-100, miR-125b, and let-7c. In addition, it appeared that miR-21, miR-194, and miR-192were progressively upregulated from NSE to BE and to EAC, suggesting that miRNA dysfunction is an early event during malig-nant progression of BE and therefore may become valuable bio-markers for malignant progression of the BE patients.In the second study, Yang et al. [24] profiled the expression of 470 human miRNAs in 16 disease tissues (including 5 LGD, 5 HGD, and 6 E AC) and their paired normal tissues. Unsupervised hierarchical clustering and class comparison analyses showed that the miRNA expression profiles clearly separated HGD and E AC tissues from their corresponding paired NSE. Eight miRNAs (miR-27b, miR-203, miR-205, let-7c, miR-342, miR-100, miR-21, and miR125b) were consistent with the previous study of Faber et al.[23] when compared EAC to NSC tissues. This study also identified many miRNA candidates that were dysregulated in HGD, or exhib-ited gradual alteration from NSE to HGD to EAC.A third study profiled miRNAs in one normal esophageal epithelial cells, 3 BE-derived cell lines, and one EAC-derived cell line, followed by the validation of top 7 differentially expressed candidates in 22 NSE, 24 BE, and 22 E AC tissues. Notably, the three members of the miR-106b-25 polycistron (miRs-25, -93, and -106b) on chromosome 7q22.1 were gradually up-regulated from NSE to BE to E AC. Four miRNAs were significantly down-regulated in E AC, including miR-100, miR-125b, miR-205, and miR-19b [25].The fourth study analyzed 377 human miRNAs by Ambion’s miRNA array in NSE of esophagus, normal gastric epithelium, BE, and EAC tissues from 16 individuals [26]. Seven miRNAs (miR-21,Table 1. Summary of miRNA Profiling Studies in Esophageal CancerStudy Array Platform Upregulated miRNAs* Downregulated miRNAs* EACFeber et al. [23] Ambion miR-21, miR-192, mir-194, miR-93, miR-200c miR-203, miR-205, miR-27b, miR-100, miR-125b, let-7cYang et al. [24] Agilent miR-126, mirR-143, miR-145, miR-146a,miR-181a & b, miR-195, and 7 more miR-203, miR-205, miR-27b, miR-99a, miR-149, miR-494, miR-221, miR-210, miR-513, miR-617Kan et al. [25] Agilent miR-93, miR-25, miR-106b miR-205, miR-100, miR-125b, miR-19bWijnhoven et al. [26] Ambion miR-21, miR-194 miR-203, miR-205Mathe et al. [27] Ohio State University miR-21, miR-192, mir-194, miR-223 miR-203EAC vs. BE: miR-145, miR143, miR-215Fassan et al. [28] Ohio State University miR-192, miR-215miR-203, miR-205, let-7cESCCGuo et al. [32] Custom miR-25, miR-151, miR-424 miR-100, miR-99a, miR-29c, mmu-miR-140*Feber et al. [23] Ambion miR-21, miR-93, miR-342 miR-203, miR-205, miR-27b, miR-100,miR-125b, let-7cMathe et al. [27] Ohio State University miR-21 miR-375Lee et al. [33] Ambion miR-330, miR-340, miR-373, let-7dOgawa et al. [34] Applied Biosystem(Taqman gene card) miR-20b, miR-34b, miR-34c, miR-129,miR-130b, miR-138 (>4 fold), miR-21,miR-25, miR-151 and 13 more (2-4 fold)miR-133a, miR-133b,miR-145, miR-139Kano et al. [35] Applied Biosystem(Taqman gene card) miR-203, miR-100, miR-99a, miR-133a & b, miR-145, miR-143, and 7 moreKimura et al. [36] Ambion miR-21miR-205Hong et al. [37] Ohio State University miR-155, miR-100, miR-146, miR-296,miR-10b, miR-203, miR-483, miR-494,miR-220miR-143, miR-375, miR-339 *MiRNAs that are consistent in at least two studies (including candidate gene studies that are not listed in this table) are shown in bold.1294 Current Pharmaceutical Design, 2013, Vol. 19, No. 7 Gu et al.miR-143, miR-145, miR-194, miR-203, miR-205 and miR-215) were chosen for validation using Taqman qRT-PCR in tissues from 32 different individuals. The expression of miR-21, miR-143, miR-145, miR-194 and miR-215 were significantly higher in columnar tissues than in squamous tissues, but the expression of miR-143, miR-145, and miR-215 was lower in EAC than in BE tissues, whereas levels of miR-203 and miR-205 were significantly lower in BE and EAC tissues than in NSE. In addition, there was a trend of progressive increase of miR-21 expression from NSE to BE and to EAC.In the fifth study, Mathe et al. [27] profiled miRNAs in 100 pairs of EAC/normal tissues (32 pairs for screening and 68 for vali-dation) using a miRNA array chip (version 3, Ohio State Univer-sity) containing 329 human and 249 mouse miRNA probes for screening followed by Taqman qRT-PCR to validate selected miR-NAs. The expressions of miR-21, miR-223, miR-192, and miR-194 were upregulated, whereas miR-203 expression was downregulated compared to normal tissues.The most recent profiling study by Fassan et al. [28] used the Ohio State University's miRNA array to profile tissue samples from 14 NSE, 14 Barett’s mucosa (BM), 7 LGD, 5 HGD and 11 EAC. They identified 13 miRNAs as the “progression signature” that were associated with the progression of BE. In the qRT-PCR vali-dation using a series of tissue samples including 15 NSE, 15 BM, 15 LGD, 15 HGD and 15 EAC, 5 miRNAs were consistently dys-regulated during BE progression, including the upregulation of miR-215 and miR-192 and downregulation of miR-205, let-7c and miR-203.In addition to the above 6 array analyses, there were a number of studies that focused on miRNA candidates. For example, Dijckmeester et al. [29] showed that the expression of miR-143 was significantly higher and that of miR-205 was significantly lower in BE than in NSE, consistent with the array analyses. Luthra et al.[30] reported that miR-196a was upregulated in E AC compared to NSE tissues, and Maru et al. [31] further showed that miR-196a expression progressively increased with higher histological grade, suggesting that miR-196a alteration is an early event in carcino-genesis of EAC.From these six independent array analyses and several candi-date gene validation, a number of miRNAs emerged as important players in the pathogenesis of EAC and may become valuable bio-markers of E AC and/or BE. MiR-21, miR-192,miR-194 were the most consistently upregulated miRNAs in EAC, whereas miR-203, miR-205, miR-100, miR-125b, miR-99a,miR-27b and let-7c were consistently downregulated in E AC (Table 1). Furthermore, for miR-21, miR-192, miR-203, miR-205, and let-7c, there appeared to be a gradual increase or decrease of expression from NSE to BE to EAC. For many other miRNAs that were identified in a single pro-filing study with small sample size, they need to be validated in independent studies.Dysregulation of miRNAs in ESCC DevelopmentESCC is the dominant histological subtypes in Far East and all of the published studies evaluating miRNAs in E SCC came from Asia [32-37].Guoet al. [32] published the first miRNA array analysis in ESCC in 31 pairs of ESCC and normal tissues (training set) and 24 paired samples and 1 unpaired ESCC sample (validation set). From a total of 191 evaluable miRNAs, 7 were identified as the best clas-sifier to distinguish E SCC tissues from normal tissues, among which 3 (miR-25, miR-424, and miR-151) were upregulated and 4 (miR-100, miR-99a, miR-29c, and mmu-miR-140*) were downre-gualted in ESCC versus normal tissues.Faberet al. [23] found that miR-21, miR-93, and miR-342 were overexpressed whereas miR-203, miR-205, miR-27b, miR-100, miR-125b, and let-7c were down-regulated in ESCC.In a small study of 5 pairs of ESCC and NSE issues, Lee et al.[33] found four miRNAs, let-7d, miR-330, miR-340, and miR-373, were upregulated by at least 1.5-fold in each of the 5 ESCC tumors. Ogawaet al. [34] quantified the expression of 73 miRNAs by qRT-PCR in 30 E SCC tumor and paired normal tissues. Twenty-one miRNAs were upregulated at least 2-fold, including afore-mentioned miR-21, miR-25, and miR-151; and 4 miRNAs were downregulated at least 2-fold (miR-133a, miR-133b, miR-139, and miR-145) in ESCC.In the study of Mathe et al. [27], 70 pairs of E SCC/NSE (44 pairs for screening and 26 for validation) were queried and the ex-pression of miR-21 was elevated while the expression of miR-375 was reduced [27].Kanoet al. [35] used Taqman human miRNA array to deter-mine the expression of 365 mature human miRNAs in 10 matched pairs of ESCC and NSE and identified 15 downregulated miRNAs in E SCC tissues, which contained 3 (miR-133a, miR-133b, and miR-145) out of the 4 downregulated miRNAs reported by Ogawa et al. [34] and 2 (miR-100 and miR-99a) out of the 4 reported by Guo et al. [32].Of interesting note, Kimura et al [36] recently showed that the expression of miR-205 was high in both malignant and benign squamous epithelia and low in cell lines and tissues other than squamous epithelia, suggesting that miR-205 may be a specific biomarker of squamous epithelia. This observation is in line with the consistent downregulation of miR-205 in EAC tissues compared to normal squamous epithelial tissues [23-26].Finally,Honget al. [37] identified a panel of 12 miRNAs dif-ferentially expressed between E SCC and normal tissues with 9 upregulated (miR-155, miR-100, miR-146, miR-296, miR-10b, miR-203, miR-483, miR-494 and miR-220) and 3 downregulated (miR-143, miR-375 and miR-339) in ESCC.In addition to the above profiling studies, there were also a number of candidate miRNA studies in ESCC. Tian et al. [38] re-ported that miR-10b was upregualted in 95% of ESCC tissues. MiR-17-92 cluster was found to be overexpressed in 75% of ESCC sam-ples [39]. MiR-31 was up-regulated in 78% of the E SCC tissues [40]. MiR-29c level was significantly lower in ESCC tumor tissues and cell lines compared to normal esophageal epithelia [41]. MiR-210 was downregulated in ESCC and derived cell lines, particularly in poorly differentiated carcinomas [42].In summary, the consistently upregulated miRNAs in ESCC (at least in two studies) include miR-21, miR-25,miR-151, and miR-10b, and downregulated miRNAs include miR205, miR-203, miR-145, miR-100, miR-99a, miR-27b, miR-125b, miR-133a,miR-133b, miR-143 and miR-375 (Table 1).MiRNA IN THE PROGNOSIS OF ECA number of recent studies have evaluated miRNAs as prog-nostic factors for EC as summarized in (Table 2), but the results are inconclusive for a number of reasons, including small sample size, tumor heterogeneity, treatment heterogeneity, and different assay methods.Guoet al. showed that high expression of human miR-103 or miR107 (the mature forms of these two miRNAs were nearly iden-tical) was associated with poor overall survival in Chinese E SCC patients in a training set (31 patients) and a testing set (22 patients) [32]. Ogawa et al. found that high expression of miR-129 conferred an 18-fold increased risk of death in 30 surgically treated Japanese E SCC patients (p=0.031) [34]. An additional 19 patients (testing set) was analyzed for independent validation (p=0.011). Mathe et al. showed that higher miR-21 expression in noncancerous tissue of 70 ESCC patients was associated with poor survival; and low levels of miR-375 in 100 EAC tissues were strongly associated with worse prognosis [27]. The prognostic effect of miR-21 has been furtherMicroRNA in the Pathogenesis and Prognosis of Esophageal Cancer Current Pharmaceutical Design, 2013, Vol. 19, No. 7 1295extended to lymph node metastasis in ESCC as shown by two other studies [43,44]. The inverse correlation of miR-375 with poor sur-vival in ESCC was later replicated by Kong et al. [45]. In addition, Nguyen et al. [46] also reported similar prognostic effect of miR-375 in EAC.A number of other miRNAs have also been reported to have prognostic value for ESCC, including miR-143 [43], miR-92a [47], miR-106 and miR-148 [44], miR-223 [48], miR-142-3p [49] and miR-133a [50]. Using a large study population (158 tissue speci-mens, 99 from EAC and 59 from ESCC patients), Hu et al. meas-ured the expression levels of 10 select miRNAs in these tissue specimens by in situ hybridization, which is capable of detect posi-tive signals at the cellular level. Kaplan-Meier analysis showed that miR-16-2 expression and miR-30e expression were associated with shorter survival in all EC patients; in addition, miR-16-2, miR-30e, and miR-200a expression were associated with shorter survival in E AC patients, but not in E SCC patients [51]. From a microarray study, Hong et al. identified that low expression of miR-296 was able to distinguish long-term survivors with node-positive disease from those dying within 20 months with an median survival time advantage of 10.8 months [37]. Feber et al. reported a combined prognostic score composed of five miRNAs (miR-100, miR-143, miR-145, miR-199a-3p, and miR-199a-5p) [52].Hummel et al. also demonstrated an inverse correlation of miR-148 expression with cancer differentiation in EAC [44].Apart from the consistent findings of miR-21 and miR-375, which were associated with poor and good survival, respectively, these mostly scattered, heterogeneous findings reflect the major challenges in clinical outcome study of rare cancers due to diffi-culty in obtaining well-characterized tissue specimens from homo-geneously treated patients. Collaborative efforts from investigators in the E C community are needed to conduct well-designed, suffi-ciently powered studies to identify miRNAs as biomarkers for the prognosis and treatment response of EC.Table 2. Summary of Studies Focusing on Prognostic Functions of miRNAs in Esophageal CancerStudy SampleSizeHistology MiRNA Prognosis Guo et al. (2008) [32] 53 ESCC miR-103/107 Poor survivalMathe et al. (2009) [27] 70 ESCC miR-21 Poor survival100E ACmiR-375 Good survivalOgawa et al. (2009) [34] 49 ESCC miR-129 Poor survivalHong et al. (2010) [37] 10 ESCC miR-296 Poor survivalNguyen et al. (2010) [46] 103 EAC miR-375 Good survivalAkagi et al. (2011) [43] 55 ESCC miR-21, miR-205 Lymph node positivity55E SCCmiR-143, miR-145 Recurrence of metastasisFeber et al. (2011) [52] 45 EAC miR-100, miR-143, miR-145, miR-199a-3p, miR-199a-5pPoor survival45E ACmiR-99b, miR-199a-3p, miR-199a-5pLymph node metastasisChen et al. (2011) [47] 107 ESCC miR-92a Poor survival, lymph node metastasis and TNMstagingHamano et al. (2011) [113] 98E SCCmiR-200c Induces chemoresistanceHu et al. (2011) [51] 158 EC miR-16-2, miR-30e Poor survival99E ACmiR-16-2, miR-30e, miR-200a Poor survivalHummel et al. (2011) [44] 21 ESCC miR-21 Lymph node metastasis21E SCCmiR-106, miR-148 Associated with lower rate of tumor-related deathand recurrence22E ACmiR-148 Inversely correlated with cancer differentiation Kong et al. (2012) [45] 60 ESCC miR-375 Inversely correlated with advanced stage, metastasis,poor overall survival and disease-free survival, nega-tively correlated with IGF1R expressionKurashige et al. (2012) [48] 109E SCCmiR-223 Poor prognosis, correlated with ubiquitin ligaseFBXW7Lin et al. (2012) [49] 91 ESCC miR-142-3p Poor prognosisSuzuki1et al. (2012) [50] 102 ESCC miR-133a Inversely correlated with CD47, an independentprognostic marker for lymph node metastasis*MiRNAs that are consistent in at least two studies are shown in bold.1296 Current Pharmaceutical Design, 2013, Vol. 19, No. 7 Gu et al.MOLECULAR MECHANISMS OF MiRNAs IN EC One of the most challenging questions in miRNA research is the identification and experimental validation of miRNA targets, more importantly, the mechanistic elucidation of physiological and pathological roles of the specific miRNA and target gene. It is well known that each miRNA can target hundreds of genes, and the same mRNA can be targeted by multiple miRNAs. The currently available target prediction programs often produce hundreds of potential target genes due to imperfect complementarity between miRNA and its target, which makes experimental validation ex-tremely important. Most of the dysregulated miRNAs, such as miR-21, miR-205, miR-203, miR-375, are also dysregulated in other cancers and there were extensive functional studies in E C and/or other cancers for a number of these miRNAs. Here, we summarize the functional studies of oncogenic miRNAs and tumor suppressor miRNAs in EC (Table 3).MiRNAs Acting as OncogenesMiR-21MiR-21 is the most commonly upregulated miRNA in human cancers that exhibits the most consistent association with both EAC and ESCC development as well as the prognosis of ESCC. MiR-21 regulates a plethora of target genes that are involved in cellular survival, apoptosis and cell invasiveness, including a number of tumor-suppressor genes such as tropomyosin-1 (TPM1), PTEN, maspin, and programmed cell death 4 (PDCD4) [53]. Hiyoshi et al.[54] showed that the protein level of PDCD4 (tumor suppressor) in ESCC cells had an inverse correlation with miR-21 expression.MiR-106-25 PolycistronM iR-106-25 polycistronic miRNA cluster is located at chromo-some 7q22.1 and encodes three miRNAs, miR-25, miR-93, and miR-106b. M iR-106-25 was upregulated progressively from NSE, to BE, and to EAC [25]. MiR-106b-25 polycistron exhibited poten-tial proliferative, anti-apoptotic, cell cycle-promoting effects in vitro and tumorigenic activity in vivo [25]. MiR-93 and miR-106b targeted tumor suppressor gene p21 via mRNA degradation, whereas miR-25 targeted Bim(Bcl-2 interacting mediator of cell death) via translational inhibition in EAC [25]. Most recently, Xu et al. [55] demonstrated that miR-25 promotes E SCC cell migration and invasion by directly targeting the 3' UTR of E-cadherin gene (CDH1) and inhibited the expression of CDH1, providing another mechanism of the ongenic activity of miR-25.MiR-17-92 PolycistronMiR-17-92 cluster, also designated as oncomir-1, is one of the best-characterized oncogenic miRNAs [56,57]. The gene is located at 13q31.3, encodes six mature miRNAs: miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92-1, and has been implicated in the oncogenesis of multiple cancers [56,57]. One study showed that miR-17-92 cluster was overexpressed 75% of E SCC tumors [39]. Furthermore, overexpression of the miR-17-92 cluster could promote cellular growth in vitro and in vivo, and inhibition of miR-19a induced apoptosis in vitro and impaired tumor growth in vivoTable 3. MiRNAs with Validated Targets in ECmiRNA Histology Validated targets [references] Function OncogenicmiR-21E SCCPDCD4[54] Cellproliferation,Migration miR-106b EAC P21 [25] Cell cycle control, ApoptosismiR-93 EAC P21 [25] Cell cycle control, ApoptosismiR-25 EAC Bim [25], CDH1 [55] Cell cycle control, ApoptosismiR-19aE SCCTNF- [39]Tumor growth, Apoptosis miR-92aE SCCCDH1[58] Migration/InvasionmiR-10bE SCCKLF4[38] Migration/InvasionmiR-196aE ACANXA1 [30], SPRR2C, S100A9, KRT5 [31] Cell proliferation, Apoptosis miR-31 ESCC EMP1, KSR2, RGS4 [40] Colony formation, Migration/invasion miR-373E SCCLATS2[33] CellproliferationTumor SuppressormiR-375 ESCC PDK1 [71], IGF1R [45] Tumorigenesis, Migration, Metastasis miR-205E SCCZE B2[76] Migration/InvasionmiR-145 ESCC FSCN1 [35] Cell proliferation, InvasionmiR-203 ESCC Np63 [85] Cell proliferation miR-133a & b ESCC FSCN1 [35] Cell proliferation, Invasion miR-29c ESCC CCNE [41] Cell cycle control, Cell proliferation miR-210 ESCC FGFRL1 [42] Cell cycle control, Cell proliferationMicroRNA in the Pathogenesis and Prognosis of Esophageal Cancer Current Pharmaceutical Design, 2013, Vol. 19, No. 7 1297[39]. TNF- (tumor necrosis factor- ) was confirmed as a direct target of miR-19a [39]. In another study, miR-92a was found to modulate the migration and invasion but not apoptosis and prolif-eration of E SCC cells in vitro. In addition, miR-92a directly tar-geted the CDH1 and repressed the expression of CDH1 [58]MiR-10bMiR-10b is overexpressed in several types of cancer [59-62] including ESCC [38]. MiR-10b was the first miRNA found to affect invasion and metastasis of human cancer (breast cancer) [63]. Simi-larly, Tian et al. [38] found that cellular miR-10b expression level correlated with cell motility and invasiveness in several human E SCC cell lines. Additionally, they identified KLF4 (Krüppel-like factor 4), a known tumor suppressor gene that has been reported to suppress esophageal cancer cell migration and invasion, as a direct target of miR-10b. KLF4 regulates the expression level of p21 and mediates p53-dependent G1/S cell cycle arrest in response to DNA damage [64]. The oncogenic function of miR-10b is at least par-tially mediated by KLF4 in ESCC.MiR-196aMiR-196a is overexpressed in several types of cancer and pre-malignant esophageal tissues [31,65-67]. Luthra et al. [30] showed that miR-196a targets Annexin A1 (ANXA1), which is a critical mediator of apoptosis and is frequently suppressed or lost in E C [68-70]. MiR-196a promotes cell proliferation and anchorage-independent growth and suppresses apoptosis, which may be par-tially explained by its targeting of ANXA1 [30]. Maru et al. [31] further identified a few additional target genes of miR-196a, includ-ing KRT5 (keratin 5), SPRR2C (small proline-rich protein 2C), and S100A9 (S100 calcium-binding protein A9), all of which are down-regulated during BE progression.Two other potential oncogenic miRNAs and their validated targets have been reported in E SCC: miR-31 targets three tumor suppressor genes, EMP1 (epithelial membrane protein 1), KSR2 (kinase suppressor of Ras 2) and RGS4 (regulator of G-protein sig-naling 4) [40]; and miR-373 targets LATS2 (large tumor suppressor 2) [33].Tumor Suppressor miRNAs in ECMiR-375The promoter of miR-375 was frequently hypermethylated in E C and miR-375 is a negative regulator of 3-phosphoinositide-dependent protein kinase-1 (PDK1) in EC [71]. Frequent promoter hypermethylation of miR-375 was also found in ESCC tissues [45]. MiR-375 also inhibits clonogenicity, cell motility, cell proliferation, tumor formation and metastasis in mice. Furthermore, miR-375 could interact with the 3'-untranslated region of IGF1R and down-regulate its expression in vitro and the expression of IGF1R was also negatively correlated with miR-375 expression in clinical sam-ples [45]. These studies provide compelling evidence supporting that the downregulation of miR-375, through promoter hypermethy-lation, is one of the molecular mechanisms involved in the devel-opment and progression of ESCC.MiR-205MiR-205 is downregulated in many different cancers [72-75]. MiR-205 plays an important role in the regulation of epithelial-to-mesenchymal transition (EMT), a process critical to tumor progres-sion and metastasis. EMT is characterized by the loss of E-cadherin and reduction of cell locomotion and invasion. Matsushima et al.[76] showed that knockdown of miR-205 expression in ESCC cells substantially increased the expression of zinc finger E-box binding homeobox 2 (ZEB2), accompanied by reduction of E-cadherin, supporting that miR-205 exerts tumor-suppressive activities with EMT inhibition by targeting ZEB2 in ESCC. MiR-145MiR-145 is downregulated in many cancers [77] and precancer-ous lesions [78,79]. A plethora of target genes of miR-145 have been experimentally validated [80-83]. In particular, Sachdeva et al.[82] showed that c-Myc is a direct target for miR-145.MiR-145 is induced by the tumor suppressor p53 transcriptionally. Therefore, miR-145 provides a direct link between p53 and c-Myc. Loss of heterogeneity (LOH) of 17p13 (p53 locus) and amplification of 8q24 (Myc locus) are both frequent molecular alterations in ESCC and EAC, suggesting that miR-145 may exhibit its tumor suppressor function in E C through the p53-Myc network. However, there has not been direct evidence showing miR-145 inhibits c-Myc in E C. On the other hand, Kano et al. [35] identified a novel target gene, FSCN1 (actin-binding protein, Fascin homolog 1), for miR-145. FSCN1 was overexpressed in E SCC tumors compared to normal epithelium, and FSCN1 overexpression was significantly associated with the extent of the tumor, lymph node metastasis, and poor prognosis [84]. These data suggest inhibition of FSCN1 may be one of the mechanisms for the tumor suppressor function of miR-145 in ESCC.Other potential tumor suppressor miRNAs and their validated targets include: miR-203 targets DeltaNp63 ( Np63), an alternative splice variant of p63 gene that has oncogenic function [85]; miR-133a and miR-133b target FSCN1 [35]; miR-29c induces cell cycle arrest by targeting CCNE (cyclin E) [41]; and miR-210 targets FGFRL1 (fibroblast growth factor receptor-like 1), an accelerator of cell proliferation [42].CIRCULATING MIRNAS AND ESOPHAGEAL CANCER Alterations of circulating miRNA expression profiles are poten-tially indicative of physiological and pathological changes. There has been great interest in the identification of circulating miRNA as a blood-based minimally invasive biomarker for early detection and prognosis of cancer since Mitchell et al. [86] reported that tumor-derived miRNA in human plasma exists in a remarkably stable form. Compared to extensive studies of circulating miRNAs in other cancer types [87-103], to date, systematic investigations of circulating miRNAs in EC were scarce and limited to ESCC. Using a two-phase study design, Zhang et al. [104] compared pooled se-rum samples by Solexa sequencing and identified 25 candidate miRNAs aberrantly expressed between samples of E SCC patients and normal subjects, which were then subjected to individual qRT-PCR validation. A panel of 7 serum miRNAs (miR-10a, miR-22, miR-100, miR-127-3p, miR-133a, miR-148b, and miR-223) was identified as potential biomarker for E SCC. Several other studies used candidate gene approach to evaluate specific circulating miR-NAs in E SCC. By comparing miRNA expression levels between tumor and adjacent normal tissues, as well as between serum sam-ples of patients and normal controls, a Chinese group reported that miR-31 is upregulated in ESCC tumor tissue and in serum of patient samples [40]. The same group also reported that miR-1322 was upregulated in both E SCC tissues and patients' serum samples [105]. Komatsu et al. [106] focused on previously reported onco-genic miR-21, miR-184 and miR-221, tumor suppressive miR-375 and confirmed the upregulation of miR-21 and downregulation of miR-375 in plasma samples of ESCC patients compared to normal subjects, and further suggested that the ratio of plasma levels of miR-21 to miR-375 was a better diagnostic marker than either markers alone. Moreover, the same Japanese group also evaluated the prognostic value of miR-21 and miR-375 and reported that high plasma level of miR-21 is correlated with higher risk of recurrence and poorer survival whereas high plasma level of miR-375 is in-dicative of better survival [106,107].。

食管癌本科-英语-精品医学课件

食管癌本科-英语-精品医学课件

Incidence
➢ The incidence of esophageal cancer ranked fifth in all cancer sites in China.
➢ Males are more than females.
➢ More likely occurred in middle and lower thoracic esophagus .
recurrent laryngeal nerves) ➢ Aspiration/cough/recurrent pneumonia ➢ Hematemesis
Diagnosis
If you have symptoms that may signal esophageal cancer, your doctor will examine you and ask you questions about your health; your lifestyle, including smoking and drinking habits; and your family medical history.
One or more of the following tests may be used to find out if you have esophageal cancer and if it has spread. These tests also may be used to find out if treatment is working.
➢ Esophageal pathology and the imaging performance of esophageal cancer
Content
✓ Definition ✓ Epidemiology ✓ Classification ✓ Signs and symptoms ✓ Diagnosis and differential diagnosis ✓ Treatment

res-base-普通外科-食管癌

res-base-普通外科-食管癌

【疾病名】食管癌【英文名】esophageal carcinoma【别名】膈症;食道癌;噎膈;carcinoma of esophagus【ICD号】C15【病因和发病机制研究的进展】1.病因研究进展 动植物中广泛存在着一大类小的非编码蛋白质的RNA,21-25个核苷酸长度,被命名为micro RNA(miRNA)。

miRNA在物种进化中相当保守,其表达有组织特异性和时序特异性。

其功能为负调控基因表达,进而调节细胞的代谢、增殖、分化和凋亡等基本的生理过程。

因此,miRNA的改变必会导致一些严重的病理过程。

研究已证实miRNA在肿瘤的发生和发展起着癌基因或抑癌基因的作用,miRNA的表达谱可用于某些肿瘤的诊断、分期和判断预后,并且在肿瘤分类方面较mRNA有更大的优越性。

食管癌变是多种因素综合作用,多基因变化先后积累或叠加形成的。

研究证实,其发生与Rb、P53等抑癌基因失活,以及环境等多因素使原癌基因H-ras、c-myc和hsl-1等激活有关,最近又在食管鳞状细胞癌中发现了1种新的癌基因GAEC1。

而miRNA作为继蛋白质之后又一高效的基因表达调控因子,并已证实在多种肿瘤的发生发展中有重要作用。

综合以上考虑,miRNA极大可能在食管癌中有更大的作用空间。

国内一项研究利用基因芯片技术,通过癌组织及癌旁正常组织的横向比较找出癌组织中特异表达的miRNA,并对各期进行纵向比较,找出肿瘤各期miRNA差异,从而完成对食管癌的诊断和分期,然后定量分析,如特异性miRNA为高表达,则有癌基因作用,如为低或无表达,则有抑癌基因的作用,进而在基因水平上通过RNAi,反义核苷酸方法对食管癌进行生物治疗,使表达异常的基因或蛋白质恢复正常。

目前存在的最大问题就是,要确定有癌基因或抑癌基因作用的miRNA的靶蛋白或其靶基因,从而指导基因治疗,并期望为肿瘤的筛查提供新的更加简便和特异的手段。

然而研究发现,同一个miRNA在对某一基因调控时,可通过参与不同的信号路径,或同一信号路径的不同环节来完成,即在不同种类的肿瘤中对靶基因的调节方式有很大差异,从而为研究带来困难,但也有利于基因治疗,因为期望的治疗工具应有高度特异性,而不是广泛的起作用。

食管癌(英文版)

食管癌(英文版)

Enhanced scanning
3. MR
The high signal fat layer exist.
There is a synechia(黏连) between the cancer and the aortic arch.
Cancer invade the trachea
T2WI:The fat layer disappeared and the wall of trachea be damaged.
ห้องสมุดไป่ตู้
Clinical feature
In the middle and advanced stage
Progressive dysphagia (进行性吞咽困难) When the tumor invade the trachea , tracheoesophageal fistula(气管食管瘘) Cachexia(恶病质)
• First: The junction of the pharynx(咽) and esophagus. • Second: located in the back of left principal bronchus. • Third: Esophageal hiatus(食管裂孔).
3 Sections of the esophagus
• The upper segment
Tracheal bifurcation (气管分叉)
• The middle segment
(Carcinoma occur most frequent)
• The lower segment
Summary
• Carcinoma of the esophagus is a common malignant tumor that occurs in a population cover 40 years old ,and in predilection for male(好发于男性).
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Power Bar niche
中国专业PPT设计交流论坛

The surrounding of the
tumor become bulged ,
and the folds of mucous
become damaged. (周围隆
起,粘膜皱襞破坏)
b .Mushroom type
Filling defect
中国专业PPT设计交流论坛
Power Bar
Early 中国专业PPT设计交流论坛 ulcerative type
Power Bar
中国专业PPT设计交流论坛
Early constrictive type
(2). Middle and advanced stage
• a. Ulcerative type(溃疡型)
Prevalence and mortality
• There are more than 300,000 people
worldwide died frPoomweesroBpahrageal cancer
each year , and 150,000 of 中国专业PPT设计交流论坛 them are Chinese.
Power BarAn 中国专业PPT设计交流论坛 expand over
the tumor
• c . Constrictive type
Pathogeny
• 1. Nitrosamine(亚硝胺)
• 2. Fungus(真菌) Power Bar 中国专业PPT设计交流论坛
• 3. Vitamin deficiency • 4. Dietary habits
Clinical feature
• In early stage
Symptoms are oPftoewnenroBtaorbvious, but 中国专业PPT设计交流论坛
the throat
and stomach.
Physiological stenosis of
esophagus
• First: The junction of the pharynx(咽) and
esophagus. Power Bar
中国专业PPT设计交流论坛
• Second: located in the back of left principal bronchus.
when swallowing the coarse food ,different degrees of uncomfortable feelings may occur.
Clinical feature
In the middle andPaodwvearnBcaerd stage
Progressive dys中p国h专业aPgPTi设a计交流(进论坛行性吞咽困难) When the tumor invade the trachea ,
1. X-ray barium meal
• (1). Early stage
➢Esophageal mucPoosawleforldBsabre beak(粘膜迂曲
、断裂)
中国专业PPT设计交流论坛
➢Single or multiple small niches(龛影)
➢Limiting filling defect(局限性充盈缺损)
Tracheal
bifurcation (气管分叉)
• The lower segment
Summary
• Carcinoma of the esophagus is a common
malignant tumor Pthoawt eorcBcuarrs in a
population cover 40 years old 中国专业PPT设计交流论坛 ,and in predilection for male(好发于男性).
Carcinoma of Esophagus
Power Bar
中国专业PPT设计交流论坛
Speaker:LiuRan
Content
• Anatomy of the Esophagus
• Summary
Power Bar
中国专业PPT设计交流论坛
• Pathogeny(发病机制)
• Clinical feature
➢Barium stream slow or temporary residence( 钡剂流动缓慢或一过性滞留)
Power BarPostoperation
中国专业PPT设计交流论坛
Recur
Power Bar
Small 中国专业PPT设计交流论坛 nodules(小结节)
PowperrotBraurde type(隆起型)
tracheoesophageal fistula(气管食管瘘) Cachexia(恶病质)
Classification of
esophageal cancer
• 1. Ulcerative type(溃疡型)
• 2. Mushroom typPeo(蕈we伞r 型Ba)r 中国专业PPT设计交流论坛
• 3. Constrictive type(缩窄型)
• 4. Medullary type(髓质型)
Diagnose
• 1. X-ray barium meal
• 2. Computed TomPowgrearpBhayr(CT) 中国专业PPT设计交流论坛
• 3. Magnetic Resonance Imaging(MR)
• Third: Esophageal hiatus(食管裂孔).
3 Sections of the esophagus
• The upper segment
Power Bar
中国专业PPT设计交流论坛
• The middle segment
(Carcinoma occur most frequent)
• Diagnose
• Differential diagnosis
ห้องสมุดไป่ตู้• Exercise
Anatomy of the Esophagus
• The esophagus is a muscular tube, which
is a digestive orgaPnower Bar
between
中国专业PPT设计交流论坛
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