Gastrointestinal stromal tumor of duodenum： a cause of upper gastrointestinal hemorrhage

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维生素D的功用

维生素D或可破解肿瘤耐药难题精选已有419次阅读2014-10-105:55|个人分类:自然科学|系统分类:海外观察维生素D为固醇类衍生物，又称抗佝偻病维生素，也是一种类固醇激素，维生素D家族成员中最重要的成员是麦角钙化醇和胆钙化醇。

早在1824年，就有人发现鱼肝油可在治疗佝偻病中起重要作用。

1918年，英国的梅兰比爵士证实佝偻病是一种营养缺乏症。

但他误认为是缺乏维生素A所致。

1930年Gottingen大学的A.Windaus 教授首先确定了维生素D的化学结构，1932年经过紫外线照射麦角固醇而得到的维生素D2的化学特性被阐明。

维生素D3的化学特性直到1936年才被确定。

最近许多研究表明，维生素D参与机体炎症免疫调节。

胰腺癌是癌症之王，是因为这是一种恶性程度很高，诊断和治疗都很困难的消化道恶性肿瘤，5年生存率<1%，是预后最差的恶性肿瘤之一。

其发病率和死亡率近年来明显上升。

胰腺癌90%为起源于腺管上皮的导管腺癌。

胰腺癌早期的确诊率不高，手术死亡率较高，治愈率非常低。

一些世界知名的人物如苹果公司创始人乔布斯和电影《人鬼情未了》男主演帕特里克都是死于这一疾病。

根据美国国NIH 的统计，美国每年有大约4.6万新确诊患者，大约4万人死于胰腺癌。

来自Salk研究所的研究人员Ronald Evans等证实，一种维生素D衍生物可以瓦解保护胰腺肿瘤的细胞屏障，使得这一坚不可摧的癌症对药物更敏感。

这一研究结果发表在最新《细胞》杂志上，这一研究给胰腺癌患者带来了新的希望。

这种维生素D衍生物能阻止纤维化过程，对于肺癌、肾癌和肝癌等一些难治性肿瘤可能也具有重要参考意义。

虽然目前并没有临床研究，但动物实验结果取得的效果非常显著，令人鼓舞，研究人员现在已经对这一手段开展的临床研究。

胰腺癌的5年生存率是所有癌症中最低，根本原因是胰腺癌容易发生耐药，但人们一直不清楚导致耐药的内在原因，更没有克服这种难题的方法。

这一研究的重要性正是因为找到一种克服肿瘤耐药的手段。

【疾病名】十二指肠腺癌【英文名】ADENOCARCINOMAO

【疾病名】十二指肠腺癌【英文名】adenocarcinoma of duodenum【缩写】【别名】adenocarcinoma of dodecadactylon；adenocarcinoma of zwolffingerdarm【ICD号】C17.0【概述】十二指肠腺癌(adenocarcinoma of duodenum)是指起源于十二指肠黏膜的腺癌。

多为单发，可由腺瘤恶变而来。

组织学上可见腺瘤-腺癌转化及腺癌中的残存腺瘤组织。

因此，腺瘤可以认为是腺瘤可以认为是腺癌的癌前病变。

【流行病学】国外文献报道十二指肠腺癌的发病率占全消化道恶性肿瘤的1%偏低，占十二指肠恶性肿瘤的80%。

国内报道本病占全消化道肿瘤的0.3%，占小肠恶性肿瘤的25%～45%，占十二指肠恶性肿瘤的65%左右。

好发于50～70岁，男性稍多于女性。

中南大学湘雅第二医院病历资料，近10年来仅发现十二指肠腺癌18例，约占同期十二指肠恶性肿瘤的70%。

【病因】目前对十二指肠腺癌的病因不甚清楚。

胆汁和胰液分泌的某些物质，如石胆酸等二级胆酸可能是致癌原，对肿瘤的形成起促进作用。

家族性息肉病、Gardner和Turcot综合征、von Reeklinghausen综合征、Lynch综合征、良性上皮肿瘤如绒毛状腺瘤等疾病，可能与十二指肠腺癌的发生有关。

另有报道十二指肠溃疡或憩室的恶变以及遗传等因素亦与十二指肠腺癌有一定关系。

【发病机制】1.好发部位十二指肠腺癌在多发生于降部乳头周围，约占60%，其次为壶腹下段，球部最少见。

2.病理形态(1)大体形态：十二指肠腺癌大体形态可分为息肉型、溃疡型、环状溃疡型和弥漫浸润型。

其中息肉型最多见，约占60%，溃疡型次之。

(2)组织形态：镜下见十二指肠腺癌多属乳头状腺癌或管状腺癌，位于十二指肠乳头附近以息肉型乳头状腺癌居多，其他部位多为管状腺癌，呈溃疡型或环状溃疡型，溃疡病灶横向扩展可致十二指肠环形狭窄(图1)。

(整理)消化病学常见英文词汇

消化病学常见英文词汇1．digestive endoscope消化内镜2. digest 消化3.Gastric mucosa 胃粘膜4.Helicopbacter pylori 幽门螺杆菌5.gastric pits 胃小凹6.gullet 食管7.Castroesophageal Reflux Disease(GERD) 胃食管反流病8.Barrett’s esophagus，Barrett食管9.lower esophageal sphincter 食管下括约肌10.reflux esophagitis 反流性食管炎11.lower esophageal sphincter LES 下食管括约肌12.non-erosive reflux disease（NERD）非糜烂性反流病13.oesophagoscopy 食管镜检查14.Hiatal Hernia, 食管裂孔疝15.oesophagoscope 食管镜,食道镜16.transient lower esophageal sphincter relaxatio n 一过性食管下括约肌松弛17.leiomyoma of esophagus.食管平滑肌瘤18.Esophageal Cancer 食管癌19..corrosive burn of esophagus腐蚀性食管灼伤20.achalasia of cardia 贲门失驰症21.stomach 胃.22.gastritis胃炎23.pangastritis 全胃炎24.acute hemorrhagic gastritis 急性出血性胃炎25 Chronic gastritis慢性胃炎26.Chronic atrophic gastritis 慢性萎缩性胃炎27.27.autoimmune gastritis 自身免疫性胃炎28.Chronic superficial gastritis 慢性浅表性胃炎29.29.superficial gastirtis 弥漫性胃窦炎30.Functional gastrointestinal disorder 功能性胃肠病30.31.functional dyspepsia 功能性消化不良32.multi-focal atrophic gastritis多灶萎缩性胃炎33.dysplasia 异型增生34.parietal cell autoantibody 壁细胞自体抗体35.intrinsic factor antibody,IFA 内因子抗体36.intestinal metaplasia of gastric epithelium 胃粘膜肠上皮化生37.Peptic Ulcer Disease (PUD), 消化性溃疡病38.ZollingerEllison syndrome 胃泌素瘤.39.kissing ulcer 对吻溃疡40.acute stress ulcer 急性应激性溃疡41.Gastrointestinal mucosa-associated lymphoid tissue lymphoma 胃粘膜相关淋巴组织淋巴瘤42.Stomach cancer 胃癌43.gastric bleeding 胃出血44.gastric canal 胃管45.gastric juice 胃液46.gaseous distention 胃胀气47.hematemesis 呕血48.gastralgia 胃痛49.gastroenteritis 胃肠炎50.Gastric Acid胃酸51.achlorhydria胃酸缺乏症52.gastrospasm 胃痉挛53.intestine肠54.tuberculose intestinale 肠结核55.Appendicitis 大腸炎56.tuberculated peritonitis结核性腹膜炎57.Intussusception 肠套叠58.Volvulus 盲腸炎59.intestinal cancer肠癌60 ileus.肠闭塞61.Enterovirus肠病毒62.intestinal hemorrhage肠出血63.63．intestinal perforation肠穿孔64.64.intestinal obstruction肠梗阻65.65.intestinal colic 肠绞痛66.66.inflammatory bowel disease 炎症性肠病67.67.Regional Enteritis (Crohn)克隆氏病68.68.Ulceratie Colitis, 溃疡性结肠炎69.69.Dierticular Disease, 肠憩室疾病70.70.carcinoid of large intestine 大肠类癌71.71.colorectal lymphoma 大肠恶性淋巴瘤72.72.Polyposis 息肉病73.family polyposis coli 家族性结肠息肉病74.irritable bowel syndrome 肠易激综合征75.肠道细菌移位76.enteral nutrition肠道营养，77.arteriovenous malformation of bowel肠动静脉畸形78.肠囊肿79.radiation injury of intestine肠放射性损伤80.end-to-side intestinal anastomosis 肠端侧吻合术81.肠扭转82.end-to-肠端端吻合术82.肠紊乱，83.intestinal lymphangiectasia肠淋巴管扩张84 intestinal bypass肠旁路术85.肠内引流式胰腺移植enteric drainage pancreas transplantation86肠袢淤滞综合征stagnant loop syndrome87.肠切除术88.肠切开术89.肠缺血90.肠缺血综合征91.肠外瘘enterocutan92.肠外营养93.肠外置术94.肠吻合术95.肠系膜动脉闭mesenteric arterial occlusion96.肠系膜动脉栓塞术97.肠系膜动脉血栓形成98.肠系膜静脉血栓形99.肠系膜囊肿100.肠系膜疝101.肠系膜上动脉综合征102肠系膜上动脉压迫综合征103.肠狭窄104.104肠旋转不良malr105.肠血管病vascular disease of bowel106.106.肠血管发育异107.107.肠血管异常108.108.肠易激综合征109.109.肠源性感染110.110.肠造口术111.肠胀气112.112.肠重复畸形duplication of intestine113.肠子宫内膜异位114.乙状结肠膀胱sigmoid conduit114.乙状结肠膀胱扩大sigmoid augmentation cystoplasty116.乙状结肠结核117.乙状结肠镜检查［术］118.回肠膀胱扩大术ileum augmentation cystoplasty119.回肠膀胱尿流改道术120.回肠膀胱术121.回肠肛管吻合术ileoanal anastomosis 122.回肠横结肠吻合术123.回肠憩室124.回肠造口术125.回盲部结核ileocecal tuberculos126.直肠膀胱一结肠腹壁造口术rectal bladder and abdominal colostomy 127.直肠固定术proctopexy，128.直肠后脓肿129.直肠后拖也吻合巨结肠根治术duhamel 130.直肠环钳吻合术ring clamp anastomosis of rectum131.直肠肌鞘拖出吻合巨结肠根治术132直肠镜检查［术］133.直肠瘘134.直肠膨出135.直肠切除术136.直肠烧灼137.直肠损伤138.直肠脱垂139.直肠狭窄140,直肠炎141.直肠乙状结肠镜检查［术］p142.直肠阴道瘘143.直肠指检144.直肠周围脓肿145.直视下活检［术］145.肛管癌146.肛裂anal fissure，147.肛门闭锁会阴瘘148.肛门闭锁尿道瘘anal atresia149.肛门闭锁前庭瘘150.肛门闭锁阴道瘘151.肛门镜152.肛门镜检查［术］153.肛门溃疡154.肛门瘙痒［症］155.肛门狭窄an156.肛门直肠瘘157.肛门直肠脓肿158.肛乳头炎anal papillitis 159.肛周脓肿，160.肝脏liver 161肝癌liver cancer 162.阑尾Appendicitis, 163.肝性脑病Hepatic encephalopathy 164.肝昏迷hepatic coma165.原发性肝癌primary carcinoma of the liver.166.病毒性肝炎virus hepatitis 167.传染性肝炎infectious hepatitis 168.急性病毒性肝炎acute viral hepatitis 169.慢性腹泻chronic diarrhea 170.酒精性肝病alcoholic lier171.自身免疫性肝炎autoimmune hepatitis 172.肝硬化cirrhosis of lier 173.腹膜炎Peritonitis, 174.干呕175.肝［性］昏迷前期176.肝被膜下出血subcapsular177.肝病性口臭178.肝肠联合移植combined liver and intestin179.肝大180肝淀粉样变性181.肝动脉造影［术］182.肝梗死183.肝结核184.肝静脉梗阻185.肝慢性阻性充血chronic passiveconge186.肝毛细线虫病capillariasis hepatica187.肝门肠吻合术portoenterostomy 188.肝内胆管结石189.肝内胆管结石病190.肝内胆汁淤积191.肝脓肿liver absces 192.肝脾大hepatosp193.肝片吸虫病194.肝肾联合移植combined liver and kidney195.肝肾综合征196.肝素辅因子heparin co-197.肝细胞移植198.肝下垂hepatoptosis 199.上消化道出血upper gastrointestinal hemorrhage200.壁细胞parietal cell 201.质子泵proton pump 202, 痔疮Hemorrhoids203.gall bladder 胆囊.pancreas 胰腺204.内镜逆行胰胆管造影endoscopic retrograde cholangiopancreatography ,ERCP 205.胆石症/胆囊炎Cholelithiasis/Cholecystitis 206.急性胰腺炎Acute Pancreatitis, 207.胰腺癌carcinoma of the Pancreatitis208.胰空肠吻合术pancreaticojejunostomy 209.胰瘘pancreatic fistula210.胰肾联合移植combined pancreas and renal transplantation211.胰十二指肠切除术pancreaticoduodenectomy212.胰十二指肠移植术pancreas-duodenal transplantation213.胰石pancreatolith，pancreatic calculus214.胰石病pancreatolithiasis215.胰腺创伤pancreatic trauma216.胰腺分裂pancreas divisum217.胰腺钙化calcification of pancreas218.胰腺假囊肿 pancreatic pseudocyst 219.胰腺囊肿 pancreatic cyst220.胰腺脓肿 abscess of pancreas 221.胰腺外瘘 external fistula of pancreas 222.胰腺炎 pancreatitis 223.胰腺移植 pancreas transplantation 224.胰腺异位 heterotopic pancreas 225.胰腺周围脓肿 peripancreatic abscess 226.胰源性腹水 pancreatic ascites 227.移动性盲肠 mobile caecum 228.移植胰假性囊肿 graft pancreatic pseudocyst 229.移植胰胰瘘 graft pancreatic fistula 230.移植胰胰腺炎 graft pancreatitis 231.胆道闭锁232.胆道测压［术］ 233.胆道出血234.胆道感染 235胆道梗阻236.胆道蛔虫病 237.胆道贾第虫病238.胆道减压术 decompression of biliary tra 239.胆道闪烁显像［术］240.胆道运动障碍 241.胆固醇结石242胆管癌 243.胆管测压造影［术］244.胆管肝炎 245.胆管空肠吻合术246.胆管扩张 cholangiec 247.胆管内置管扩张［术］248.胆管腺瘤 249.胆管炎250.胆管造影［术］ 251.胆管周围炎252.胆红素脑病 bilirubin encephalopathy ， 253.胆红素尿254.胆绞痛 biliary colic 255.胆瘘 256.胆囊癌257.胆囊肠瘘258.胆囊超声显像［术］259.胆囊穿孔 260.胆囊钙化261.胆囊积脓 262.胆囊积气 pneu-263.胆囊积水 264.胆囊积血265.胆囊镜检查［术］ 266.胆囊空肠吻合术267.胆囊扭转 268.胆囊切除术269.胆囊切除术后综合征 postcholecystectomy syndrome 270,胆囊十二指肠吻合术ch 271.胆囊收缩素 272.胆囊炎273.胆囊造口术 274胆囊造影术275.胆囊周围脓肿 276.胆石性肠梗阻277.胆总管结石 calculus of common bile duct 278.胆小管炎 cholangiolitis279.胆血症 280.胆总管梗阻 281.胆汁反流性胃炎 282.胆总管端端吻合术283.胆汁浓缩综合征 284.胆汁性腹膜炎 biliary peritonitis ，285.胆汁性肝硬化 286.胆总管十二指肠吻合术choledochoduodenostomy 287.胆汁引流 288.胆汁淤积289.胆汁粘稠综合征290.［内镜］操纵部, ［endoscopic ］291.［内镜］插入管, ［endoscopic ］292.［内镜］充气/水阀, ［endoscopic ］293.［内镜］导光连接部, ［endoscopic ］light guide connector section 294.［内镜］导光束, ［endoscopic ］295.［内镜］导像束, ［endoscopic ］296.［内镜］光导纤维, ［endoscopic ］optical fibers297.［内镜］活检管道开口, ［endoscopic ］biopsy channel opening298.［内镜］角度锁钮, ［endoscopic］locking299.［内镜］角度旋钮, ［endoscopic］300.［内镜］冷光源, ［endoscopic］cold light source301.［内镜］弯曲部, ［endoscopic］302.［内镜］吸引阀, ［endoscopic］---------------------------------------------------------------------------------------------------------消化学名词［内镜］操纵部, ［endoscopic］control section［内镜］插入管, ［endoscopic］insertion tube［内镜］充气/水阀, ［endoscopic］air/water valve［内镜］导光连接部, ［endoscopic］light guide connector section［内镜］导光束, ［endoscopic］light guide bundles［内镜］导像束, ［endoscopic］image guide bundles［内镜］光导纤维, ［endoscopic］optical fibers［内镜］活检管道开口, ［endoscopic］biopsy channel opening［内镜］角度锁钮, ［endoscopic］locking knob［内镜］角度旋钮, ［endoscopic］angulation knob［内镜］冷光源, ［endoscopic］cold light source［内镜］弯曲部, ［endoscopic］bending section［内镜］吸引阀, ［endoscopic］suction valve阿米巴［性］肝脓肿, amebic liver abscessEhlers-Danlos综合征, Ehlers-Danlos syndrome嗳气, belch凹陷性病变, excavated lesion, depressed lesionOddi括约肌成形术, plastic repair of Oddi sphincterOddi括约肌切开术, sphincterotomy of OddiOddi括约肌狭窄, stenosis of Oddi sphincterOsler-Weber-Rendu病, Osler-Weber-Rendu diseaseBudd-Chiari综合征, Budd-Chiari syndromeBarrett's食管, Barrett's esophagus板状强直, board-like rigidity半成形便, semiformed stool半乳糖耐量, galactose tolerance伴有先天性综合征的毛细管扩张, telangiectasia associated with congenital syndrome 贝尔西食管裂孔疝修补术, Belsey hiatal hernia repair背驮式肝移植, piggyback liver transplantation贲门成形术, cardioplasty贲门肌切开术, cardiomyotomy鼻胆管引流［术］, nasobiliary drainageBillroth II式吻合［术］, Billroth II anastomosisBillroth I式吻合［术］, Billroth I anastomosis闭袢性肠梗阻, closed loop intestinal obstruction闭塞性肝静脉内膜炎, endophlebitis hepatica obliterans壁外性压迫, extrinsic compression of wall壁细胞迷走神经切断术, parietal cell vagotomy便血, hematochezia变应性直肠炎, allergic proctitis丙型病毒性肝炎, viral hepatitis type C病毒性腹泻, viral diarrhea病毒性肝炎, viral hepatitis病毒性胃肠炎, viral gastroenteritisPeutz-Jegher's综合征, Peutz-Jegher's syndrome剥脱活检, strip biopsy博尔德莫尔食管吻合术, Beordmore anastomosis of esophagus Braun’s吻合［术］, Braun anastomosis部分肠梗阻, partial intestinal obstruction擦拭法细胞学检查［术］, abrasive cytologic examination残留结石, residual stone, retained stone残胃, gastric remnant藏毛病, pilonidal disease侧侧吻合［术］, side-to-side anastomosis侧视内镜, side-viewing endoscope产毒性腹泻, toxigenic diarrhea肠闭锁, intestinal atresia肠壁囊样积气, pneumatosis cystoides intestinalis肠壁囊样积气［症］, pneumatosis cystoides intestinalis肠侧侧吻合［术］, side-to-side intestinal anastomosis肠穿孔, perforation of intestine肠道细菌内毒素移位, endotoxin translocation from intestine肠道细菌移位, bacterial translocation from intestine肠道营养, enteral nutrition肠动静脉畸形, arteriovenous malformation of bowel肠端侧吻合［术］, end-to-side intestinal anastomosis肠端端吻合［术］, end-to-end intestinal anastomosis肠放射性损伤, radiation injury of intestine肠梗阻, intestinal obstruction, ileus肠结核, tuberculosis of intestine肠淋巴管扩张, intestinal lymphangiectasia肠内引流式胰腺移植, enteric drainage pancreas transplantation肠囊肿, enteric cyst肠扭转, volvulus肠袢淤滞综合征, stagnant loop syndrome肠旁路术, intestinal bypass肠切除术, intestinal resection肠切开术, enterotomy肠缺血, ischemia of intestine肠缺血综合征, intestinal ischemic syndrome肠套叠, intussusception肠外瘘, enterocutaneous fistula肠外营养, parenteral nutrition肠外置术, intestinal exteriorization肠吻合［术］, intestinal anastomosis肠紊乱, bowel disturbance肠系膜动脉闭塞, mesenteric arterial occlusion肠系膜动脉栓塞术, mesenteric artery embolization肠系膜动脉血栓形成, mesenteric artery thrombosis肠系膜静脉血栓形成, mesenteric venous thrombosis肠系膜囊肿, mesenteric cyst肠系膜疝, mesenteric hernia肠系膜上动脉综合征, superior mesenteric artery syndrome肠系膜上动脉压迫综合征, superior mesenteric artery compression syndrome 肠狭窄, intestinal stenosis肠旋转不良, malrotation of intestine肠血管病, vascular disease of bowel肠血管发育异常, angiodysplasia of bowel肠血管异常, vascular abnormality of intestine肠易激综合征, irritable bowel syndrome肠源性感染, enterogenic infection肠造口术, enterostomy肠胀气, intestinal tympanites肠重复畸形, duplication of intestine肠子宫内膜异位, endometriosis in bowel超声腹腔镜, ultrasonic laparoscope超声内镜, ultrasonic endoscope成形便, formed stool冲洗法细胞学检查［术］, lavage cytologic examination虫蚀样边缘, eroded edge出血性胃炎, hemorrhagic gastritis出血性胰腺炎, hemorrhagic pancreatitis穿孔, perforation穿孔性阑尾炎, perforating appendicitis穿透, penetration穿透性溃疡, penetrating ulcer大便失禁, fecal incontinence大肠梗阻, large bowel obstruction, colonic obstruction大网膜及肠系膜囊肿, omental cyst and mesenteric cyst单纯性集群性憩室病, simple massed diverticulosis单极电凝［术］, monopolar electrocoagulation胆［结］石, gallstone胆道闭锁, biliary atresia胆道测压［术］, manometry of biliary tract胆道出血, hemobilia胆道感染, infection of biliary tract胆道梗阻, obstruction of biliary tract胆道蛔虫病, biliary ascariasis胆道贾第虫病, giardiasis of biliary tract胆道减压术, decompression of biliary tract胆道闪烁显像［术］, cholescintigraphy胆道运动障碍, biliary dyskinesia胆固醇结石, cholesterol calculus胆管癌, carcinoma of bile duct胆管测压造影［术］, manometric cholangiography胆管肝炎, cholangiohepatitis胆管空肠吻合术, cholangiojejunostomy胆管扩张, cholangiectasis胆管内置管扩张［术］, biliary stent dilatation胆管腺瘤, cholangioadenoma胆管炎, cholangitis胆管造影［术］, cholangiography胆管周围炎, pericholangitis胆红素脑病, bilirubin encephalopathy, kernicterus胆红素尿, bilirubinuria胆绞痛, biliary colic胆瘘, biliary fistula胆囊癌, carcinoma of gallbladder胆囊肠瘘, cholecystoenteric fistula胆囊超声显像［术］, cholecystosonography胆囊穿孔, perforation of gallbladder胆囊钙化, calcification of gallbladder胆囊积脓, empyema of gallbladder胆囊积气, pneu-gallbladder胆囊积水, hydrops of gallbladder胆囊积血, hemocholecyst胆囊镜检查［术］, cholecystoscopy胆囊空肠吻合术, cholecystojejunostomy胆囊扭转, torsion of gallbladder胆囊切除术, cholecystectomy胆囊切除术后综合征, postcholecystectomy syndrome胆囊十二指肠吻合术, cholecystoduodenostomy胆囊收缩素, cholecystokinin胆囊炎, cholecystitis胆囊造口术, cholecystostomy胆囊造影术, cholecystography胆囊周围脓肿, pericholecystic abscess胆石性肠梗阻, gallstone ileus胆石症, cholelithiasis胆小管炎, cholangiolitis胆血症, cholemia胆胰管汇合异常, choledochopancreatic junction anomaly胆汁反流性胃炎, bile reflux gastritis胆汁尿, choleuria, choluria胆汁浓缩综合征, inspissated bile syndrome胆汁性腹膜炎, biliary peritonitis, choleperitoneum胆汁性肝硬化, biliary cirrhosis胆汁胸, cholothorax胆汁引流, biliary drainage胆汁淤积, cholestasis胆汁粘稠综合征, biliary hyperviscosity syndrome胆总管端端吻合术, choledochocholedochostomy胆总管梗阻, obstruction of common bile duct胆总管结石, calculus of common bile duct, choledocholith胆总管结石病, choledocholithiasis胆总管空肠Roux-en-Y形吻合术, choledochojejunostomy Roux-en-Y胆总管扩张, choledochectasia胆总管囊肿, choledochal cyst胆总管囊肿切除术, choledochocystectomy胆总管切开术, choledochotomy胆总管十二指肠吻合术, choledochoduodenostomy胆总管狭窄, stricture of common bile duct胆总管炎, choledochitis胆总管造口术, choledochostomy弹性假黄色瘤, pseudoxanthoma elasticum蛋白丢失性肠病, protein-losing enteropathyDevine结肠造口术, Devine colostomy电子内镜检查［术］, electronic endoscopy, videoendoscopy淀粉酶-肌酸酐清除率之比, amylase-creatinine clearance ratio淀粉酶清除率, clearance of amylase丁型病毒性肝炎, viral hepatitis type D，delta hepatitis动脉胆道瘘, arteriobiliary fistula痘疮样胃炎, gastritis varioliformisDubin-Johnson综合征, Dubin-Johnson syndrome端侧吻合［术］, end-to-side anastomosis端端吻合［术］, end-to-end anastomosis端式结肠造口术, terminal colostomy短肠, short gut短肠综合征, short-bowel syndrone多发性静脉扩张, multiple phlebectasia,多极电凝［术］, multipolar electrocoagulation多囊肝, polycystic liver二期小肠移植, two-stage intestine transplantation翻出型肛门外吻合巨结肠根治术, Swenson procedure翻转法内镜检查［术］, reverse method of endoscopy反流性食管炎, reflux esophagitis反跳痛, rebound tenderness反胃, regurgitation放大腹腔镜检查［术］, magnifying laparoscopy放大内镜检查［术］, magnifying endoscopy放射性结肠炎, radiation colitis放射性小肠炎, radiation enteritis非闭塞性肠梗死, nonocclusive intestinal infarction肥厚性胃炎, hypertrophic gastritis肥厚性幽门狭窄, hypertrophic pylorostenosis肥皂性结肠炎, soap colitis粪便嵌塞, fecal impaction粪瘘, fecal fistula蜂窝织炎性阑尾炎, phlegmonous appendicitis蜂窝织炎性胃炎, phlegmonous gastritis缝线肉芽肿, suture granuloma弗纳-莫里森综合征, Verner-Morrison syndrome辅助性肝移植, auxiliary liver transplantation腐蚀性食管狭窄, caustic stricture of esophagus腐蚀性胃炎, corrosivegastritis复发性胆总管结石病, recurrent choledocholithiasis复发性溃疡, recurrent ulcer复发性阑尾炎, recurrent appendicitis复合性胃和十二指肠溃疡, combined gastric and duodenal ulcers腹部结核, abdominal tuberculosis腹鸣, borborygmus腹膜刺激征, peritoneal irritation sign腹膜炎, peritonitis腹膜粘连, peritoneal adhesion腹腔穿刺［术］, peritoneocentesis, abdominal paracentesis腹腔动脉压迫综合征, celiac artery compression syndrome腹腔灌洗, peritoneal lavage腹腔积血, hemoperitoneum腹腔镜胆囊切除［术］, laparoscopic cholecystectomy腹腔镜检查［术］, laparoscopy腹腔镜治疗［术］, therapeutic laparoscopy腹腔内引流式胰腺移植, free-drainage intraperitoneal pancreas transplantation腹腔脓肿, peritoneal abscess腹水, ascites腹主动脉瘤, abdominal aortic aneurysm改良的黑勒贲门肌切开术, modified Heller operation钙乳胆汁, milk of calcium bile干呕, retch肝［性］昏迷, hepatic coma肝［性］昏迷前期, hepatic precoma肝被膜下出血, subcapsular hemorrhage of liver肝病性口臭, fetor hepaticus肝肠联合移植, combined liver and intestine transplantation肝大, hepatomegaly肝淀粉样变性, amyloidosis of liver肝动脉造影［术］, hepatic arteriography肝梗死, infarction of liver肝结核, tuberculosis of liver肝静脉梗阻, hepatic venous obstruction肝慢性阻性充血, chronic passive congestion of liver肝毛细线虫病, capillariasis hepatica肝门肠吻合术, portoenterostomy, Kasai procedure肝内胆管结石, calculus of intrahepatic duct肝内胆管结石病, hepatolithiasis肝内胆汁淤积, intrahepatic cholestasis肝脓肿, liver abscess肝脾大, hepatosplenomegaly肝片吸虫病, fascioliasis hepatica肝肾联合移植, combined liver and kidney transplantation肝肾综合征, hepatorenal syndrome肝素辅因子, heparin co-factor肝素化, heparinization肝素化逆转, heparinization reversal肝细胞移植, hepatocyte transplantation肝下垂, hepatoptosis肝纤维化, hepatic fibrosis肝心联合移植, combined liver and heart transplantation肝性昏迷, hepatic coma肝性脑病, hepatic encephalopathy肝炎后肝硬化, posthepatitic cirrhosis肝胰联合移植, combined liver and pancreas transplantation肝移植, liver transplantation肝硬化, cirrhosis of liver肝周炎, perihepatitis感染性腹泻, infectious diarrhea感染性胃炎, infectious gastritis肛管癌, cancer of anal canal肛裂, anal fissure,肛门闭锁会阴瘘, anal atresia with perineal fistula肛门闭锁尿道瘘, anal atresia with urethral fistula肛门闭锁前庭瘘, anal atresia with vestibular fistula肛门闭锁阴道瘘, anal atresia with vaginal fistula肛门镜, anoscope肛门镜检查［术］, anoscopy肛门溃疡, anal ulcer肛门瘙痒［症］, pruritus ani肛门狭窄, anal stenosis肛门直肠瘘, anorectal fistula肛门直肠脓肿, anorectal abscess肛乳头炎, anal papillitis肛周脓肿, perianal abscess高胆红素血［症］, hyperbilirubinemia高淀粉酶血［症］, hyperamylasemia高峰酸排出量, peak acid outputGrey Turner征, Grey Turner sign膈膨升, eventration of diaphragm膈疝, diaphragmatic hernia膈下脓肿, subphrenic abscess梗阻性阑尾炎, obstructive appendicitis孤立性非特异性溃疡, isolated nonspecific ulcer骨盆直肠窝脓肿, pelvirectal abscess管探查［术］, exploration of common bile duct光动力学治疗［术］, photodynamic therapy光凝固［术］, photocoagulation果糖不耐受［症］, fructose intolerance黑粪, melena黑勒贲门肌切开术, heller operation,横结肠造口术, transverse colostomy呼气试验breath test糊状便, mushy stool滑动性食管裂孔疝, sliding hiatus hernia滑管, sliding tube化脓性腹膜炎, purulent peritonitis化脓性阑尾炎, suppurative appendicitis化脓性胰腺炎, purulent pancreatitis化生性息肉, metaplastic polyp化学性腹膜炎, chemical peritonitis坏疽性胆囊炎, gangrenous cholecystitis坏疽性阑尾炎, gangrenous appendicitis坏死后肝硬化, postnecrotic cirrhosis坏死性胰腺炎, necrotizing pancreatitis环状胰腺, annular pancreas黄疸, jaundice, icterus黄色肉芽肿性胆囊炎, xanthogranulomatous cholecystitis磺溴酞钠试验, bromsulphalein test回肠膀胱扩大术, ileum augmentation cystoplasty, ileocystoplasty回肠膀胱尿流改道术, ileal conduit diversion回肠膀胱术, ileal conduit, Bricker operation回肠肛管吻合术, ileoanal anastomosis回肠横结肠吻合术, ileotransversostomy回肠憩室, ileal diverticulum回肠造口术, ileostomy回盲部结核, ileocecal tuberculosisWhipple病, Whipple disease混合性结石, mixed stone, mixed calculus混合性毛细血管-海绵状血管瘤, mixed capillary-cavernous hemangioma活动性肝炎, active hepatitis活体部分肝移植, partial living liver transplantation获得性巨结肠, acquired megacolon机械性肠梗阻, mechanical intestinal obstruction, mechanical ileus基础酸排出量, basal acid outputKillian憩室, Killian diverticulum激光治疗［术］, laser therapy急腹症, acute abdomen急性肠系膜淋巴结炎, acute mesenteric lymphadenitis急性出血性胰腺炎, acute hemorrhagic pancreatitis急性腐蚀性食管炎, acute corrosive esophagitis急性肝［功能］衰竭, acute hepatic failure急性梗阻性化脓性胆管炎, acute obstructive suppurative cholangitis急性坏死性胰腺炎, acute necrotizing pancreatitis急性间质性胰腺炎, acute interstitial pancreatitis急性卡他性阑尾炎, acute catarrhal appendicitis急性弥漫性腹膜炎, acute diffuse peritonitis,急性水肿性胰腺炎, acute edematous pancreatitis急性胃扩张, acute dilatation of stomach急性胃扩张, acute gastric dilatation急性应激性溃疡, acute stress ulcer急性重型肝炎, acute severe hepatitis, fulminant hepatitis急诊肝移植, emergency liver transplantation继发性巨结肠, secondary megacolon寄生虫性腹泻, parasitic diarrheaGardner综合征, Gardner syndrome家族性肠息肉病, familial intestinal polyposis家族性结肠息肉病, familial polyposis coli甲胎蛋白测定, alpha-fetoprotein detemination甲型病毒性肝炎, viral hepatitis type A假膜性结肠炎, pseudomembranous colitis假膜性小肠结肠炎, pseudomembranous enterocolitis假憩室, pseudodiverticulum假息肉, pseudopolyp假性感染性直肠炎, pseudoinfectious proctitis假性结肠梗阻, false colonic obstruction, Ogilvie syndrome减体积肝移植, reduced-size liver transplantation碱性反流性胃炎, alkaline reflux gastritis浆液性腹膜炎, serous peritonitis胶原性结肠炎, collagenous colitis绞窄性肠梗阻, strangulated intestinal obstruction节段小肠移植, segmental small intestine transplantation节段性肠扩张, segmental dilatation of intestine节段胰腺移植, segmental pancreas transplantation结肠癌, cancer of colon结肠癌Dukes分类法, Dukes classification for colon cancer结肠膀胱瘘, colovesical fistula结肠穿孔, colonic perforation结肠次全切除术, subtotal colectomy结肠非特异性溃疡, nonspecific ulcer of colon结肠孤立性溃疡, colonic solitary ulcer结肠黑色素沉着病, melanosis coli结肠后胃空肠吻合术, retrocolic gastrojejunostomy结肠回肠侧吻合术, Martin procedure结肠结核, tuberculosis of colon结肠镜检查［术］, colonoscopy结肠憩室病, diverticular disease of colon结肠前胃空肠吻合术, antecolic gastrojejunostomy结肠切除术, colectomy结肠切开术, colotomy结肠缺血, colonic ischemia结肠息肉, polyp of colon结肠息肉病, polyposis coli结肠腺瘤, adenoma of colon结肠造口术, colostomy结肠直肠切除术, coloproctectomy结核性腹膜炎, tuberculous peritonitis结石性胰腺炎, calcareus pancreatitis近侧胃迷走神经切断术, proximal gastric vagotomy经腹骶直肠切除术, abdominosacral resection, anterior resection经颈静脉胆管造影［术］, transjugular cholangiography经口胆管镜检查［术］, peroral cholangioscopy经皮经肝胆管镜检查［术］, percutaneous transhepatic cholangioscopy 经皮经肝胆管造影［术］, percutaneous transhepatic cholangiography经皮经肝胆囊镜检查［术］, percutaneous transhepatic cholecystoscopy经皮经肝栓塞, percutaneous transhepatic embolization经皮内镜胃造瘘［术］, percutaneous endoscopic gastrostomy经直肠活检, transrectal biopsy精神性便秘, psychogenic constipation颈部食管胃吻合术, cervical esophagogastrostomy痉挛性肠梗阻, spastic intestinal obstruction痉挛性肛部痛, proctalgia fugax痉挛性结肠憩室病, spastic colon diverticulosis静脉闭塞性病, veno-occlusive disease静脉胆管造影［术］, intravenous cholangiography静脉胆囊造影［术］, intravenous cholecystography静脉切开术, venesection, phlebotomy静脉曲张, varicosis, varix静脉曲张性溃疡, varicose ulcer静脉造影［术］, phlebography酒精性肝炎, alcoholic hepatitis酒精性肝硬化, alcoholic cirrhosis酒精性胰腺炎, alcoholic pancreatitis局限性肠炎, regional enteritis, Crohn disease局限性腹膜炎, localized peritonitis巨大肥厚性胃炎, giant hypertrophy gastritis巨大皱襞, giant folds, giant ruga巨结肠, megacolon巨十二指肠, megaduodenum菌群失调性肠炎, flora imbalance enteritisCullen征, Cullen signCanada-Cronkhite综合征, Canada-Cronkhite syndrome可控性回肠膀胱术, continent ileal reservoirCrigler-Najjar综合征, Crigler-Najjar syndromeCruveilhier-Baumgarten综合征, Cruveilhier-Baumgarten syndrome克罗恩病, Crohn’s disease空肠回肠旁路术, jejunoileal bypass空肠间置代胆道术, choledochoplasty by jejunal interposition空肠移植, jejunum transplantation空肠造口术, jejunostomy口服胆囊造影［术］, oral cholecystographyCourvoisier征, Courvoisier sign溃疡性结肠炎, ulcerative colitis拉埃内克肝硬化, Laennec’s cirrhosis阑尾残端, appendiceal stump阑尾粪石, appendiceal fecalith阑尾切除术, appendectomy阑尾炎, appendicitis阑尾粘液囊肿, appendiceal mucocele阑尾周围脓肿, periappendiceal abscess类癌, carcinoid类癌综合征, carcinoid syndrome里急后重, tenesmus隆起性病变, protrusion lesion鲁氏Y形吻合［术］, Roux-en-Y anastomosisRotor综合征, Rotor syndrome麻痹性肠梗阻, paralytic ileusMallory-Weiss综合征, Mallory-Weiss syndrome慢性非化浓性破坏性胆管炎, chronic nonsuppurative destructive cholangitis 慢性溃疡性结肠炎, chronic ulcerative colitis慢性重型肝炎, chronic severe hepatitis盲肠膀胱扩大术, cecum augmentation cystoplasty盲肠后位阑尾, retrocecal appendix盲肠炎, typhlitis, cecitis盲肠造口术, cecostomy盲袢综合征, blind loop syndrome毛石, trichobezoar毛植物石, trichophytobezoarMeckel憩室, Meckel diverticulumMenetrier病, Menetrier disease门静脉高压, portal hypertension门静脉脓血症, portal pyemia门静脉血栓形成, thrombosis of portal vein门静脉炎, pylephlebitis门脉性肝硬化, portal cirrhosis门体脑病, portosystemic encephalopathy弥漫性腹膜炎, diffuse peritonitis弥漫性食管痉挛, diffuse spasm of esophagus迷走神经干切断术, truncal vagotomy迷走神经切断术, vagotomy糜烂性胃炎, erosive gastritis米库利兹结肠造口术, Mikulicz colostomy面团感, doughy sensationMurphy征, Murphy sign内镜, endoscope内镜超声检查［术］, endoscopic ultrasonography内镜胆管引流［术］, endoscopic biliary drainage内镜复位［术］, endoscopic reduction内镜检查术, endoscopy内镜逆行胰胆管造影［术］, endoscopic retrograde cholangio pancreatography内镜取石［术］, endoscopic stone extraction technique内镜碎石［术］, endoscopic lithotripsy内镜胰管引流［术］, endoscopic drainage of pancreatic duct内镜粘膜下肿瘤切除［术］, endoscopic enucleation of submucosal tumor内镜治疗［术］, therapeutic endoscopy内镜置管［术］, endoprosthesis内镜注射治疗［术］, endoscopic injection therapy逆蠕动吻合［术］, antiperistaltic anastomosis凝结物, concretion诺沃克组病毒性胃肠炎, norwalk agents gastroenteritis呕血, hematemesis袢式结肠造口术, loop colostomy喷射性呕吐, projectile vomiting盆腔内吻合巨结肠根治术, rehbein procedure劈裂式肝移植, split liver transplantation皮革样胃, leather bottle stomach, linitis plastica脾大, splenomegaly脾功能亢进, hypersplenism脾门静脉造影术, splenoportography脾曲综合征, splenic flexure syndrome屁, flatus胼胝性溃疡, callous ulcer, indolent ulcer平坦性病变, flat lesionPlummer-Vinson综合征, Plummer-Vinson syndrome脐肠瘘, omphalo-enteric fistula气腹, pneumoperitoneum气管食管瘘, tracheo-esophageal fistula气囊扩张器, balloon dilator气囊填塞, balloon tamponade气体扩张器, pneumatic dilator气胀, flatulence, gaseous distention气肿性胆囊炎, emphysematous cholecystitis憩室, diverticulum憩室病, diverticulosis憩室前期, prediverticular stage憩室切除术, diverticulectomy憩室炎, diverticulitis迁延性肝炎, persistent hepatitis前视内镜, forward-viewing endoscope钳夹活检［术］, forceps biopsy浅表性胃炎, superficial gastritis腔静脉造影［术］, venacavography桥形皱襞, bridging fold倾倒综合征, dumping syndrome球后十二指肠溃疡, postbulbar duodenal ulcer曲张静脉切除术, varicectomy圈套器, snare圈套烧灼术, snare cautery全部吸收不良, panmalabsorption全结肠切除术, total colectomy全结肠炎, pancolitis全上消化道内镜检查［术］, panendoscopy全小肠移植, whole small intestine transplantation全胰十二指肠切除术, total pancreaticoduodenectomy全胰腺移植, whole pancreas transplantation缺血性结肠炎, ischemic colitis热活检, hot biopsy热探头凝固［术］, heater probe coagulationGillbert综合征, Gillbert syndrome肉芽肿性胃炎, granulomatous gastritis乳糜性腹膜炎, chyle peritonitis乳糖不耐受［症］, lactose intolerance乳糖酶缺乏, lactase deficiency乳头括约肌切开［术］, sphincterotomy, papillotomy乳头切开刀, papillotome乳头上部切开, suprapapillary incision三次肝移植, tertiary liver transplantation色素内镜检查［术］, dye endoscopy, chromoendoscopy色素性结石, pigmented stone,Sengstaken-Blakemore管, Sengstaken-Blakemore tube上腔静脉梗阻, obstruction of superior vena cava上腔静脉综合症, superior vena cava syndrome失弛缓症, achalasia十二指肠闭锁, duodenal atresia十二指肠残端漏, duodenal stump leakage十二指肠梗阻, obstruction of duodenum十二指肠钩虫病, capillariasis hepatica十二指肠假憩室, pseudodiverticulum of duodenum十二指肠镜检查［术］, duodenoscopy十二指肠空肠襻不全旋转, incomplete rotation of duodenojejunal loop 十二指肠溃疡, duodenal ulcer十二指肠旁疝, paraduodenal hernia十二指肠蹼, duodenal web十二指肠胃反流, duodenogastric reflux十二指肠狭窄, duodenal stenosis十二指肠炎, duodenitis食管癌, esophageal carcinoma。

第7节肠胃药物Gastrointestinaldrugs

第7節腸胃藥物 Gastrointestinal drugs7.1 消化性潰瘍用藥：1.藥品種類：(1)制酸懸浮劑：各廠牌瓶裝、袋裝制酸懸浮劑及袋裝顆粒制酸劑。

(2)乙型組織胺受體阻斷劑：各廠牌乙型組織胺受體阻斷劑之口服製劑與針劑。

(3)氫離子幫浦阻斷劑：各廠牌氫離子幫浦阻斷劑。

(4)細胞保護劑：如gefarnate、cetraxate、carbenoxolone等。

(5)其他消化性潰瘍用藥：dibismuth trioxide, sucralfate, pirenzepine HCl, Gaspin, Caved-S,misoprostol, proglumide及其他未列入之同類藥品，價格與其相當者比照辦理。

2.使用規定：(106/12/1)(1)使用於治療活動性（active）或癒合中（healing）之消化性潰瘍及逆流性食道炎。

(92/10/1)(2)瘢痕期（scar stage）之消化性潰瘍復發預防，其劑量依照醫理減量使用。

(3)消化性潰瘍及逆流性食道炎符合洛杉磯食道炎分級表（The Los AngelesClassification of Esophagitis※備註）Grade A或Grade B者，欲使用消化性潰瘍用藥，其使用期間以四個月為限，申報費用時需檢附四個月內有效之上消化道內視鏡檢查或上消化道Ｘ光攝影報告，其針劑限使用於消化道出血不能口服之病人急性期替代療法。

(92/10/1)(4)經上消化道內視鏡檢查，診斷為重度逆流性食道炎，且符合洛杉磯食道炎分級表（The Los Angeles Classification of Esophagitis※備註）Grade C或Grade D 者，得經消化系專科醫師之確認後可長期使用消化性潰瘍用藥一年。

另外，下列病患得比照辦理：(92/10/1)Ⅰ.胃切除手術縫接處產生之潰瘍。

Ⅱ.經消化系專科醫師重覆多次（三次以上）上消化道內視鏡檢查確認屬難治癒性之潰瘍。

SMAD3_对消化道恶性肿瘤调控作用的研究进展

- 160 -*基金项目：国家自然科学基金项目（82260483；81502556）；云南省科技厅基础研究专项-重点项目（202301AS070015）；云南省消化内镜临床医学中心项目（2022LCZXKF-XH19）①昆明理工大学医学院　云南　昆明　650500②云南省第一人民医院通信作者：郭强SMAD3对消化道恶性肿瘤调控作用的研究进展*李西沙①　唐慧②　刘中建②　郭强② 【摘要】　消化道恶性肿瘤的发生及进展机制一直是国内外研究的热点。

SMAD3作为一种受体调节型蛋白，参与了癌症信号通路，对多数消化道恶性肿瘤的增殖、迁移及侵袭等起着重要的调控作用，与肿瘤患者的预后密切相关。

本文就SMAD3的结构功能、其在消化道恶性肿瘤中的作用机制的最新研究做一综述，以对SMAD3有更全面的了解。

【关键词】　SMAD3　消化道恶性肿瘤　癌基因 Research Progress on the Regulatory Effect of SMAD3 on Gastrointestinal Malignant Tumor/LI Xisha, TANG Hui, LIU Zhongjian, GUO Qiang. //Medical Innovation of China, 2023, 20(36): 160-164 [Abstract]　The occurrence and progression mechanism of gastrointestinal malignant tumor have been the focus of research at home and abroad. As a receptor regulated protein, SMAD3 is involved in cancer signaling pathway and plays an important regulatory role in the proliferation, migration and invasion of most gastrointestinal malignant tumor, which is closely related to the prognosis of tumor patients. In this paper, the structure and function of SMAD3 and its mechanism of action in gastrointestinal malignant tumor are reviewed, so as to have a more comprehensive understanding of SMAD3. [Key words]　SMAD3　Gastrointestinal malignant tumor　Oncogene First-author's address: School of Medicine, Kunming University of Science and Technology, Kunming 650500, China doi：10.3969/j.issn.1674-4985.2023.36.036 肿瘤的发生发展是一个复杂多步骤的生物学过程，多基因参与了肿瘤的调控，在肿瘤的调控网络中存在着一些关键基因。

EMT有关基因

MINI REVIEW ARTICLEpublished:17September2013doi:10.3389/fonc.2013.00221 Role of epithelial-mesenchymal transition in pancreatic ductal adenocarcinoma:is tumor budding the missing link? Eva Karamitopoulou1,2*1Clinical Pathology Division,Institute of Pathology,University of Bern,Bern,Switzerland2Translational Research Unit,Institute of Pathology,University of Bern,Bern,SwitzerlandEdited by:Inti Zlobec,University of Bern, SwitzerlandReviewed by:Parham Minoo,University of Calgary, CanadaQianghua Xia,The Children’s Hospital of Philadelphia,USA*Correspondence:Eva Karamitopoulou,Clinical Pathology Division,Institute of Pathology,University of Bern, Murtenstrasse31,CH-3010Bern, Switzerlande-mail:eva.diamantis@pathology.unibe.ch Pancreatic ductal adenocarcinoma(PDAC)ranks as the fourth commonest cause of cancer death while its incidence is increasing worldwide.For all stages,survival at5years is<5%. The lethal nature of pancreatic cancer is attributed to its high metastatic potential to the lymphatic system and distant ck of effective therapeutic options contributes to the high mortality rates of PDAC.Recent evidence suggests that epithelial-mesenchymal transition(EMT)plays an important role to the disease progression and development of drug resistance in PDAC.Tumor budding is thought to reﬂect the process of EMT which allows neoplastic epithelial cells to acquire a mesenchymal phenotype thus increasing their capacity for migration and invasion and help them become resistant to apoptotic signals. In a recent study by our own group the presence and prognostic signiﬁcance of tumor budding in PDAC were investigated and an association between high-grade budding and aggressive clinicopathological features of the tumors as well as worse outcome of the patients was found.The identiﬁcation of EMT phenotypic targets may help identifying new molecules so that future therapeutic strategies directed speciﬁcally against them could potentially have an impact on drug resistance and invasiveness and hence improve the prognosis of PDAC patients.The aim of this short review is to present an insight on the morphological and molecular aspects of EMT and on the factors that are involved in the induction of EMT in PDAC.Keywords:pancreatic cancer,epithelial-mesenchymal transition,tumor budding,prognosis,biomarkerPANCREATIC CANCERPancreatic ductal adenocarcinoma(PDAC)is a common can-cer with dismal prognosis(1)that escapes early detection and resists treatment(2).Most patients have advanced stage dis-ease at presentation with a median survival of less than1year (1,3).Surgical resection is the only potentially curative treat-ment of PDAC(3).Classical histomorphological features like tumor size,blood vessel,or lymphatic invasion,and presence of lymph node metastases constitute essential prognostic deter-minants in pancreatic cancer and are invariably included in the pathology reports,with tumor stage being the most important of all(3).The lethal nature of PDAC has been attributed to the propensity of PDAC cells to rapidly disseminate to the lym-phatic system and distant organs(4).However,even patients with completely resected,node-negative PDACs eventually die of their disease.Within this context and considering the fact that the management of PDAC remains suboptimal and that adjuvant therapy has resulted to limited progress,the identiﬁcation of addi-tional reliable and reproducible prognostic markers that would enable better patient stratiﬁcation and eventually provide a guide toward a more successful and individualized therapy,is mandatory (1,5).EPITHELIAL-MESENCHYMAL TRANSITIONEpithelial-mesenchymal transition is a biologic process that allows epithelial cells to undergo the biochemical changes that enable them to acquire a mesenchymal phenotype,including enhanced migratory capacity,invasiveness,elevated resistance to apoptosis, and increased production of extracellular matrix(ECM)compo-nents(6,7).EMT is characterized by loss of cell adhesion,down regulation of E-cadherin expression,acquisition of mesenchy-mal markers(including N-cadherin,Vimentin,and Fibronectin), and increased cell motility(6).Both EMT and mesenchymal-epithelial transition(MET),the reversion of EMT,are essential for developmental and repair processes like implantation,embryo for-mation,and organ development as well as wound healing,tissue regeneration,and organﬁbrosis(8).However,EMT also occurs in neoplastic cells that have undergone genetic and epigenetic changes.These changes affect both oncogenes and tumor sup-pressor genes that enable cancer cells to invade and metastasize. Moreover,some neoplastic cells may go through EMT retaining many of their epithelial properties while other cells are becoming fully mesenchymal(9).Many molecular processes are involved in the initiation of EMT including activation of transcription factors,expression of speciﬁc cell-surface proteins,reorganization and expression of cytoskeletal proteins,production of ECM-degrading enzymes,and changes in the expression of speciﬁc microRNAs(miRNAS).The above fac-tors can also be used as biomarkers to detect cells in EMT state(10). EMT has been linked to cellular self-renewal programs of cancer stem cells and apoptosis-anoikis resistance,which are features of therapeutic resistance(11).The zincﬁnger transcription factors Snail,Slug,Zeb1,and Twist repress genes responsible for the epithelial phenotype and represent important regulators of EMT(6,7,12).In PDAC Snail expression has been reported to be seen in nearly80%of the cases and Slug expression in50%(13).Snail expression was inversely correlated with E-cadherin expression and decreased E-cadherin expression was associated with higher tumor grade. Similarly,poorly differentiated pancreatic cancer cell lines showed higher levels of Snail and lower levels of E-cadherin compared with moderately differentiated cell lines(13)while silencing of Zeb1leaded to up-regulation of E-cadherin and restoration of an epithelial phenotype(14).Zeb1expression in PDAC also corre-lated with advanced tumor grade and worse outcomes(14–16) and was shown to be primarily responsible for the acquisition of an EMT phenotype,along with increased migration and inva-sion in response to NF-κB signaling in pancreatic cancer cells (16).EMT AND TUMOR BUDDINGTumor budding reﬂects a type of diffusely inﬁltrative growth con-sisting of detached tumor cells or small cell clusters of up toﬁve cells at the invasive front of gastrointestinal carcinomas(17–22). Tumor buds represent a non-proliferating,non-apoptotic,highly aggressive subpopulation of tumor cells that display migratory and invasive capacities(23).The aim of tumor buds seems to be the invasion of the peritumoral connective tissue,the avoidance of the host’s defense andﬁnally the inﬁltration of the lymphatic and blood vessels with the consequence of local and distant metastasis. The EMT process by allowing a polarized cell to assume a more mesenchymal phenotype with increased migratory capacity,inva-siveness,and resistance to apoptosis seems to play a major role in the development of tumor buds.In fact,tumor buds are thought to result from the process of EMT.Thus,although formally tumor budding cannot be equated with EMT,several similarities between the two processes,including activation in WNT signaling,can be shown(24).The detachment of tumor buds from the main tumor body is accomplished by loss of membranous expression of the adhesion molecule E-cadherin.Activation of WNT sig-naling is further suggested by nuclear expression of b-catenin in tumor-budding cells,as well as increase of laminin5gamma2and activation of Slug and Zeb1(24,25).The presence of high-grade tumor budding has been consis-tently associated with negative clinicopathologic parameters in gastrointestinal tumors(26–30).In a previous study from our group we could show that tumor budding occurs frequently in pancreatic cancer and is a strong,independent,and reproducible, highly unfavorable prognostic factor that may be used as a para-meter of tumor aggressiveness and as an indicator of unfavorable outcome,even within this group of patients with generally poor prognosis.Moreover,tumor budding was proven to have a more powerful prognostic ability than other more classic prognostic fac-tors including TNM stage,thus adding relevant and independent prognostic information(31).EMT AND miRNAsMicroRNAS are small non-coding RNAs of18–25nucleotides, excised from60to110nucleotide RNA precursor structures (32).MiRNAs are involved in crucial biological processes, including development,differentiation,apoptosis,and pro-liferation,through imperfect pairing with target messenger RNAs of protein-coding genes and the transcriptional or post-transcriptional regulation of their expression(33,34).Recent studies illustrate the role of miRNAs on the regula-tion of gene expression and proteins in metastasis.For exam-ple,it has been shown that miR-10b,which is up-regulated by EMT transcription factor Twist,is associated with increased invasiveness and metastatic potential(35,36).Furthermore,it was shown that the miR-200family(miR-200a,miR-200b,miR-200c,miR-141,and miR-429)and miR-205play critical roles in regulating EMT by directly targeting the mRNAs encoding E-cadherin repressors Zeb1and Zeb2(37).Moreover,recent studies showed that members of the miR-200family by induc-ing EMT can regulate the sensitivity to epidermal growth fac-tor receptor(EGFR)in bladder cancer cells and to gemcitabine in pancreatic cancer cells(38).Conversely,Zeb1represses the transcription of miR-200genes by directly binding to their promoter region,thereby forming a double-negative feedback loop(39).On the other hand,miR-200family can also pro-mote the conversion of mesenchymal cells to epithelial-like cells (MET)suggesting that these miRNAs may also favor metastatic outgrowth.Recent studies aiming at the evaluation of miRNAs in pan-creatic cancer have shown that speciﬁc miRNAs are dysregulated in PDAC while the higher expression of some miRNA species was able to distinguish between benign and malignant pancre-atic tissue(40).For example,miR-21was shown to be over-expressed in79%of pancreatic cancers as opposed to27%of chronic pancreatitis(41).In resected PDAC specimens high lev-els of miR-200c expression strongly correlated with E-cadherin levels and were associated with signiﬁcantly better survival rates compared with patients whose tumors had low levels of miR-200c expression(42).CHEMORESISTANCE AND EMTCells undergoing EMT become invasive and develop resistance to chemotherapeutic agents.Moreover,EMT can be induced by chemotherapeutic agents,and stress conditions such as exposure to radiation or hypoxia(43,44).Up-regulation of Twist has been shown to be associated with resistance to paclitaxel in nasopharyngeal,bladder,ovarian,and prostate cancers(45).In colorectal cancer cell lines,chronic expo-sure to oxaliplatin leaded to the development of the ability to migrate and invade with phenotypic changes resembling EMT(spindle-cell shape,loss of polarity,intercellular separa-tion,and pseudopodia formation)by the oxaliplatin-resistant cells(46).Pancreatic cancer remains today an extremely lethal disease largely because of its resistance to existing treatments(47).EMT has been shown to contribute signiﬁcantly to chemoresistance in several cancers,including pancreatic cancer(30,48,49).Induction of gemcitabine resistance in previously sensitive cell lines resulted in development of an EMT phenotype and was associated with an increased migratory and invasive ability compared to gemc-itabine sensitive cells(49).Moreover,gene expression proﬁling ofchemoresistant cells showed a strong association between expres-sion of the EMT transcription factors Zeb1,Snail,and Twist and decreased expression of E-cadherin(39,50).Silencing of Zeb1 with siRNA resulted to MET(51)and restored chemosensitivity (14).Interestingly,maintenance of chemoresistance in cell lines that have undergone EMT is dependent on Notch and NF-κB signaling(30).Inhibition of Notch-2down regulates Zeb1,Snail, and Slug expression,attenuates NF-κB signaling,and reduces the migratory and invasive capacity of the gemcitabine resistant cells(30).Epithelial-mesenchymal transition can also confer resistance to targeted agents.For example,lung cancer cell lines that have undergone EMT,became resistant to the growth inhibitory effects of EGFR kinase inhibition(erlotinib)in vitro and in xenografts(47)as well as other EGFR inhibitors such as geﬁtinib and cetuximab(48)Thus,EMT can lead to resis-tance to multiple agents and result to rapid progression of the tumor.Clarifying the correlation between EMT and drug resistance may help clinicians select an optimal treat-ment.CONCLUSIONPancreatic cancer remains an extremely lethal disease partly because of the poor response to existing treatments.Accumulat-ing evidence suggests that EMT plays an important role in PDAC progression,is associated with stem cell features of the PDAC cells and seems to signiﬁcantly contribute to the chemoresistance of pancreatic cancer.Moreover,is associated with more aggressive tumor characteristics and with poor patient survival.Because of its role in therapy response and tumor progression,targeting EMT could potentially reduce drug resistance and have a great impact in the survival of PDAC patients.Tumor budding thought to be the result of the EMT process is commonly observed in PDAC and high-grade tumor budding has been proven to have an independent adverse prognostic impact in the survival of PDAC patients.Figure1depicts tumor bud-ding as a possible transition between a fully epithelial and a fully mesenchymal phenotype of the tumor cells in PDAC.Moreover, cancer cells in tumor buds have been shown to have EMT and cancer stem cell characteristics.The further characterization of the budding cells at a protein and gene level in order to iden-tify a“molecular budding-promoting proﬁle”will lead to a better understanding of the tumor-stroma interaction at the area of the invasive front and help to further elucidate the similarities between budding cells,EMT process and cancer stem cells in pancreatic cancer.Investigating these issues will allow us to gain further insight into pancreatic carcinogenesis,and provide us with a platform on which to build future studies leading to the identiﬁcation of new therapeutic interventions.REFERENCES1.Hidalgo M.Pancreatic cancer.NEngl J Med(2010)362:1605–17.doi:10.1056/NEJMra09015572.Tuveson DA,Hingorani SR.Duc-tal pancreatic cancer in humans and mice.Cold Spring Harb Symp Quant Biol(2005)70:65–72.doi:10.1101/ sqb.2005.70.0403.Fernandez-del-Castillo C,JimenezRE,Steer ML.Surgery in the treatment of exocrine pancreas and prognosis.In:Tanabe KK,edi-tor(2013).Available from:www.4.Li Y,Kong D,Ahmad A,Bao B,Sarkar FH.Pancreatic cancer stem cells:emerging target for designing novel therapy.Cancer Lett(2012).Available from:/10.1016/j canlet.2012.03.018,5.Welsch T,Kleeff J,Friess H.Molecu-lar pathogenesis of pancreatic can-cer:advances and challenges.Curr Mol Med(2007)7:504–21.doi:10.2174/1566524077813870826.Kalluri R,Weinberg RA.The basicsof epithelial-mesenchymal transi-tion.J Clin Invest(2009)119:1420–8.doi:10.1172/JCI391047.Thiery JP,Acloque H,Huang RYJ,Nieto MA.Epithelial-mesenchymal transitions in development and dis-ease.Cell(2009)139:871–90.doi:10.1016/j.cell.2009.11.0078.Rasheed ZA,Yang J,Wang Q,Kowal-ski J,Freed I,Murter C,et al.Prog-nostic signiﬁcance of tumorigenic cells with mesenchymal features in pancreatic adenocarcinoma.J Natl Cancer Inst(2010)102:340–51.doi:10.1093/jnci/djp5359.Iwatsuki M,Mimori K,YokoboriT,Ishi H,Beppu T,Nakamori S.Epithelial–mesenchymal transi-tion in cancer development and its clinical signiﬁcance.Cancer Sci (2010)101(2):293–9.doi:10.1111/j.1349-7006.2009.01419.x10.Kalluri R.EMT:when epithelial cellsdecide to become mesenchymal-like cells.J Clin Invest(2009)119:1417–9.doi:10.1172/JCI3967511.Krantz SB,Shields MA,Dangi-Garimella S,Munshi HG,Bentrem DJ.Contribution of epithelial-to-mesenchymal transition and cancer stem cells to pancreatic cancer progression.J Surg Res(2012)173: 105–12.doi:10.1016/j.jss.2011.09.02012.Lee JM,Dedhar S,Kalluri R,Thompson EW.The epithelial-mesenchymal transition:new insights in signaling,devel-opment,and disease.J Cell Biol(2006)172:973–81.doi:10.1083/jcb.20060101813.Hotz B,Arndt M,Dullat S,BhargavaS,Buhr HJ,Hotz HG.Epithelial tomesenchymal transition:expressionof the regulators snail,slug,andtwist in pancreatic cancer.ClinCancer Res(2007)13:4769–76.doi:10.1158/R-06-292614.Arumugam T,Ramachandran V,Fournier KF,Wang H,MarquisL,Abbruzzese JL,et al.Epithe-lial to mesenchymal transition con-tributes to drug resistance in pan-creatic cancer.Cancer Res(2009)69:5820–8.doi:10.1158/0008-5472.CAN-08-281915.Buck E,Eyzaguirre A,Barr S,Thompson S,Sennello R,Y oung D,et al.Loss of homotypic cell adhe-sion by epithelial-mesenchymaltransition or mutation limits sen-sitivity to epidermal growth factorreceptor inhibition.Mol CancerTher(2007)6:532–41.doi:10.1158/1535-7163.MCT-06-046216.Maier HJ,Schmidt-Strassburger U,Huber MA,Wiedemann EM,BeugH,Wirth T.NF-kappaB promotesepithelial-mesenchymal transition,migration and invasion of pancre-atic carcinoma cells.Cancer Lett(2010)295:214–28.doi:10.1016/j.canlet.2010.03.00317.Prall F.Tumour budding in col-orectal carcinoma.Histopathology(2007)50:151–62.doi:10.1111/j.1365-2559.2006.02551.x18.Brown M,Sillah K,Grifﬁths EA,Swindell R,West CM,Page RD,et al.Tumour budding and a lowhost inﬂammatory response areassociated with a poor progno-sis in oesophageal and gastro-oesophageal junction cancers.Histopathology(2010)56:893–9.doi:10.1111/j.1365-2559.2010.03559.x19.Koike M,Kodera Y,Itoh Y,Nakayama G,Fujiwara M,Hamajima N,et al.Multivariateanalysis of the pathologic featuresof esophageal squamous cell cancer:tumor budding is a signiﬁcantindependent prognostic factor.AnnSurg Oncol(2008)15:1977–82.doi:10.1245/s10434-008-9901-620.Miyata H,Y oshioka A,YamasakiM,Nushijima Y,Takiguchi S,Fujiwara Y,et al.Tumor bud-ding in tumor invasive front pre-dicts prognosis and survival ofpatients with esophageal squa-mous cell carcinomas receivingneoadjuvant chemotherapy.Cancer(2009)115:3324–34.doi:10.1002/cncr.2439021.Roh MS,Lee JI,Choi PJ.Tumorbudding as a useful prognosticmarker in esophageal squamous cellcarcinoma.Dis Esophagus(2004)17:333–7.doi:10.1111/j.1442-2050.2004.00436.x22.Ohike N,Coban I,Kim GE,Bas-turk O,Tajiri T,Krasinskas A,etal.Tumor budding as a strongprognostic indicator in invasiveampullary adenocarcinomas.Am JSurg Pathol(2010)34:1417–24.doi:10.1097/PAS.0b013e3181f0b05a23.Zlobec I,Lugli A.Epithelial mes-enchymal transition and tumorbudding in aggressive colorectalcancer:tumor budding as oncotar-get.Oncotarget(2010)1:651–61.24.Muto T,Mochizuki H,Masaki T edi-tors.Tumor Budding in ColorectalCancer:Recent Progress in ColorectalCancer Research(Horizons in Can-cer Research).(Vol.8).Tokyo:Nova(2006).25.Schmalhofer O,Brabletz S,Brabletz T.E-cadherin,beta-catenin,and ZEB1in malignantprogression of cancer.CancerMetastasis Rev(2009)28:151–66.doi:10.1007/s10555-008-9179-y26.Karamitopoulou E,Zlobec I,KölzerV,Kondi-Paﬁti A,Patsouris ES,Gen-natas K,et al.Proposal for a10-high-power-ﬁelds scoring methodfor the assessment of tumor bud-ding in colorectal cancer.ModPathol(2013)26:295–301.doi:10.1038/modpathol.2012.15527.Nakamura T,Mitomi H,KikuchiS,Ohtani Y,Sato K.Evaluationof the usefulness of tumor bud-ding on the prediction of metasta-sis to the lung and liver after cura-tive excision of colorectal cancer.Hepatogastroenterology(2005)52:1432–5.28.Ueno H,Mochizuki H,HashiguchiY,Hatsuse K,Fujimoto H,HaseK.Predictors of extrahepatic recur-rence after resection of colorectalliver metastases.Br J Surg(2004)91:327–33.doi:10.1002/bjs.442929.Ueno H,Murphy J,Jass JR,Mochizuki H,Talbot IC.Tumour‘budding’as an indexto estimate the potential ofaggressiveness in rectal cancer.Histopathology(2002)40:127–32.doi:10.1046/j.1365-2559.2002.01324.x30.Wang LM,Kevans D,Mulcahy H,O’Sullivan J,Fennelly D,Hyland J,et al.Tumor budding is a strong andreproducible prognostic marker inT3N0colorectal cancer.Am J SurgPathol(2009)33:134–41.doi:10.1097/PAS.0b013e318184cd5531.Karamitopoulou E,Zlobec I,BornD,Kondi-Paﬁti A,Patsouris E,Gen-natas K,et al.Tumor budding isa strong and independent prognos-tic factor in pancreatic cancer.EurJ Cancer(2013)49:1032–9.doi:10.1016/j.ejca.2012.10.02232.Calin GA,Croce CM.Micro RNAsignatures in human cancers.NatRev Cancer(2006)6:857–66.doi:10.1038/nrc199733.McShane L,Altman DG,SauerbreiW,Taube SE,Gion M,Clark GM,etal.REporting recommendations fortumor MARKer prognostic studies(REMARK).Eur J Cancer(2005)41:1690–6.doi:10.1016/j.ejca.2005.03.03234.Pasquinelli AE,Hunter S,BrachtJ.MicroRNAs:a developing story.Curr Opin Gen Dev(2005)15:200–5.doi:10.1016/j.gde.2005.01.00235.Peter ME.Let-7and miR-200microRNAs:guardians againstpluripotency and cancer progres-sion.Cell Cycle(2009)8:843–52.doi:10.4161/cc.8.6.790736.Preis M,Gardner TB,Gordon SR,Pipas JM,Mackenzie TA,Klein EE,et al.MicroRNA10b expression cor-relates with response to neoadju-vant therapy and survival in pan-creatic ductal adenocarcinoma.ClinCancer Res(2011)17:5812–21.doi:10.1158/R-11-069537.Gregory PA,Bert AG,Paterson EL,Barry SC,Tsykin A,Farshid G,et al.The miR-200family and miR-205regulate epithelial to mesenchymaltransition by targeting ZEB1andSIP1.Nat Cell Biol(2008)10:593–601.doi:10.1038/ncb172238.Burk U,Schubert J,Wellner U,Schmalhofer O,Vincan E,SpadernaS,et al.A reciprocal repressionbetween ZEB1and members of themiR-200family promotes EMT andinvasion in cancer cells.EMBO Rep(2008)9:582–9.doi:10.1038/embor.2008.7439.Wellner U,Schubert J,Burk UC,Schmalhofer O,Zhu F,Sonntag A,et al.The EMT-activator ZEB1pro-motes tumorigenicity by repress-ing stemness-inhibiting microR-NAs.Nat Cell Biol(2009)11:1487–95.doi:10.1038/ncb199840.Panarelli NC,Chen YT,ZhouXK,Kitabayashi N,Yantiss RK.MicroRNA expression aids thepreoperative diagnosis of pancre-atic ductal adenocarcinoma.Pan-creas(2012)41:685–90.doi:10.1097/MPA.0b013e318243a90541.Dillhoff M,Liu J,Frankel W,CroceC,Bloomston M.MicroRNA-21is overexpressed in pan-creatic cancer and a potentialpredictor of survival.J Gas-trointest Surg(2008)12:2171–6.doi:10.1007/s11605-008-0584-x42.Yu J,Ohuchida K,Mizumoto K,Sato N,Kayashima T,Fujita H, et al.MicroRNA,hsa-miR-200c, is an independent prognos-tic factor in pancreatic cancer and its upregulation inhibits pancreatic cancer invasion but increases cell prolifera-tion.Mol Cancer(2010)9:169.doi:10.1186/1476-4598-9-169 43.Li C,Heidt DG,Dalerba P,BurantCF,Zhang L,Adsay V,et al.Identiﬁcation of pancreatic can-cer stem cells.Cancer Res(2007) 67:1030–7.doi:10.1158/0008-5472.CAN-06-203044.Lee CJ,Dosch J,Simeone DM.Pan-creatic cancer stem cells.J Clin Oncol(2008)26:2806–12.doi:10.1200/JCO45.Hong SP,Wen J,Bang S,ParkS,Song SY.CD44-positive cells are responsible for gemc-itabine resistance in pancreatic cancer cells.Int J Cancer(2009)125:2323–31.doi:10.1002/ijc.2457346.Hermann PC,Huber SL,HerrlerT,Aicher A,Ellwart JW,GubaM,et al.Distinct populations ofcancer stem cells determine tumorgrowth and metastatic activity inhuman pancreatic cancer.Cell StemCell(2007)1:313–23.doi:10.1016/j.stem.2007.06.00247.Li Y,VandenBoom TG,Kong D,Wang Z,Ali S,Philip PA,et al.Up-regulation of miR-200and let-7bynatural agents leads to the reversalof epithelial-to-mesenchymal tran-sition in gemcitabine-resistant pan-creatic cancer cells.Cancer Res(2009)69:6704–12.doi:10.1158/0008-5472.CAN-09-129848.Yang AD,Fan F,Camp ER,vanBuren G,Liu W,Somcio R,etal.Chronic oxaliplatin resistanceinduces epithelial-to-mesenchymaltransition in colorectal cancercell lines.Clin Cancer Res(2006)12:4147–53.doi:10.1158/1078-R-06-003849.Shah AN,Summy JM,Zhang J,Park S,Parikh N,Gallick GE.Development and characterizationof gemcitabine-resistant pancre-atic tumor cells.Ann Surg Oncol(2007)14:3629–37.doi:10.1245/s10434-007-9583-550.Shimono Y,Zabala M,ChoRW,Lobo N,Dalerba P,QianD,et al.Downregulation ofmiRNA-200c links breast cancerstem cells with normal stemcells.Cell(2009)138:592–603.doi:10.1016/j.cell.2009.07.01151.Conroy T,Paillot B,Francois E,Bugat R,Jacob JH,Stein U,etal.Irinotecan plus oxaliplatin andleucovorin-modulatedﬂuorouracilin advanced pancreatic cancer–aGroupe Tumeurs Digestives of theFederation Nationale des Centres deLutte Contre le Cancer study.J ClinOncol(2005)23:1228–36.doi:10.1200/JCO.2005.06.050Conﬂict of Interest Statement:Theauthor declares that the research wasconducted in the absence of anycommercial orﬁnancial relationshipsthat could be construed as a potentialconﬂict of interest.Received:24July2013;accepted:11August2013;published online:17Sep-tember2013.Citation:Karamitopoulou E(2013)Role of epithelial-mesenchymal tran-sition in pancreatic ductal adenocar-cinoma:is tumor budding the miss-ing link?Front.Oncol.3:221.doi:10.3389/fonc.2013.00221This article was submitted to Gastroin-testinal Cancers,a section of the journalFrontiers in Oncology.Copyright©2013Karamitopoulou.Thisis an open-access article distributed underthe terms of the Creative CommonsAttribution License(CC BY).The use,distribution or reproduction in otherforums is permitted,provided the origi-nal author(s)or licensor are credited andthat the original publication in this jour-nal is cited,in accordance with acceptedacademic practice.No use,distribution orreproduction is permitted which does notcomply with these terms.。

双钳道胃镜在治疗贲门-胃底黏膜下肿瘤中的临床应用评价

双钳道胃镜在治疗贲门-胃底黏膜下肿瘤中的临床应用评价王珊珊;沈磊【摘要】目的评价双钳道内镜在治疗贲门-胃底部黏膜下肿瘤(SMT)中的安全性及疗效性.方法回顾性分析28例贲门-胃底部SMT患者在双钳道胃镜下行内镜治疗的资料,包括基本情况、病变大小、治疗经过及病理结果等,并统计并发症及术后随访结果.结果 28例患者均顺利完成内镜治疗,病变最大径在0.6～4.0 cm,平均2.3 cm,内镜下病灶完整取出,手术时间35～120 min,平均65 min,术后住院5～10 d,平均7.5 d,无转外科继续治疗者.目前正在随访的患者胃镜复查均未见病变残留及复发.结论双钳道内镜在治疗贲门-胃底部SMT时能够达到完整切除的目标并具有较好的临床疗效.【期刊名称】《中国内镜杂志》【年(卷),期】2018(024)012【总页数】4页(P95-98)【关键词】双钳道胃镜;贲门-胃底部;消化道黏膜下肿瘤【作者】王珊珊;沈磊【作者单位】武汉大学人民医院消化内科,湖北武汉 430060;武汉大学人民医院消化内科,湖北武汉 430060【正文语种】中文【中图分类】R735消化道黏膜下肿瘤（submucosal tumor，SMT）是指突向浆膜层生长起源于固有肌层的肿瘤性疾病，内镜下多表现为表面覆盖正常黏膜的隆起性病变[1]。

随着消化道内镜技术的发展，这类病变多能在内镜下完全切除[2]，相关手术方式包含内镜黏膜下剥离术（endoscopic submucosal dissection，ESD）及其相关技术，如内镜下黏膜挖除术、黏膜下隧道切除术和内镜下全层切除术等。

目前对双钳道胃镜治疗SMT病变的报道相对较少，我院2015年1月－2017年12月利用双钳道胃镜对SMT完整治疗的28例贲门-胃底部SMT的治疗效果较好。

现报道如下：1 资料与方法1.1 一般资料2015年1月－2017年12月普通胃镜检查发现的贲门-胃底部异常病灶，结合超声胃镜及CT结果，诊断考虑突向黏膜下生长且在内镜下切除术中发现与浆膜层紧密粘连的起源于固有肌层的贲门-胃底部SMT患者共28例。

舒尼替尼label

HIGHLIGHTS OF PRESCRIBING INFORMATIONThese highlights do not include all the information needed to use SUTENT safely and effectively. See full prescribing information for SUTENT.SUTENT® (sunitinib malate) capsules, oralInitial U.S. Approval: 2006----------------------------RECENT MAJOR CHANGES-------------------------- Indications and Usage, Advanced Renal Cell Carcinoma (1.2) 2/2007 Warnings and Precautions, Left Ventricular Dysfunction (5.2) 2/2007 Warnings and Precautions, QT Interval Prolongation andTorsade de Pointes (5.3) 2/2007 Warnings and Precautions, Hypertension (5.4) 2/2007 Warnings and Precautions, Hemorrhagic Events (5.5) 2/2007 Warnings and Precautions, Hypothyroidism (5.6) 2/2007----------------------------INDICATIONS AND USAGE--------------------------- SUTENT is a kinase inhibitor indicated for the treatment of: •Gastrointestinal stromal tumor after disease progression on or intolerance to imatinib mesylate. (1.1)•Advanced renal cell carcinoma. (1.2)----------------------DOSAGE AND ADMINISTRATION----------------------- •50 mg orally once daily, with or without food, 4 weeks on treatment followed by 2 weeks off. (2.1)•Dose adjustments of 12.5 mg recommended based on individual safety and tolerability. (2.2)---------------------DOSAGE FORMS AND STRENGTHS---------------------- •Capsules: 12.5 mg, 25 mg, 50 mg (3)-------------------------------CONTRAINDICATIONS------------------------------ •None (4)-----------------------WARNINGS AND PRECAUTIONS------------------------ •Women of childbearing potential should be advised of the potential hazard to the fetus and to avoid becoming pregnant. (5.1) •Left ventricular ejection fraction declines to below the lower limit of normal have occurred. Monitor patients for signs and symptoms ofcongestive heart failure. (5.2)•Prolonged QT intervals and Torsade de Pointes have been observed.Use with caution in patients at higher risk for developing QT intervalprolongation. When using SUTENT, monitoring with on-treatmentelectrocardiograms and electrolytes should be considered. (5.3) •Hypertension may occur. Monitor blood pressure and treat as needed.(5.4)•Hemorrhagic events including tumor-related hemorrhage have occurred.Perform serial complete blood counts and physical examinations. (5.5) •Hypothyroidism may occur. Patients with signs and symptoms suggestive of hypothyroidism should have laboratory monitoring ofthyroid function performed and be treated as per standard medicalpractice. (5.6)•Adrenal hemorrhage was observed in animal studies. Monitor adrenal function in case of stress such as surgery, trauma or severe infection.(5.7)------------------------------ADVERSE REACTIONS------------------------------- •The most common adverse reactions (≥20%) are fatigue, asthenia, diarrhea, nausea, mucositis/stomatitis, vomiting, dyspepsia, abdominalpain, constipation, hypertension, rash, hand-foot syndrome, skindiscoloration, altered taste, anorexia, and bleeding. (6)To report SUSPECTED ADVERSE REACTIONS, contact Pfizer, Inc. at1-800-438-1985 or FDA at 1-800-FDA-1088 or /medwatch.------------------------------DRUG INTERACTIONS------------------------------- •CYP3A4 Inhibitors: Consider dose reduction of SUTENT when administered with strong CYP3A4 inhibitors. (7.1)•CYP3A4 Inducers: Consider dose increase of SUTENT when administered with CYP3A4 inducers. (7.2)See 17 for PATIENT COUNSELING INFORMATION and FDA-approved patient labeling.Revised:2/2007_______________________________________________________________________________________________________________________________________ FULL PRESCRIBING INFORMATION: CONTENTS*1INDICATIONS AND USAGE1.1Gastrointestinal stromal tumor1.2Advanced renal cell carcinoma2DOSAGE AND ADMINISTRATION2.1Recommended Dose2.2Dose Modification3DOSAGE FORMS AND STRENGTHS4CONTRAINDICATIONS5WARNINGS AND PRECAUTIONS5.1Pregnancy5.2Left Ventricular Dysfunction5.3QT Interval Prolongation and Torsade de Pointes5.4Hypertension5.5Hemorrhagic Events5.6Hypothyroidism5.7Adrenal Function5.8Laboratory Tests6ADVERSE REACTIONS6.1 Adverse Reactions in GIST Study A6.2 Adverse Reactions in the Treatment-Naïve MRCC Study6.3 Venous Thromboembolic Events6.4 Reversible Posterior Leukoencephalopathy Syndrome6.5 Pancreatic and Hepatic Function7DRUG INTERACTIONS7.1CYP3A4 Inhibitors7.2CYP3A4 Inducers7.3In Vitro Studies of CYP Inhibition and Induction 8USE IN SPECIFIC POPULATIONS8.1Pregnancy8.3Nursing Mothers8.4Pediatric Use8.5Geriatric Use8.6 Hepatic Impairment10 OVERDOSAGE11 DESCRIPTION12 CLINICAL PHARMACOLOGY12.1 Mechanism of Action12.3 Pharmacokinetics12.4 Cardiac Electrophysiology13NONCLINICAL TOXICOLOGY13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility14 CLINICAL STUDIES14.1 Gastrointestinal Stromal Tumor14.2 Renal Cell Carcinoma16 HOW SUPPLIED/STORAGE AND HANDLING17 PATIENT COUNSELING INFORMATION17.1 Gastrointestinal Disorders17.2 Skin Effects17.3 Other Common Events17.4 Concomitant Medications17.5 FDA-Approved Patient Labeling* Sections or subsections omitted from the full prescribing information are not listed._______________________________________________________________________________________________________________________________________FULL PRESCRIBING INFORMATION:1 INDICATIONS AND USAGE1.1 GastrointestinalStromalTumorSUTENT is indicated for the treatment of gastrointestinal stromal tumor after disease progression on or intolerance to imatinib mesylate.1.2 Advanced Renal Cell CarcinomaSUTENT is indicated for the treatment of advanced renal cell carcinoma.2 DOSAGE AND ADMINISTRATION2.1 Recommended DoseThe recommended dose of SUTENT for gastrointestinal stromal tumor (GIST) and advanced renal cell carcinoma (RCC) is one 50 mg oral dose taken once daily, on a schedule of 4 weeks on treatment followed by 2 weeks off (Schedule 4/2). SUTENT may be taken with or without food.2.2 DoseModificationDose increase or reduction of 12.5 mg increments is recommended based on individual safety and tolerability.Strong CYP3A4 inhibitors such as ketoconazole may increase sunitinib plasma concentrations. Selection of an alternate concomitant medication with no or minimal enzyme inhibition potential is recommended. A dose reduction for SUTENT to a minimum of 37.5 mg daily should be considered if SUTENT must be co-administered with a strong CYP3A4 inhibitor [see Drug Interactions (7.1) and Clinical Pharmacology (12.3)].CYP3A4 inducers such as rifampin may decrease sunitinib plasma concentrations. Selection of an alternate concomitant medication with no or minimal enzyme induction potential is recommended. A dose increase for SUTENT to a maximum of 87.5 mg daily should be considered if SUTENT must be co-administered with a CYP3A4 inducer. If dose is increased, the patient should be monitored carefully for toxicity [see Drug Interactions (7.2) and Clinical Pharmacology (12.3)].3 DOSAGE FORMS AND STRENGTHS12.5 mg capsulesHard gelatin capsule with orange cap and orange body, printed with white ink “Pfizer” on the cap and “STN 12.5 mg” on the body.25 mg capsulesHard gelatin capsule with caramel cap and orange body, printed with white ink “Pfizer” on the cap and “STN 25 mg” on the body.50 mg capsulesHard gelatin capsule with caramel top and caramel body, printed with white ink “Pfizer” on the cap and “STN 50 mg” on the body.4 CONTRAINDICATIONSNone5 WARNINGS AND PRECAUTIONS5.1 PregnancyPregnancy Category DAs angiogenesis is a critical component of embryonic and fetal development, inhibition of angiogenesis following administration of SUTENT should be expected to result in adverse effects on pregnancy. There are no adequate and well-controlled studies of SUTENT in pregnant women. If the drug is used during pregnancy, or if the patient becomes pregnant while receiving this drug, the patient should be apprised of the potential hazard to the fetus. Women of childbearing potential should be advised to avoid becoming pregnant while receiving treatment with SUTENT.Sunitinib was evaluated in pregnant rats (0.3, 1.5, 3.0, 5.0 mg/kg/day) and rabbits (0.5, 1, 5, 20 mg/kg/day) for effects on the embryo. Significant increases in the incidence of embryolethality and structural abnormalities were observed in rats at the dose of 5 mg/kg/day (approximately 5.5 times the systemic exposure [combined AUC of sunitinib + primary active metabolite] in patients administered the recommended daily doses [RDD]). Significantly increased embryolethality was observed in rabbits at 5 mg/kg/day while developmental effects were observed at ≥1 mg/kg/day (approximately 0.3 times the AUC in patients administered the RDD of 50 mg/day). Developmental effects consisted of fetal skeletal malformations of the ribs and vertebrae in rats. In rabbits, cleft lip was observed at 1 mg/kg/day and cleft lip and cleft palate were observed at 5 mg/kg/day (approximately 2.7 times the AUC in patients administered the RDD). Neither fetal loss nor malformations were observed in rats dosed at ≤3 mg/kg/day (approximately 2.3 times the AUC in patients administered the RDD).5.2 Left Ventricular DysfunctionIn the presence of clinical manifestations of congestive heart failure (CHF), discontinuation of SUTENT is recommended. The dose of SUTENT should be interrupted and/or reduced in patients without clinical evidence of CHF but with an ejection fraction <50% and >20% below baseline.More patients treated with SUTENT experienced decline in left ventricular ejection fraction (LVEF) than patients receiving either placebo or interferon-α(IFN-α). In GIST Study A, 22/209 patients (11%) on SUTENT and 3/102 patients (3%) on placebo had treatment-emergent LVEF values below the lower limit of normal (LLN). Nine of 22 GIST patients on SUTENT with LVEF changes recovered without intervention. Five patients had documented LVEF recovery following intervention (dose reduction: one patient; addition of antihypertensive or diuretic medications: four patients). Six patients went off study without documented recovery. Additionally, three patients on SUTENT had Grade 3 reductions in left ventricular systolic function to LVEF <40%; twoof these patients died without receiving further study drug. No GIST patients on placebo had Grade 3 decreased LVEF. In GIST Study A, 1 patient on SUTENT and 1 patient on placebo died of diagnosed heart failure; 2 patients on SUTENT and 2 patients on placebo died of treatment-emergent cardiac arrest.In the treatment-naïve MRCC study, 78/375 (21%) and 44/360 (12%) patients on SUTENT and IFN-α, respectively, had an LVEF value below the LLN. Thirteen patients on SUTENT (4%) and four on IFN-α (1%) experienced declines in LVEF of >20% from baseline and to below 50%. Left ventricular dysfunction was reported in three patients (1%) and CHF in one patient (<1%) who received SUTENT.Patients who presented with cardiac events within 12 months prior to SUTENT administration, such as myocardial infarction (including severe/unstable angina), coronary/peripheral artery bypass graft, symptomatic CHF, cerebrovascular accident or transient ischemic attack, or pulmonary embolism were excluded from SUTENT clinical studies. It is unknown whether patients with these concomitant conditions may be at a higher risk of developing drug-related left ventricular dysfunction. Physicians are advised to weigh this risk against the potential benefits of the drug. These patients should be carefully monitored for clinical signs and symptoms of CHF while receiving SUTENT. Baseline and periodic evaluations of LVEF should also be considered while the patient is receiving SUTENT. In patients without cardiac risk factors, a baseline evaluation of ejection fraction should be considered.5.3 QT Interval Prolongation and Torsade de PointesSUTENT has been shown to prolong the QT interval in a dose dependent manner, which may lead to an increased risk for ventricular arrhythmias including Torsade de Pointes. Torsade de Pointes has been observed in <0.1%of SUTENT-exposed patients.SUTENT should be used with caution in patients with a history of QT interval prolongation, patients who are taking antiarrhythmics, or patients with relevant pre-existing cardiac disease, bradycardia, or electrolyte disturbances. When using SUTENT, periodic monitoring with on-treatment electrocardiograms and electrolytes (magnesium, potassium) should be considered. Concomitant treatment with strong CYP3A4 inhibitors, which may increase sunitinib plasma concentrations, should be used with caution and dose reduction of SUTENT should be considered [see Dosage and Administration (2.2)].5.4 HypertensionPatients should be monitored for hypertension and treated as needed with standard anti-hypertensive therapy. In cases of severe hypertension, temporary suspension of SUTENT is recommended until hypertension is controlled.Of patients receiving SUTENT for treatment-naïve MRCC, 111/375 patients (30%) receiving SUTENT compared with 13/360 patients (4%) on IFN-α experienced hypertension. Grade 3 hypertension was observed in 36/375 treatment-naïve MRCC patients (10%) on SUTENT compared to 1/360 patient (<1%) on IFN-α. While all-grade hypertension was similar in GIST patients on SUTENT compared to placebo, Grade 3 hypertension was reported in 9/202 GIST patients on SUTENT (4%), and none of the GIST patients on placebo. No Grade 4 hypertension was reported. SUTENT dosing was reduced or temporarily delayed for hypertension in 18/375 patients (5%) on the treatment-naive MRCC study. Two treatment-naïve MRCC patients, including one with malignant hypertension, and no GIST patients discontinued treatment due to hypertension. Severe hypertension (>200 mmHg systolic or 110 mmHg diastolic) occurred in 8/202 GIST patients on SUTENT (4%), 1/102 GIST patients on placebo (1%), and in 20/375 treatment-naïve MRCC patients (5%) on SUTENT and 2/360 patients (1%) on IFN-α.5.5 HemorrhagicEventsIn patients receiving SUTENT for treatment-naïve MRCC, 112/375 patients (30%) had bleeding events compared with 27/360 patients (8%) receiving IFN-α. Bleeding events occurred in 37/202 patients (18%) receiving SUTENT in GIST Study A, compared to 17/102 patients (17%) receiving placebo. Epistaxis was the most common hemorrhagic adverse event reported. Less common bleeding events in GIST or MRCC patients included rectal, gingival, upper gastrointestinal, genital, and wound bleeding. In GIST Study A, 14/202 patients (7%) receiving SUTENT and 9/102 patients (9%) on placebohad Grade 3 or 4 bleeding events. In addition, one patient in Study A taking placebo had a fatal gastrointestinal bleeding event during Cycle 2. Most events in MRCC patients were Grade 1 or 2; there was one Grade 5 event of gastric bleed in a treatment-naïve patient.Tumor-related hemorrhage has been observed in patients treated with SUTENT. These events may occur suddenly, and in the case of pulmonary tumors may present as severe and life-threatening hemoptysis or pulmonary hemorrhage. Fatal pulmonary hemorrhage occurred in 2 patients receiving SUTENT on a clinical trial of patients with metastatic non-small cell lung cancer (NSCLC). Both patients had squamous cell histology. SUTENT is not approved for use in patients with NSCLC. Treatment-emergent Grade 3 and 4 tumor hemorrhage occurred in 5/202 patients (3%) with GIST receiving SUTENT on Study A. Tumor hemorrhages were observed as early as Cycle 1 and as late as Cycle 6. One of these five patients received no further drug following tumor hemorrhage. None of the other four patients discontinued treatment or experienced dose delay due to tumor hemorrhage. No patients with GIST in the Study A placebo arm were observed to undergo intratumoral hemorrhage. Tumor hemorrhage has not been observed in patients with MRCC. Clinical assessment of these events should include serial complete blood counts (CBCs) and physical examinations.Serious, sometimes fatal gastrointestinal complications including gastrointestinal perforation have occurred rarely in patients with intra-abdominal malignancies treated with SUTENT.5.6 HypothyroidismBaseline laboratory measurement of thyroid function is recommended and patients with hypothyroidism should be treated as per standard medical practice prior to the start of SUTENT treatment. All patients should be observed closely for signs and symptoms of hypothyroidism on SUTENT treatment. Patients with signs or symptoms suggestive of hypothyroidism should have laboratory monitoring of thyroid function performed and be treated as per standard medical practice.Treatment-emergent acquired hypothyroidism was noted in eight GIST patients (4%) on SUTENT versus one (1%) on placebo. Hypothyroidism was reported as an adverse reaction in eleven patients (3%) on SUTENT in the treatment-naïve MRCC study and in one patient (<1%) in the IFN-α arm. An additional seven patients (2%) with no prior history of hypothyroidism were started on thyroid replacement therapy while on study.5.7 Adrenal FunctionPhysicians prescribing SUTENT are advised to monitor for adrenal insufficiency in patients who experience stress such as surgery, trauma or severe infection.Adrenal toxicity was noted in non-clinical repeat dose studies of 14 days to 9 months in rats and monkeys at plasma exposures as low as 0.7 times the AUC observed in clinical studies. Histological changes of the adrenal gland were characterized as hemorrhage, necrosis, congestion, hypertrophy and inflammation. In clinical studies, CT/MRI obtained in 336 patients after exposure to one or more cycles of SUTENT demonstrated no evidence of adrenal hemorrhage or necrosis. ACTH stimulation testing was performed in approximately 400 patients across multiple clinical trials of SUTENT. Among patients with normal baseline ACTH stimulation testing, one patient developed consistently abnormal test results during treatment that are unexplained and may be related to treatment with SUTENT. Eleven additional patients with normal baseline testing had abnormalities in the final test performed, with peak cortisol levels of 12-16.4 mcg/dL (normal >18 mcg/dL) following stimulation. None of these patients were reported to have clinical evidence of adrenal insufficiency.5.8 LaboratoryTestsCBCs with platelet count and serum chemistries including phosphate should be performed at the beginning of each treatment cycle for patients receiving treatment with SUTENT.6 ADVERSE REACTIONSThe data described below reflect exposure to SUTENT in 577 patients who participated in a placebo-controlled trial (n=202) for the treatment of GIST or an active-controlled trial (n=375) for the treatment of MRCC. In these two studies, 225 patients were exposed to SUTENT for at least 6 months and 16 were exposed for greater than one year. The population was 23 - 87 years of age and 69% male and 31% female. The race distribution was 92% White, 3% Asian, 2% Black and 3% not reported. The patients received a starting oral dose of 50 mg daily on Schedule 4/2 in repeated cycles.The most common adverse reactions (≥20%) in patients with GIST or MRCC are fatigue, asthenia, diarrhea, nausea, mucositis/stomatitis, vomiting, dyspepsia, abdominal pain, constipation, hypertension, rash, hand-foot syndrome, skin discoloration, altered taste, anorexia, and bleeding. The potentially serious adverse reactions of left ventricular dysfunction, QT interval prolongation, hemorrhage, hypertension, and adrenal function are discussed in Warnings and Precautions (5). Other adverse reactions occurring in GIST and MRCC studies are described below.Because clinical trials are conducted under widely varying conditions,adverse reaction rates observed in the clinical trials of a drug cannot be directlycompared to rates in the clinical trials of another drug and may not reflect therates observed in practice.6.1 Adverse Reactions in GIST Study AMedian duration of blinded study treatment was two cycles for patients onSUTENT (mean 3.0, range 1-9) and one cycle (mean 1.8, range 1-6) for patientson placebo. Dose reductions occurred in 23 patients (11%) on SUTENT andnone on placebo. Dose interruptions occurred in 59 patients (29%) on SUTENTand 31 patients (30%) on placebo. The rates of treatment-emergent, non-fataladverse reactions resulting in permanent discontinuation were 7% and 6% in theSUTENT and placebo groups, respectively.Most treatment-emergent adverse reactions in both study arms were Grade1 or2 in severity. Grade3 or4 treatment-emergent adverse reactions werereported in 56% versus 51% of patients on SUTENT versus placebo,respectively. Table 1 compares the incidence of common (≥10%) treatment-emergent adverse reactions for patients receiving SUTENT and reported morecommonly in patients receiving SUTENT than in patients receiving placebo.Table 1. Adverse Reactions Reported in Study A in at Least 10% of GISTPatients who Received SUTENT and More Commonly Than in PatientsGiven Placebo*GISTSUTENT (n=202) Placebo (n=102)Adverse Reaction,n (%) All Grades Grade 3/4 All Grades Grade 3/4Any 114(56) 52(51) GastrointestinalDiarrheaMucositis/stomatitisConstipation81 (40)58 (29)41 (20)9 (4)2 (1)0 (0)27 (27)18 (18)14 (14)0 (0)2 (2)2 (2)CardiacHypertension 31 (15) 9 (4) 11 (11) 0 (0)DermatologySkin discolorationRashHand-foot syndrome61 (30)28 (14)28 (14)0 (0)2 (1)9 (4)23 (23)9 (9)10 (10)0 (0)0 (0)3 (3)NeurologyAltered taste 42 (21) 0 (0) 12 (12) 0 (0)MusculoskeletalMyalgia/limb pain 28 (14) 1 (1) 9 (9) 1 (1)Metabolism/NutritionAnorexia aAsthenia67 (33)45 (22)1 (1)10 (5)30 (29)11 (11)5 (5)3 (3)* Common Terminology Criteria for Adverse Events (CTCAE), Version 3.0a Includes decreased appetiteOral pain other than mucositis/stomatitis occurred in 12 patients (6%) onSUTENT versus 3 (3%) on placebo. Hair color changes occurred in 15 patients(7%) on SUTENT versus 4 (4%) on placebo. Alopecia was observed in 10patients (5%) on SUTENT versus 2 (2%) on placebo.Table 2 provides common (≥10%) treatment-emergent laboratoryabnormalities.Table 2. Laboratory Abnormalities Reported in Study A in at Least 10% of GIST Patients Who Received SUTENT or Placebo* GIST SUTENT (n=202) Placebo (n=102) Laboratory Parameter, n (%) All Grades* Grade 3/4*a All Grades*Grade 3/4*b Any68 (34) 22 (22) Gastrointestinal AST / ALT Lipase Alkaline phosphatase Amylase Total bilirubin Indirect bilirubin 78 (39) 50 (25) 48 (24) 35 (17) 32 (16) 20 (10) 3 (2) 20 (10) 7 (4) 10 (5) 2 (1) 0 (0) 23 (23) 17 (17) 21 (21) 12 (12) 8 (8) 4 (4) 1 (1) 7 (7) 4 (4) 3 (3) 0 (0) 0 (0) CardiacDecreased LVEF 22 (11) 2 (1) 3 (3) 0 (0) Renal/MetabolicCreatinine Potassium decreased Sodium increased 25 (12) 24 (12) 20 (10) 1 (1) 1 (1) 0 (0) 7 (7) 4 (4) 4 (4) 0 (0)0 (0)1 (1) Hematology Neutrophils Lymphocytes Platelets Hemoglobin 107 (53) 76 (38) 76 (38) 52 (26) 20 (10) 0 (0) 10 (5) 6 (3) 4 (4) 16 (16) 4 (4) 22 (22) 0 (0) 0 (0) 0 (0) 2 (2) LVEF=Left ventricular ejection fraction* Common Terminology Criteria for Adverse Events (CTCAE), Version 3.0aGrade 4 laboratory abnormalities in patients on SUTENT included alkalinephosphatase (1%), lipase (2%), creatinine (1%), potassium decreased (1%),neutrophils (2%), hemoglobin (2%), and platelets (1%).bGrade 4 laboratory abnormalities in patients on placebo included amylase(1%), lipase (1%) and hemoglobin (2%).6.2 Adverse Reactions in the Treatment-Naïve MRCC StudyThe as-treated patient population for the interim safety analysis of thetreatment-naive MRCC study included 735 patients, 375 randomized toSUTENT and 360 randomized to IFN-α. The median duration of treatment was5.6 months (range: 0.4-15.6) for SUTENT treatment and 4.1 months (range:0.1-13.7) on IFN-α treatment. Dose reductions occurred in 121 patients (32%)on SUTENT and 77 patients (21%) on IFN-α. Dose interruptions occurred in142 patients (38%) on SUTENT and 115 patients (32%) on IFN-α. The rates oftreatment-emergent, non-fatal adverse reactions resulting in permanentdiscontinuation were 9% and 12% in the SUTENT and IFN-α groups,respectively. Most treatment-emergent adverse reactions in both study armswere Grade 1 or 2 in severity. Grade 3 or 4 treatment-emergent adversereactions were reported in 67% versus 51% of patients on SUTENT versusIFN-α, respectively.Table 3 compares the incidence of common (≥10%) treatment-emergentadverse reactions for patients receiving SUTENT versus IFN-α.Table 3. Adverse Reactions Reported in at Least 10% of Patients with MRCC Who Received SUTENT or IFN-α*Treatment-Naïve MRCCSUTENT (n=375) IFN-α (n=360)Adverse Reaction, n (%) All Grades Grade 3/4a All Grades Grade 3/4bAny 370 (99) 250 (67) 354 (98) 184(51) ConstitutionalFatigue Asthenia Fever Weight decreased Chills 218 (58) 79 (21) 62 (17) 45 (12) 42 (11) 35 (9) 27 (7) 3 (1) 0 (0) 3 (1) 199 (55) 85 (24) 129 (36) 54 (15) 108 (30) 50 (14) 20 (6) 0 (0) 2 (1) 0 (0) GastrointestinalDiarrhea Nausea Mucositis/stomatitis Vomiting DyspepsiaAbdominal paincConstipationDry mouthGERD/refluxesophagitisFlatulenceOral pain Glossodynia 218 (58) 183 (49) 162 (43) 105 (28) 105 (28) 83 (22) 60 (16) 45 (12) 42 (11) 39 (10) 38 (10) 37 (10) 22 (6) 16 (4) 12 (3) 15 (4) 4 (1) 10 (3) 0 (0) 0 (0) 0 (0) 0 (0) 0 (0) 0 (0) 72 (20) 136 (38) 14 (4) 51 (14) 14 (4) 42 (12) 44 (12) 26 (7) 3 (1) 8 (2) 2 (1) 2 (1) 0 (0) 5 (1)2 (<1)3 (1) 0 (0) 5 (1) 1 (<1) 1 (<1) 0(0) 0 (0) 0 (0) 0 (0) Cardiac Hypertension Edema, peripheral 111 (30) 42 (11) 36 (10) 2 (1) 13 (4) 15 (4) 1 (<1) 2 (1) Dermatology Rash Hand-foot syndrome Skin discoloration/ yellow skin Dry skin Hair color changes 103 (27) 78 (21) 72 (19) 67 (18) 56 (16) 3 (1) 20 (5) 0 (0) 1 (<1) 0 (0) 40 (11) 3 (1) 0 (0) 23 (6) 1 (<1) 2 (1) 0 (0) 0 (0) 0 (0) 0 (0) Neurology Altered taste dHeadache Dizziness 166 (44) 68 (18) 28 (7) 1 (<1) 3 (1) 1 (<1) 52 (14) 61 (17) 42 (12) 0 (0) 0 (0) 1 (<1) Musculoskeletal Back pain Arthralgia Pain in extremity/ limb discomfort 70 (19) 69 (18) 65 (17) 13 (3) 5 (1) 6 (2) 44 (13) 60 (17) 28 (8) 6 (2) 1 (<1) 4 (1) Respiratory Cough Dyspnea 64 (18) 58 (15) 2 (1) 15 (4) 45 (12) 65 (18) 0 (0) 14 (4) Metabolism/Nutrition Anorexia e Dehydration 142 (38) 30 (8) 6 (2) 8 (2) 145 (40) 17 (5) 7 (2) 2 (1)Hemorrhage/BleedingBleeding, all sites 112 (30) 10 (3)f27 (8) 2 (1) PsychiatricInsomnia Depression g 42 (11) 29 (8) 1 (<1) 0 (0) 31 (9) 47 (12) 0 (0) 5 (1) * Common Terminology Criteria for Adverse Events (CTCAE), Version 3.0 aGrade 4 ARs in patients on SUTENT included back pain (1%),arthralgia (<1%), asthenia (<1%), dehydration (<1%), fatigue (<1%), limb pain (<1%) and rash (<1%). bGrade 4 ARs in patients on IFN-α included dyspnea (1%), fatigue (1%) and depression (<1%). cIncludes flank pain dIncludes ageusia, hypogeusia and dysgeusia eIncludes decreased appetite fIncludes one patient with Grade 5 gastric hemorrhage gIncludes depressed moodTreatment-emergent Grade 3/4 laboratory abnormalities are presented in Table 4.。

消化系统疾病名称

胃：acute/chronic gastritis急/慢性胃炎chronic superficial gastritis 慢性浅表性胃炎chronic atrophic gastritis:慢性萎缩性胃炎acute hemorrhagic gastritis：急性出血性胃炎gastric ulcer 胃溃疡duodenal ulcer 十二指肠溃疡digestive tract ulcer 消化道溃疡Gastric Volvulus 胃扭转['vɔlvjuləs] 扭转gastrolithiasis：胃石症gastrinoma 胃泌素瘤esophagus/ leiomyosarcoma 食道平滑肌瘤leiomyoma of stomach 胃平滑肌瘤gastric stromal tumor 胃间质瘤stromal ['strəuməl]：基质的；gastric cancer 胃癌pyloric obstruction幽门梗阻Gastroduodenal bleeding 胃十二指肠出血Gastroduodenal vascular malformation 胃十二指肠血管畸形foreign body in stomach 胃内异物functional dyspepsia 功能性消化不良anastomotic obstruction 吻合口梗阻肠：acute hemorrhagic necrotizing enteritis 急性出血性坏死性肠炎ulcerative colitis 溃疡性结肠炎enterophthisis 肠结核intestinal polyp 肠息肉rectal polyp 直肠息肉Colon Polyps 结肠息肉carcinoma of ampulla 十二指肠壶腹癌colorectal cancer 结直肠癌duodenal ulcer 十二指肠溃疡duodenitis 十二指肠炎irritable bowel syndrome (IBS):肠易激综合征Crohn disease 克罗恩病intestinal obstruction肠梗阻Acute gastroenteritis 急性胃肠炎Radiation enteritis 放射性肠炎tuberculosis of intestine 肠结核[tju:,bə:kju'ləusis]结核ischemic bowel disease 缺血性肠病[is'ki:mik]appendicitis 阑尾炎肝胆：hepatitis gravis 重型肝炎acute severe hepatitis 急性重型肝炎hepatitis B 乙型肝炎post-hepatitis B liver cirrhosis 乙型肝炎后肝硬化alcoholic hepatitis 酒精性肝炎drug-induced hepatitis 药物性肝炎autoimmune hepatitis 自身免疫性肝炎Hepatitis cholestasis 胆汁淤积型肝炎[,kəuli'steisis]hepatic encephalopathy肝性脑病Liver cirrhosis 肝硬化Hepatocellular Carcinoma 肝细胞癌Fatty liver 脂肪肝Hepatic cyst 肝囊肿Multiple hepatic cysts 多囊肝Hepatic hemangioma 肝血管瘤[hi,mændʒi'əumə]血管瘤hepatorenal syndrome 肝肾综合征liver colonorchiasis 肝吸虫病cholecystitis 胆囊炎hepatocholangeitis 肝胆管炎sclerosing cholangitis 硬化性胆管炎Gallbladder polyps 胆囊息肉intrahepatic bile duct stone 肝内胆管结石choledocholithiasis 胆总管结石cholelithiasis 胆石症tumors of biliary tract胆道肿瘤obstructive jaundice 梗阻性黄疸pyogeniccholangitis 化脓性胆管炎pyogenic [,paiəu'dʒenik] 化脓的胰腺：pancreatitis 胰腺炎Pancreatolithiasis 胰石病 lithiasis [li'θaiəsis] 结石病pancreatic cancer 胰腺癌pancreatic abscess 胰腺脓肿pancreatic pseudocyst 胰腺假性囊肿Stricture of pancreatic duct 胰管狭窄Stricture of pancreatic duct 胰管狭窄食管: reflux esophagitis 反流性食管炎Gastroesophageal reflux disease 胃食管反流性疾病Cardiaoesophagus lost atony disease 贲门失弛缓症hiatal hernia 食管裂孔疝cancer of the esophagus 食管癌oesophageal phlebeurysma食管静脉曲张Esophagostenosis 食道狭窄Esophagostoma 食道瘘foreign body in esophagus 食管异物MalloryWeiss syndrome 贲门黏膜撕裂综合症leiomyoma of esophagus 食道平滑肌瘤[,laiəumai'əumə]Esophageal stromal tumor 食道间质瘤Esophagostenosis 食道狭窄其他：splenic abscess脾脓肿。

gastrointestina terminologyl医学英语

History of present illness
On May 19, 2008 she had an episode of severe epigastric pain after drinking water, then she went to the Second Affiliated Hospital of Zhejiang University. There, the plain abdominal radiograph showed "obvious gas accumulation in bowels", abdominal CT showed "significant dilation of right colon, stricture in the middle of transverse colon is considered”. He was given antispasmodic and anti-inflammatory agent. The symptoms were partially relieved and she was discharged.
Teeth Dent/o --- dentist Odont/o --- orthodontist Gum Gingiv/o --- gingivitis Esophagus Esophag/o --- esophagoscope Stomach Gastr/o --- gastroscopy Pharynx Pharyng/o --- pharyngitis Pylorus Pylor/o --- pylorotomy

Through Dia- — diarrhea Bad,painful Dys- — dystrophy Excessive Hyper- --- hyperemesis Around Perianal Under, below Sublingual

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