中国基层医药
中國基層醫藥
중국기층의약
Chinese Journal of Primary Medicine and Pharmacy
2015年
22期
3440-3444,3445
,共6页
肝细胞癌%E-钙黏素%胰岛素样生长因子 1 受体%复发%预后
肝細胞癌%E-鈣黏素%胰島素樣生長因子 1 受體%複髮%預後
간세포암%E-개점소%이도소양생장인자 1 수체%복발%예후
Hepatocellular carcinoma%E -cad%IGF -1R%Recurrence%Prognosis
目的:探讨 E-cad 和 IGF-1R 表达与原发性肝细胞癌(HCC)患者肝切除术后复发的关系。方法收集2010年1月至2012年12月因原发性 HCC 实施肝切除术的具备完整资料的91例连续病例,通过RT-PCR 方法测定组织标本中 E-cad 和 IGF-1R 表达,分别分析 E-cad 和 IGF-1R 的表达与临床病理因素以及肝切除术后复发的关系。结果 E-cad 在肝癌组织中的表达率较正常组织显著下降(38.7%比75.0%)。E-cad 阴性组患者其术后复发率明显增高(71.1%),其肿瘤侵及肝被膜者多(χ2=5.144,P =0.036),TNM分期 II ~Ⅳ期者多(χ2=7.161,P =0.009)。IGF-1R 在肝癌组织中的表达率较正常组织显著上升(66.1%比20.0%),IGF-1R 阳性患者术后复发率显著增高(68.3%),其肿瘤侵及肝被膜者多(χ2=5.144,P =0.036),无瘤包膜者多(χ2=7.201,P =0.012),TNM分期 II ~Ⅳ期者多(χ2=4.195,P =0.014),门脉癌栓者多(χ2=6.538,P =0.032)。E-cad 与 IGF-1R 表达存在显著负相关关系(χ2=14.329,P =0.000)。结论 E-cad 在肝癌组织中表达显著低于正常肝组织。IGF-1R 在肝癌组织中表达显著高于正常组织。两者表达均与肝癌侵袭转移及患者术后复发相关。同时 E-cad 与 IGF-1R 在肝癌组织标本中的表达存在相关性,两者可能在肝癌发生发展中起协调作用。
目的:探討 E-cad 和 IGF-1R 錶達與原髮性肝細胞癌(HCC)患者肝切除術後複髮的關繫。方法收集2010年1月至2012年12月因原髮性 HCC 實施肝切除術的具備完整資料的91例連續病例,通過RT-PCR 方法測定組織標本中 E-cad 和 IGF-1R 錶達,分彆分析 E-cad 和 IGF-1R 的錶達與臨床病理因素以及肝切除術後複髮的關繫。結果 E-cad 在肝癌組織中的錶達率較正常組織顯著下降(38.7%比75.0%)。E-cad 陰性組患者其術後複髮率明顯增高(71.1%),其腫瘤侵及肝被膜者多(χ2=5.144,P =0.036),TNM分期 II ~Ⅳ期者多(χ2=7.161,P =0.009)。IGF-1R 在肝癌組織中的錶達率較正常組織顯著上升(66.1%比20.0%),IGF-1R 暘性患者術後複髮率顯著增高(68.3%),其腫瘤侵及肝被膜者多(χ2=5.144,P =0.036),無瘤包膜者多(χ2=7.201,P =0.012),TNM分期 II ~Ⅳ期者多(χ2=4.195,P =0.014),門脈癌栓者多(χ2=6.538,P =0.032)。E-cad 與 IGF-1R 錶達存在顯著負相關關繫(χ2=14.329,P =0.000)。結論 E-cad 在肝癌組織中錶達顯著低于正常肝組織。IGF-1R 在肝癌組織中錶達顯著高于正常組織。兩者錶達均與肝癌侵襲轉移及患者術後複髮相關。同時 E-cad 與 IGF-1R 在肝癌組織標本中的錶達存在相關性,兩者可能在肝癌髮生髮展中起協調作用。
목적:탐토 E-cad 화 IGF-1R 표체여원발성간세포암(HCC)환자간절제술후복발적관계。방법수집2010년1월지2012년12월인원발성 HCC 실시간절제술적구비완정자료적91례련속병례,통과RT-PCR 방법측정조직표본중 E-cad 화 IGF-1R 표체,분별분석 E-cad 화 IGF-1R 적표체여림상병리인소이급간절제술후복발적관계。결과 E-cad 재간암조직중적표체솔교정상조직현저하강(38.7%비75.0%)。E-cad 음성조환자기술후복발솔명현증고(71.1%),기종류침급간피막자다(χ2=5.144,P =0.036),TNM분기 II ~Ⅳ기자다(χ2=7.161,P =0.009)。IGF-1R 재간암조직중적표체솔교정상조직현저상승(66.1%비20.0%),IGF-1R 양성환자술후복발솔현저증고(68.3%),기종류침급간피막자다(χ2=5.144,P =0.036),무류포막자다(χ2=7.201,P =0.012),TNM분기 II ~Ⅳ기자다(χ2=4.195,P =0.014),문맥암전자다(χ2=6.538,P =0.032)。E-cad 여 IGF-1R 표체존재현저부상관관계(χ2=14.329,P =0.000)。결론 E-cad 재간암조직중표체현저저우정상간조직。IGF-1R 재간암조직중표체현저고우정상조직。량자표체균여간암침습전이급환자술후복발상관。동시 E-cad 여 IGF-1R 재간암조직표본중적표체존재상관성,량자가능재간암발생발전중기협조작용。
Objective To investigate the relationship between expression of E -cad and IGF -1R and the recurrence of patients with primary hepatocellular carcinoma (HCC)who underwent liver resection.Methods The clinical data of 91 cases of primary HCC underwent liver resection from January 2010 to December 2012 were analyzed retrospectively.The expression of E -cad and IGF -1R was detected by RT -PCR,and the relationship between expression of E -cad and IGF -1R and the recurrence of patients was analyzed.Results The expression of E -cad was obviously lower in HCC tissues than that in normal liver tissues,with the expression percentage of 38.7% vs. 75.0%.The recurrence rate of E -cad negative group was higher(71.1%).The TNM Ⅱ -Ⅳ stage (χ2 =7.161, P =0.009)and liver capsule invasion (χ2 =5.144,P =0.036)in E -cad negative group were higher than E -cad positive group.The expression of IGF -1R was obviously higher in HCC tissues than that in normal liver tissues,with the expression percentage of 66.1% vs.20.0%.The recurrence rate of IGF -1R negative group was higher(68.3%). The TNMⅡ-Ⅳ stage (χ2 =4.195,P =0.014),liver capsule invasion (χ2 =5.144,P =0.036),non -tumor capsularin (χ2 =7.201,P =0.012)and PVTT(χ2 =6.538,P =0.032)in E -cad negative group were higher than E -cad positive group.And there was negative correlation between the expression of E -cad and IGF -1R(χ2 =14.329,P =0.000).Conclusion The mRNA expression of E -cad in the tissues of HCC is obviously lower than normal liver tissues.The mRNA expression of IGF -1R in the tissues of HCC is obviously higher than normal liver tissues.The expressions of E -cad and IGF -1R are associated with the degree of local invasion and malignant.The E -cad and IGF -1R expression is correlated in the tissues of HCC,which means that E -cad and IGF -1R play synergistic effect in HCC genesis.