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机构地区:[1]西安交通大学医学部第一附属医院妇产科,陕西西安710061 [2]西安市第四医院妇产科,陕西西安710004
出 处:《西安交通大学学报(医学版)》2015年第3期337-340,共4页Journal of Xi’an Jiaotong University(Medical Sciences)
基 金:国家自然科学基金资助(No.81172489)~~
摘 要:目的探索缺氧诱导因子-1α(HIF-1α)和碳酸酐酶IX(CAIX)在妊娠滋养细胞疾病发生、发展中的作用。方法应用免疫组化S-P法检测32例正常早孕绒毛(NP)、33例葡萄胎(HM)和26例侵袭性葡萄胎(IM)组织中HIF-1α和CAIX的表达情况。结果 HIF-1α在NP、HM和IM中的阳性表达率分别为28.1%(9/32)、45.5%(15/33)和73.1%(19/26)。在IM中的表达水平明显高于HM组和NP组,差异具有统计学意义(P<0.05);HM组与NP组差异无统计学意义(P>0.05)。CAIX在NP、HM和IM中的阳性表达率分别为31.2%(10/32)、3.0%(1/33)、57.7%(15/26)。在IM中的表达水平明显高于HM组和NP组,差异具有统计学意义(P<0.05);在HM组织中几乎呈阴性表达,与NP组差异具有统计学意义(P<0.05)。HIF-1α和CAIX在IM中的表达无显著性关联(P>0.05)。结论 HIF-1α和CAIX的表达水平随着滋养细胞恶性程度的增加而明显升高,提示两者可能与妊娠滋养细胞疾病的发生发展及恶性转化有关。Objective To explore the role of hypoxia-inducible factor 1α(HIF-1α)and carbonic anhydrase IX (CAIX)in oncogenesis and development of gestational trophoblastic disease (GTD).Methods The expressions of HIF-αand CAIX were determined immunohistochemically by specific antibodies on formalin-fixed paraffin sections of normal pregnancy villi (32 cases),hydatidiform moles (33 cases),and invasive hydatidiform moles (26 cases). Results The positive rate of HIF-1α in normal pregnancy villi (NP),hydatidiform moles (HM)and invasive hydatidiform moles (IM) was 28.1% (9/32 ), 45.5% (1 5/33 ) and 73.1% (1 9/26 ), respectively. It was significantly higher in IM than in HM and NP(P 〈0.05),and there was no statistical difference between the latter two groups (P 〉0.05).The positive rate of CAIX in NP,HM and IM was 31.2 (10/32),3.0(1/33)and 57.7%(1 5/26),respectively.It was significantly higher in IM than in HM and NP (P 〈 0.05 ),and CAIX was almost negatively expressed in HM group,which differed significantly from that in NP group (P 〈0.05 ).There was no correlation between HIF-1αand CAIX expressions in IM (P 〉0.05).Conclusion The expressions of HIF-1αand CAIX were both higher in gestational trophoblastic neoplasia than in normal pregnancy and hydatidiform moles, which indicates that HIF-1αand CAIX may play a role in oncogenesis and development of malignant transformation of trophoblastic cells.
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