【摘要】：目的：探討腫瘤壞死因子α(TNF-α)基因-308GA、白介素10(IL-10)基因-1082AG位點多態(tài)與非霍奇金淋巴瘤(Non-Hodgkin's lymphoma,NHL)易感性的關(guān)系。方法：系統(tǒng)檢索Pubmed. EMBASE、MEDLINE、 ISI Web of Science中文數(shù)據(jù)庫中國生物醫(yī)學(xué)文獻數(shù)據(jù)庫(CBM)、中國知網(wǎng)數(shù)據(jù)庫(CNKI)、重慶維普(VIP)數(shù)據(jù)庫和萬方數(shù)據(jù)庫等中外文數(shù)據(jù)庫,收集關(guān)于TNF-α基因-308GA和IL-10基因-1082AG位點基因多態(tài)性與NHL關(guān)聯(lián)的病例對照研究和隊列研究,并追蹤參考文獻利于百度、Google等搜索引擎進行全面檢索,檢索時間從建庫到2013年5月。納入公開發(fā)表的試驗設(shè)計嚴謹,試驗方法可靠的病例對照和隊列研究,并且其結(jié)果均可提供提供各基因型在病例和對照中的分布頻率或者例數(shù)或者比值比(odds ratio, OR)和95%可信區(qū)間(95%confidence interval,95%CI),對納入的研究文獻采用量表進行質(zhì)量評價。本論文所有的研究分析均采用R軟件meta程序包進行,分別分析等位基因遺傳模型、顯性遺傳模型、隱性遺傳模型、加性遺傳模型和超顯性遺傳模型與NHL的關(guān)系,選用OR及其95%CI作為合并效應(yīng)值。同時進行亞組分析上述五種模型與彌漫性大B細胞淋巴瘤(diffuse large B cell lymphoma, DLBCL)和濾泡性淋巴瘤(follicular lymphoma, FNHL)的關(guān)系,并且在剔除低質(zhì)量研究文獻后進行敏感性分析。利用漏斗圖和Egger's檢驗來綜合評價研究文獻的發(fā)表偏倚。結(jié)果：(1)TNF-α基因-308GA位點多態(tài)與NHL的關(guān)系：等位基因遺傳模型(A allele vs. G allele, OR=1.18,95%CI=[1.04,1.34],P=0.0128)、顯性遺傳模型(GA+AA vs. GG, OR=1.15,95%CI=[1.01,1.31], P=0.0394).隱性遺傳模型(AA vs. GG+GA, OR=1.46,95%CI=[1.12,1.90], P=0.005)、加性遺傳模型(AA vs. GG,OR=1.51,95%CI=[1.15,1.99],P=0.0031)均顯示會增加NHL的發(fā)病風(fēng)險,而超顯性遺傳模型(GG+AA vs. GA, OR=0.94,95%CI=[0.84,1.06],P=0.3073)與NHL易感性無關(guān)聯(lián)�；贜HL腫瘤類型的亞組分析,我們分析了DLBCL和FNHL兩種NHL亞型與該位點的關(guān)系,結(jié)果顯示在DLBCL亞組中,該位點與DLBCL易感性有關(guān)聯(lián),但是未發(fā)現(xiàn)其與FNHL易感性存在著關(guān)聯(lián)。(2)IL-10基因-1082AG位點多態(tài)與NHL的關(guān)系：顯性遺傳模型(AG+GG vs. AA, OR=1.16,95%CI=[1.04,1.30], P=0.0073)會增加NHL的發(fā)病風(fēng)險�；贜HL腫瘤類型的亞組分析,我們分析了DLBCL和FNHL兩種NHL亞型與IL-10基因-1082AG位點的關(guān)系,結(jié)果顯示在DLBCL亞組中,顯性遺傳模型(AG+GG vs. AA, OR=1.25,95%CI=[1.01,1.54], P=0.0363)會增加DLBCL的發(fā)病風(fēng)險,超顯性遺傳模型(AA+GG vs. AG, OR=0.85,95%CI=[0.73,0.97],P=0.0199),則會降低DLBCL的發(fā)病風(fēng)險；在FNHL亞組中加性遺傳模型(GG vs.AA, OR=3.22,95%CI=[2.40,4.32], P0.0001)會增加FNHL的發(fā)病風(fēng)險。結(jié)論：(1)TNF基因-308GA多態(tài)位點A等位基因可顯著增加NHL,特別是DLBCL的發(fā)病風(fēng)險。(2)IL-10基因-1082AG多態(tài)位點可能與NHL易感性有關(guān)。
[Abstract]:Objective: to investigate the relationship between polymorphism of tumor necrosis factor 偽 (TNF- 偽) gene -308GA, interleukin-10 (IL-10) gene -1082 AG and susceptibility to non Hodgkin's lymphoma (NHL). Methods: Pubmed. were searched systematically. ISI Web of Science Chinese database, Chinese biomedical literature database, (CBM), China knowledge network database, (CNKI), Chongqing Weipu (VIP) database, Wanfang database and other Chinese and foreign language databases, Case control studies and cohort studies on the association of NHL with TNF- 偽 gene -308GA and IL-10 gene -1082AG locus polymorphism were collected. To include publicly published case-control and cohort studies with rigorous design and reliable trial methods, The results can provide the distribution frequency or the number of cases or the ratio of each genotype in the case and control group than (odds ratio, OR) and 95% confidence interval (95%confidence interval-95 CI). The quality evaluation of the included research literature was carried out by using the scale. All the research and analysis in this paper are carried out with R software meta package. The relationships between allele genetic model, dominant genetic model, recessive genetic model, additive genetic model and superdominant genetic model and NHL are analyzed, respectively. OR and its 95%CI were selected as the combined effect value. The relationship between the above five models and diffuse large B-cell lymphoma (diffuse large B cell lymphoma, DLBCL) and follicular lymphoma (follicular lymphoma, FNHL) was analyzed by subgroup analysis. Funnel diagram and Egger's test were used to evaluate the publication bias of the research literature. Results: (1) the relationship between polymorphism of TNF- 偽 gene -308GA locus and NHL: the allelic genetic model (A allele vs. G allele, OR1.18995 CI = [1.04n1.34] PN0.0128), and the dominant genetic model (GA AA vs. GG, OR-1.1595CI = [1.01n1.31], P0.0394). The recessive genetic model (AA vs. GG GA, OR1. 466 / 95 CI = [1.121.90], P0. 005) and additive genetic model (AA vs.) GGG OR1. 51 ~ 95CI= [1. 151.99] P0. 0031) all showed that the risk of NHL was increased, but the overdominance genetic model (GG AA vs. GA, OR0. 949 5CII = [0. 841.06] Pu 0.3073) was not associated with the susceptibility of NHL. Based on the subgroup analysis of NHL tumor types, we analyzed the relationship between DLBCL and FNHL NHL subtypes and this locus. The results showed that in the DLBCL subgroup, this locus was associated with DLBCL susceptibility. (2) the relationship between polymorphism of IL-10 gene -1082AG and NHL: the dominant genetic model (AG GG vs. AA, OR1.16995 CI = [1.04N 1.30], P0. 0073) could increase the risk of NHL. Based on the subgroup analysis of NHL tumor types, we analyzed the relationship between the NHL subtypes of DLBCL and FNHL and the IL-10 gene -1082 AG locus. The results showed that in DLBCL subgroup, the dominant genetic model (AG GG vs. AA, OR1. 25 ~ 95 CI = [1. 01 + 1. 54], Pn0. 0363) increased the risk of DLBCL. The risk of DLBCL was decreased by (AA GG vs. AG, OR0.85 / 95CI = [0.730.97] P0.0199, and the risk of FNHL was increased by the additive genetic model (GG vs.AA, OR3.22C95CI= [2.404.32], P0.0001) in the FNHL subgroup. Conclusion: (1) allele A of TNF gene -308GA polymorphism can increase the risk of NHL, especially the risk of DLBCL. (2) the polymorphism of IL-10 gene -1082 AG may be related to the susceptibility of NHL.
【學(xué)位授予單位】：瀘州醫(yī)學(xué)院
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2013
【分類號】：R733.1

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本文編號：2149219