胃黏膜相关淋巴组织淋巴瘤BCL10核表达与其对幽门螺杆菌根除治疗无反应相关

背景：经幽门螺杆菌（H．pylori）根除治疗，约75％的早期胃黏膜相关淋巴组织（MALT）淋巴瘤患者可获得完全缓解。肿瘤细胞有BCL10核表达和t（11；18）（q21；q21）可能提示胃MALT淋巴瘤对根除治疗无反应。目的：探讨单纯H．pylori根除治疗对国人早期胃MALT淋巴瘤的疗效，以及肿瘤细胞BCL10核表达和t（11；18）（q21；q21）对治疗方案选择的提示作用。方法：收集19例早期胃MALT淋巴瘤患者，以免疫组化方法检测BCL10核表达，以间期荧光原位杂交方法检测t（11：18）（q21；q21）。所有患者均首选H．pylori根除治疗，并行内镜活检病理随访。结果：本组19例早期胃MALT淋巴瘤患者中10例（52．6％）经单纯H．pylori根除治疗获得完全缓解。10例完全缓解者中2例（20，0％）肿瘤细胞BCL10核表达阳性，9例对根除治疗无反应者中7例（77．8％）阳性，阳性率显著高于完全缓解者（P〈0．05）。14例患者行t（11；18）（q21；q21）检测，8例完全缓解者均未检出该易位，6例对根除治疗无反应者中3例（50．0％）检出该易位．两组检出率差异无统计学意义（P〉0．05）。结论：单纯H．pylori根除治疗可使本组52．6％的早期胃MALT淋巴瘤患者获得完全缓解。胃MALT淋巴瘤肿瘤细胞BCL10核表达与其对根除治疗无反应相关。     

肺黏膜相关B淋巴细胞淋巴瘤中BCL10蛋白表达和染色体易位的关系

目的 检测肺黏膜相关B淋巴细胞淋巴瘤(MALT淋巴瘤)中BCL10蛋白表达及目前报道的染色体易位的发生率.包括t(11;18)/AP12-MALTI、t(1;14)/BCLIO-lgH及t(14;18)/MALTI-IgH.探讨BCL10异常表达和染色体易位的关联程度.方法 收集复旦大学附属肿瘤医院病理科2000～2007年诊断的23例肺MALT淋巴瘤患者的病理组织蜡块,其中男19例,女4例,年龄27～84岁,平均55.8岁.用免疫组织化学EnVision法检测BCL10蛋白的表达,用荧光原位杂交(FISH)法分别检测API2-MALTI、BCL10、MALTl和IgH基因的异常,并对可联络到的10例病例进行随访.结果 23例中19例BCL10蛋白表达阳性,其中细胞质阳性9例,细胞核阳性者10例;用FISH方法榆测了全部病例,其中9例可检测到API2-MALTI融合基因.1例町能为BCL10-IgH融合,未发现IgH-MALT1基因异常.细胞核BCL10蛋白表达阳性的10例中,仅5例同时伴有基因异常;BCL10异常核表达与染色体易位无明显相关性(x2=0.306,P=0.685).有随访资料的10例患者全部生存(随访时间7～35个月),但治疗方式各异(单纯化疗、手术或手术加化疗).结论 肺MALT淋巴瘤患者组织内BCL10在细胞核中表达率较高,t(11;18)/AP12-MALT1融合基因是肺MALT淋巴瘤中最常见的染色体异常,而t(1;14)/BCL10-IgH和t(14;18)/MALT1-IgH在肺MALT淋巴瘤中不常见;核表达BCL10与发生染色体异常是瓦相独立的凶素,但这些特点对肺MALT淋巴瘤的诊断有一定的辅助价值,特别是对纤维支气管镜活检小标本组织的诊断更有帮助.     

原发性胃淋巴瘤凋亡抑制蛋白2-黏膜相关淋巴瘤转位基因1融合基因检测的意义

目的 研究原发性胃淋巴瘤(PGL)内镜活检组织中凋亡抑制蛋白2-黏膜相关淋巴瘤转位基因1（API2-MALT1）融合基因检测的可行性,探讨该融合基因在PGL的表达及其在PGL诊断、治疗等方面的临床价值。方法对32例疑诊为PGL者进行超声内镜检查和黏膜活检,活检标本分别进行组织病理、免疫组织化学检查和用荧光定量RT-PCR测定API2-MALT1融合基因。总结、分析诊断明确的PGL中API2-MALT1融合基因的表达以及该融合基因与PGL诊断、分型和治疗等方面的关系。结果32例疑诊PGL者中14例经病理检查和免疫组织化学检查确诊为PGL,其中胃黏膜相关淋巴组织(MALT)淋巴瘤11例,胃弥漫性大B细胞淋巴瘤(DLBCL)3例。API2-MALT1融合基因检测阳性5例,均为胃MALT淋巴瘤,约占胃MALT淋巴瘤(5/11)的45％。3例DLBCL患者API2-MALT1融合基因检测均阴性。API2-MALT1融合基因阴性组病变浸润深度和淋巴结浸润状况较阳性组严重。5例API2-MALT1融合基因阳性者中幽门螺杆菌(Hp)阳性2例,9例阴性者中Hp阳性5例。API2-MALT1融合基因阳性组5例行抗Hp治疗皆无效,但化学治疗有效;阴性组中5例Hp阳性者完全缓解2例,4例Hp阴性者抗Hp治疗无效。结论 API2-MALT1融合基因是胃MALT淋巴瘤的常见遗传学异常。内镜定位活检标本通过荧光定量PCR法检测该融合基因在临床上是可行的,该融合基因的检测对PGL诊断、治疗和预后评估均有一定的价值。     

组织学结合分子生物学参数诊断早期胃黏膜相关淋巴组织淋巴瘤

背景：胃黏膜相关淋巴组织（MALT）是幽门螺杆菌（H．pylori）感染的特殊征象，临床上较为常见．而胃MALT淋巴瘤则极为少见，两者在形态学上难以鉴别。目的：建立胃活检组织胃MALT淋巴瘤的阶梯式诊断流程，为H.pylori根除治疗提供依据。方法：收集31例胃淋巴样增生（GLH）病例，行组织学、蛋白质、DNA和染色体水平的阶梯式检查。GLH组织学分级参照Isaacson标准，以免疫组化方法检测L26、UCHL-1、免疫球蛋白轻链κ、λ和Ki-67，半巢式聚合酶链反应（PCR）检测免疫球蛋白重链（IgH）基因重排，逆转录（RT）-PCR检测AP12-MALT1融合。29例H.pylori感染者接受根除治疗，比较治疗前后的内镜和组织学表现。结果：23例GLH病例组织学分级为Ⅱ或Ⅲ级。仅2例为胃MALT淋巴瘤（组织学Ⅴ级）。1例胃MALT淋巴瘤表达λ轻链限制，10例GLH（包括2例胃MALT淋巴瘤）检测到单克隆IgH基因重排，2例胃MALT淋巴瘤检测到API2-MALT1融合。随着GLH组织学分级的递增．Ki-67标记率和单克隆IgH基因重排榆出率显著增高（P〈0．05）。根除H．pylori后随访1．5～37个月，18例内镜和组织学完全缓解。4例部分缓解。7例无变化。结论：组织学结合Ki-67、IgH基因重排和API2-MALT1融合检测的阶梯式诊断流程有助于诊断早期胃MALT淋巴瘤，亦有助于药物治疗后的随访。     

幽门螺旋菌清除后胃粘膜相关淋巴样组织中原发性低度恶性B细胞胃淋巴瘤的消退

胃原发性低度恶性B淋巴细胞淋巴瘤具有粘膜相关淋巴样组织(MALT)的特征。据统计,90％以上的胃MALT淋巴瘤中可找到幽门螺旋菌(HP)。在低分化胃MALT淋巴瘤中,母细胞转化、上皮下浆细胞分化和淋巴滤泡中心有肿瘤细胞特异性定位,提示此淋巴瘤为免疫反应引起的。可能是幽门螺旋菌激起免疫反应,刺激肿瘤生长。如此则幽门螺旋菌的清除应能抑制低度恶性胃淋巴瘤的生长。     

胃黏膜相关淋巴样组织淋巴瘤早期诊治的探讨

目的　探讨胃黏膜相关淋巴样组织 (MALT)淋巴瘤早期诊断的方法及根除幽门螺杆菌(Hp)治疗的临床意义。方法　观察胃淋巴增殖症 (GLH)患者根除Hp前后组织学、Ki 6 7标记率及免疫球蛋白重链 (IgH)重排克隆性变化的情况 ,组织学参照Isaacson组织学评分标准 ,免疫组化检测L2 6、UCHL 1、抗κ、抗λ及抗Ki 6 7,半巢式PCR检测IgH重排。结果　 31例GLH以慢性胃炎及胃溃疡为主 ,男女比例 1.8∶1,平均病程 6 .8年。 2 9例感染Hp。组织学评分以Ⅱ、Ⅲ级者多见。仅 1例表达λ轻链限制性 ,10例 (32 .3% )检测到单克隆IgH重排。随着组织学分级递增 ,Ki 6 7标记率及单克隆重排递增 (P <0 .0 5 )。对 2 8例抗Hp治疗 ,2 4例获得根除 ,平均随访 4 .6个月。治疗后 18例组织学及内镜完全缓解 ,10例部分或无缓解。 4例Ⅳ级以下者Ki 6 7标记率全部下降且逆转为多克隆 ,而 4例Ⅳ级无变化。结论　组织学、Ki 6 7及IgH重排结合 ,有助于筛选早期干预病例及早期诊断胃MALT淋巴瘤。PCR检测IgH重排对Ⅲ或Ⅳ级的病例意义更大。     

Ki-67核抗原在良、恶性胃粘膜病变中的表达及临床意义

目的　研究Ki 6 7核抗原在良、恶性胃粘膜病变中的表达及与胃癌生物学行为的关系。方法　采用免疫组化技术检测 36例正常胃粘膜和 6 4例胃癌Ki 6 7核抗原的蛋白表达。结果　正常胃粘膜中Ki 6 7核抗原的表达率为 5 6 %,胃癌中Ki 6 7核抗原的表达率为 43 8%,二者相比具有显著性差异 (P <0 0 1) ;侵犯肌层或浆膜层胃癌的Ki 6 7核抗原表达率 ( 5 4 5 %)显著高于局限于粘膜层和粘膜下层者 ( 2 0 0 %) (P <0 0 5 ) ;低分化胃癌的Ki 6 7核抗原表达率 ( 5 6 8%)显著高于高、中分化胃癌 ( 2 5 0 %) (P <0 0 5 ) ;淋巴结转移阳性组胃癌Ki 6 7核抗原表达率 ( 6 7 7%)显著高于淋巴结转移阴性组 ( 2 1 2 %) (P <0 0 5 )。结论　Ki 6 7核抗原的表达与胃癌的侵袭、低分化、淋巴结转移显著相关 ,是判断胃癌患者预后的一项有价值的参考指标。     

COX-2和PCNA在胃黏膜相关淋巴组织淋巴瘤中的表达

目的:探讨环氧合酶-2(COX-2)在胃黏膜相关淋巴组织(MALT)淋巴瘤中的表达及其与细胞增殖和预后的关系.方法:采用免疫组化SP法检测43例胃MALT淋巴瘤和10例正常胃黏膜中COX-2和增殖细胞核抗原(PCNA)的表达.结果:COX-2在胃MALT淋巴瘤中的阳性表达率为55.8%,明显高于对照组45.8%,差异具有显著性(χ2=5.119,P=0.024).COX-2的表达与胃MALT淋巴瘤的临床分期具有相关性(χ2=4.408,P=0.036).胃MALT淋巴瘤平均增殖指数(MPI)为41.5%±5.1%;COX-2表达阳性组的MPI(43.4%±4.8%)显著高于阴性组(37.5%±2.9%),侵袭性胃MALT淋巴瘤的MPI(44.0%±5.6%)显著高于惰性组(38.9%±4.6%),差异有显著性(t=3.16,P=0.008和t=2.98,P=0.045).COX-2表达阴性患者的5a生存率要高于COX-2表达阳性患者(χ2=6.056,P=0.014).COX-regression模型显示COX-2是一个独立的不良预后指标(P<0.01).结论:胃MALT淋巴瘤中COX-2表达上调.COX-2蛋白可以通过促进淋巴瘤细胞的增殖而参与胃MALT淋巴瘤的发生和发展,并且在胃MALT淋巴瘤中是一个有用的预后指标.     

胃肠粘膜相关淋巴瘤误诊分析

胃肠粘膜相关淋巴瘤是发生在胃肠粘膜相关淋巴组织 (MALT)的恶性淋巴瘤 ,其发病率约占MALT淋巴瘤的 51 %。由于其临床表现缺乏特异性 ,X线钡餐及内镜下表现与胃溃疡、胃癌相似 ,故临床较易误诊。我科 1 992～ 1 999年共收治胃肠MALT淋巴瘤 2 8例 ,但在外院和门诊误诊 2 6例 ,误诊率达 92 .9% ,大多在手术后经病理确诊。现总结报告如下。1 　 临床资料2 8例中 ,男 1 7例 ,女 1 1例 ;年龄 1 1～ 69岁 ,>45岁 2 0例。死亡 2例 ,失随访 6例。生存期超过1年者 1 3例 ,超过 2年者 7例。发病部位 :胃 1 9例 ,其中胃体 8例 ,胃角 3例 ,胃窦 5…     

原发性胃恶性淋巴瘤与幽门螺杆菌感染的相关性初探

为了探讨原发性胃恶性淋巴瘤(RGML)与幽门螺杆菌(Hp)感染的相关性，本收集39例PGML以及22例巴性胃炎、32例Hp无关疾病的胃粘膜行对照研究。结果：PGML组Hp检出率87．18％，显高于对照的63.64、53.13%（P<0．005)。粘膜相关淋巴样组织(MALT)来源的淋巴留占92.31％，Hp检出率达86．11％，瘤周慢性活动性胃炎及淋巴滤泡检出率分别为84.62、56．41％，且炎症活动程度与Hp分布密度相关。组织学研究提示胃B细胞MALT淋巴瘤与Hp感染相关。     

BCL10 nuclear expression and t(11;18)(q21;q21) indicate nonresponsiveness to Helicobacter pylori eradication of Chinese primary gastric MALT lymphoma

The eradication of Helicobacter pylori (H. pylori) with antibiotics induces complete remission in 75% of patients with gastric MALT lymphoma. We investigated the efficacy of H. pylori eradication and assessed the predictive value of BCL10 nuclear expression and t(11;18)(q21;q21) regarding resistance to H. pylori eradication in primary gastric mucosa-associated lymphoid tissue lymphoma (MALT lymphoma) patients from mainland China. Twenty-two gastric MALT cases (Stage I_E) underwent H. pylori eradication with antibiotics, and sequential endoscopic-bioptic follow-ups were performed and assessed with regular morphologic and immunohistochemical examinations. BCL10 nuclear expression and interphase fluorescence in situ hybridization (FISH) for MALT1 and API2/MALT1 were tested. Thirteen out of the 22 cases (59.1%) achieved complete regression (CR) after the eradication of H. pylori. The longest follow-up period in the 22 patients was 68 months, with 12 patients longer than 24 months. For the 13 CR patients, the longest follow-up period after H. pylori eradication was 53 months, with 6 patients longer than 24 months. BCL10 nuclear expression was detected by immunohistochemical staining in 9 cases, including 7 (77.8%) of 9 cases who showed no response (NR) and 2 (15.4%) of 13 patients who achieved CR following eradication therapy (P < 0.05). t(11;18)(q21;q21) was evaluated by interphase FISH in 18 cases including 11 CR and 7 NR patients after H. pylori eradication. t(11;18)(q21;q21) was found in 4 (57.1%) of 7 patients who showed NR following H. pylori eradication, but one in 11 CR patients (P < 0.05). A total of 59.1% of patients with early gastric MALT lymphoma recruited in this study achieved CR after H. pylori eradication. BCL10 nuclear expression and t(11;18)(q21;q21)-positive gastric MALT lymphomas are likely to be related to a failure to respond to H. pylori eradication in Chinese patients. Both G. Dong and C. Liu are treated as co-first authors.     

Gastric mucosa-associated lymphoid tissue lymphomas and Helicobacter pylori infection: a Colombian perspective

AIM: To assess the significance of chromosome translocation t(11;18)(q21;q21), B-cell lymphoma 10 (BCL-10) protein and Helicobacter pylori (H. pylori) infection in gastric mucosa-associated lymphoid tissue (MALT) lymphoma in Colombia.METHODS: Fifty cases of gastric MALT lymphoma and their respective post-treatment follow-up biopsies were examined to assess the presence of the translocation t(11;18)(q21;q21) as identified by fluorescence in situ hybridization; to detect protein expression patterns of BCL10 using immunohistochemistry; and for evaluation of tumor histology to determine the correlation of these factors and resistance to H. pylori eradication.RESULTS: Infection with H. pylori was confirmed in all cases of gastric MALT lymphoma in association with chronic gastritis. Bacterial eradication led to tumor regression in 66% of cases. The translocation t(11;18)(q21;q21) was not present in any of these cases, nor was there evidence of tumor transformation to diffuse large B-cell lymphoma. Thirty-four percent of the patients showed resistance to tumor regression, and within this group, 7 cases, representing 14% of all those analyzed, were considered to be t(11;18)(q21;q21)-positive gastric MALT lymphomas. Protein expression of BCL10 in the nucleus was associated with the presence of translocation and treatment resistance. Cases that were considered unresponsive to therapy were histologically characterized by the presence of homogeneous tumor cells and a lack of plasmacytic differentiation. Responder cases exhibited higher cellular heterogeneity and a greater frequency of plasma cells.CONCLUSION: Both t(11;18)(q21;q21)-positive MALT lymphoma cases and those with nuclear BCL10 expression are considered resistant to H. pylori eradication. It is suggested that chronic antigenic stimulation is not a dominant event in resistant cases.     

BCL10 mutation does not represent an important pathogenic mechanism in gastric MALT-type lymphoma, and the presence of the API2-MLT fusion is associated with aberrant nuclear BCL10 expression

Two recurrent translocations have been associated with mucosa-associated lymphoid tissue (MALT)-type lymphoma, t(11;18)(q21;q21) and t(1;14)(p22;q32). The first, t(11;18)(q21;q21), results in the fusion protein API2-MLT (API2-MALT1). Through t(1;14)(p22;q32), the BCL10 gene is entirely transferred to the IgH gene, resulting in its overexpression. Wild-type BCL10 is implicated in apoptosis, and it has been suggested that mutated forms gain oncogenic activity. The occurrence of genomic BCL10 mutations in 35 gastric MALT-type lymphomas with or without t(11;18)(q21;q21) (10 and 25 cases, respectively) was investigated. DNA extracted from either whole tissue sections or microdissected clusters of tumor cells was used. Five polymerase chain reactions amplifying the coding exons were performed and were followed by direct sequencing of the products. Twenty differences with the published BCL10 sequence, all single nucleotide substitutions, were detected in 16 cases. Of these, 12 represented known polymorphisms, either at codon 8, 213, or 5. Of the remaining 8 substitutions, 2 were silent and 6 resulted in amino acid substitutions. Mutation analysis results were correlated with the BCL10 expression pattern. Aberrant nuclear BCL10 expression was detected in 14 cases. No association could be demonstrated between the latter and the presence of BCL10 mutations. In contrast, all 10 cases carrying t(11;18)(q21;q21) showed nuclear expression, whereas this staining pattern was absent in 21 of 25 cases without t(11;18)(q21;q21). These results demonstrate that BCL10 mutations are rare in gastric MALT-type lymphoma and are not related to the aberrant nuclear expression of BCL10. In contrast, they indicate that the presence of the API2-MLT fusion protein is associated with aberrant nuclear BCL10 expression.     

Update on MALT lymphomas

Gastric mucosa associated lymphoid tissue (MALT) lymphoma is a histologically distinct tumour derived from MALT acquired as a result of Helicobacter pylori infection. Eradication of H. pylori causes clinical regression of the lymphoma in 75% of cases. In seeking to identify those cases resistant to this therapy, and in the interests of further understanding the biology of MALT lymphoma, genetic alterations of MALT lymphomas have been investigated. Three translocations, t(11;18)(q21;q21), t(1;14)(p22;q32) and t(14;18)(q32;q21) are specifically associated with MALT lymphoma and the genes involved have been identified. T(11;18) results in a chimeric fusion between the API2 and MALT1 genes and is specifically associated with gastric MALT lymphomas that do not respond to eradication of H. pylori. T(1;14) and t(14;18) deregulate BCL10 and MALT1 expression, respectively. These three chromosomal translocations that involve different genes appear to share common oncogenic properties by targeting the same nuclear factor kappa B (NF kappa B) oncogenic pathway.     

Clinical impact of genetic aberrations in gastric MALT lymphoma: a comprehensive analysis using interphase fluorescence in situ hybridisation

BACKGROUND AND AIMS: There is a need for genetic biomarkers to guide prognosis and management of gastric mucosa-associated lymphoid tissue (MALT) lymphomas. We assessed the incidence and clinical significance of the MALT lymphoma-associated genetic abnormalities t(11;18)/API2-MALT1, t(1;14)/BCL10-IGH, t(14;18)/IGH-MALT1, t(3;14)/FOXP1-IGH, and extra copies of MALT1 and FOXP1 in gastric MALT lymphomas from Japan. METHODS: The presence of translocations and copy number changes involving MALT1, IGH and FOXP1 were assessed in 90 cases of gastric MALT lymphoma using interphase fluorescence in situ hybridisation (FISH). In cases carrying a MALT1 translocation, FISH for API2-MALT1 was performed, whereas in those carrying an IGH translocation, FISH was performed for BCL10, BCL6, BCL2, c-MYC and/or CCND1. RESULTS: t(11;18)/API2-MALT1 was detected in 18 of 87 (21%) cases and was significantly associated with Helicobacter pylori-negativity, resistance to H pylori eradication and Bcl10 nuclear expression. Four of 68 (6%) cases carried a translocation involving IGH and FOXP1 (n = 1), BCL2 (n = 1) or an unknown partner (n = 2). Neither t(1;14)/BCL10-IGH nor t(14;18)/IGH-MALT1 was detected. Extra copies of MALT1 and FOXP1 were detected in 18 of 71 (25%) cases and 10 of 59 (17%) cases, respectively. The presence of extra copies of MALT1 was significantly associated with progression or relapse of lymphoma, and was an independent adverse prognostic factor for event-free survival as determined by multivariate analysis. CONCLUSIONS: t(11;18)/API2-MALT1 is frequent, whereas IGH-involved translocations are rare in gastric MALT lymphoma in Japan. The presence of extra copies of MALT1, often suggestive of partial or complete trisomy 18, is a frequent genetic aberration in gastric MALT lymphoma, which appears to predict adverse clinical behaviour.     

MALT1 and the API2-MALT1 fusion act between CD40 and IKK and confer NF-kappa B-dependent proliferative advantage and resistance against FAS-induced cell death in B cells

The most frequently recurring translocations in mucosa-associated lymphoid tissue (MALT) B-cell non-Hodgkin lymphoma, t(11;18)(q21;q21) and t(14;18)(q32; q21), lead to formation of an API2-MALT1 fusion or IgH-mediated MALT1 overexpression. Various approaches have implicated these proteins in nuclear factor kappaB (NF-kappa B) signaling, but this has not been shown experimentally in human B cells. Immunohistochemistry showed that MALT1 is predominantly expressed in normal and malignant germinal center B cells, corresponding to the differentiation stage of MALT lymphoma. We expressed MALT1 and apoptosis inhibitor-2 API2/MALT1 in human B-cell lymphoma BJAB cells and found both transgenes in membrane lipid rafts along with endogenous MALT1 and 2 binding partners involved in NF-kappa B signaling, B-cell lymphoma 10 (BCL10) and CARMA1 (caspase recruitment domain [CARD]-containing membrane-associated guanylate kinase [MAGUK] 1). API2-MALT1 and exogenous MALT1 increased constitutive NF-kappa B activity and enhanced I kappa B kinase (IKK) activation induced by CD40 stimulation. Both transgenes protected BJAB cells from FAS (CD95)-induced death, consistent with increases in NF-kappa B cytoprotective target gene expression, and increased their proliferation rate. Expression of a dominant-negative I kappa B alpha mutant showed that these survival and proliferative advantages are dependent on elevated constitutive NF-kappa B activity. Our findings support a model in which NF-kappa B signaling, once activated in a CD40-dependent immune response, is maintained and enhanced through deregulation of MALT1 or formation of an API2-MALT1 fusion.     

Nuclear expression of BCL10 or nuclear factor kappa B helps predict Helicobacter pylori-independent status of low-grade gastric mucosa-associated lymphoid tissue lymphomas with or without t(11;18)(q21;q21)

The t(11;18)(q21;q21) translocation is a specific marker for Helicobacter pylori-independent status of low-grade gastric mucosa-associated lymphoid tissue (MALT) lymphoma. However, there are no reliable markers to predict tumor response to H pylori eradication in patients without t(11;18)(q21;q21). Nuclear expression of BCL10 and nuclear factor kappa B (NF-kappaB) was recently found to be closely associated with H pylori-independent status of the high-grade counterpart of gastric MALT lymphoma, which usually lacks t(11;18)(q21;q21). This study examined whether these 2 markers can also predict H pylori-independent status of low-grade gastric MALT lymphomas without t(11; 18)(q21;q21). Sixty patients who underwent successful H pylori eradication for low-grade gastric MALT lymphomas were included. Forty-seven (78.3%) patients were negative for t(11;18)(q21;q21); among them, 36 (76.6%) were H pylori dependent and 11 (23.4%) were H pylori independent. Nuclear expression of BCL10 was significantly higher in H pylori-independent than in H pylori-dependent tumors (8 of 11 [72.7%] vs 3 of 36 [8.3%]; P < .001). Nuclear expression of NF-kappaB was also significantly higher in H pylori-independent than in H pylori-dependent tumors (7 of 11 [63.6%] vs 3 of 36 [8.3%]; P < .001). Further, nuclear translocation of BCL10 and NF-kappaB was observed in 12 of the 13 patients with t(11;18)(q21;q21), and all these 12 patients were H pylori independent. In summary, nuclear expression of BCL10 or NF-kappaB is predictive of H pylori-independent status of low-grade gastric MALT lymphoma with or without t(11;18)(q21; q21).