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Masao Seto - One of the best experts on this subject based on the ideXlab platform.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Won Seog Kim, Y D Kim, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Younghyeh Ko, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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genome wide array based comparative genomic hybridization of ocular Marginal Zone b cell lymphoma comparison with pulmonary and nodal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2007Co-Authors: Won Seog Kim, Keiichiro Honma, Sivasundaram Karnan, Hiroyuki Tagawa, Yoon Duck Kim, Masao SetoAbstract:The genetic changes in Marginal Zone B cell lymphomas (MZBCL) vary according to the anatomical region. This study aimed to investigate genomic aberrations in ocular MZBCL and to compare them with those of tumors from other anatomical sites. The study population comprised 24 cases of primary ocular MZBCL, 11 pulmonary MZBCL, and seven nodal MZBCL. For array CGH, fresh tumor tissues were analyzed with a genome-wide scanning array containing 2,304 BAC/PAC clones which cover the whole human genome at a resolution of 1.3 Mb. FISH analysis for MALT1 gene alteration was performed for ocular and nodal MZBCL and RT-PCR for the detection of API2-MALT1 transcripts was performed for pulmonary MZBCL. The recurrent genomic alterations in ocular MZBCL were losses of chromosome bands 6q23.3 (9/24, 38%), 7q36.3 (2/24, 8%), and 13q34 (2/24, 8%), and gains of chromosomes 3 (9/24, 38%), and 15 (4/24, 16%), and chromosome arms 18q (4/24, 16%), and 6p (2/24, 8%). The t(11;18)(q21;q21) was not detected. The genomic alterations of pulmonary MZBCL included recurrent loss of 18q21 (2/11, 19%). A t(11;18)(q21;q21) fusion transcript was detected in five out of eight cases (63%). Nodal MZBCL showed neither recurrent genome alterations nor any change in MALT1 gene copy number. In conclusion, the array CGH profile of ocular MZBCL is distinct from those of pulmonary and nodal MZBCL. Deletion of chromosome band 6q23.3 in ocular MZBCL is a novel finding and may constitute a crucial genetic alteration in the pathogenesis of ocular MZBCL. © 2007 Wiley-Liss, Inc.
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detection of ap12 malt1 chimaeric gene in extranodal and nodal Marginal Zone b cell lymphoma by reverse transcription polymerase chain reaction pcr and genomic long and accurate pcr analyses
British Journal of Haematology, 2001Co-Authors: Masakatsu Yonezumi, Tadashi Yoshino, Shigeo Nakamura, Ritsuro Suzuki, Yoshitaka Hosokawa, Masahiro Asaka, Hiroko Suzuki, Kouichi Oshima, Yasuo Morishima, Masao SetoAbstract:t(11;18)(q21;q21) has been recognized as a characteristic chromosomal translocation in mucosa-associated lymphoid tissue (MALT)-type lymphoma, and recent studies have demonstrated that this translocation results in the chimaeric transcript of API2 (apoptosis inhibitor 2)-MALT1 (mucosa-associated lymphoid tissue lymphoma translocation gene 1). In this study, we used reverse transcription polymerase chain reaction (RT–PCR) to analyse the incidence of this fusion product in a large series of MALT lymphoma, nodal Marginal Zone B-Cell lymphoma (nMZBCL) and extranodal diffuse large B-Cell lymphoma (DLBL) cases. RT–PCR analysis revealed that 17 of the 95 (17·9%) MALT lymphomas but none of the nine nMZBCLs or 16 DLBLs had API2-MALT1 fusion transcripts. The incidence of API2-MALT1 varied among MALT lymphomas arising from different sites and was highest for pulmonary MALT lymphomas (10 out of 16 cases, 62·5%). The presence of the API2-MALT1 fusion gene was also confirmed by long and accurate (LA)–PCR with genomic DNA, and the result correlated well with that obtained with the RT–PCR assay, thus demonstrating the usefulness of LA–PCR for the detection of the API2-MALT1 fusion gene.
Keiichiro Honma - One of the best experts on this subject based on the ideXlab platform.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Won Seog Kim, Y D Kim, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Younghyeh Ko, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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genome wide array based comparative genomic hybridization of ocular Marginal Zone b cell lymphoma comparison with pulmonary and nodal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2007Co-Authors: Won Seog Kim, Keiichiro Honma, Sivasundaram Karnan, Hiroyuki Tagawa, Yoon Duck Kim, Masao SetoAbstract:The genetic changes in Marginal Zone B cell lymphomas (MZBCL) vary according to the anatomical region. This study aimed to investigate genomic aberrations in ocular MZBCL and to compare them with those of tumors from other anatomical sites. The study population comprised 24 cases of primary ocular MZBCL, 11 pulmonary MZBCL, and seven nodal MZBCL. For array CGH, fresh tumor tissues were analyzed with a genome-wide scanning array containing 2,304 BAC/PAC clones which cover the whole human genome at a resolution of 1.3 Mb. FISH analysis for MALT1 gene alteration was performed for ocular and nodal MZBCL and RT-PCR for the detection of API2-MALT1 transcripts was performed for pulmonary MZBCL. The recurrent genomic alterations in ocular MZBCL were losses of chromosome bands 6q23.3 (9/24, 38%), 7q36.3 (2/24, 8%), and 13q34 (2/24, 8%), and gains of chromosomes 3 (9/24, 38%), and 15 (4/24, 16%), and chromosome arms 18q (4/24, 16%), and 6p (2/24, 8%). The t(11;18)(q21;q21) was not detected. The genomic alterations of pulmonary MZBCL included recurrent loss of 18q21 (2/11, 19%). A t(11;18)(q21;q21) fusion transcript was detected in five out of eight cases (63%). Nodal MZBCL showed neither recurrent genome alterations nor any change in MALT1 gene copy number. In conclusion, the array CGH profile of ocular MZBCL is distinct from those of pulmonary and nodal MZBCL. Deletion of chromosome band 6q23.3 in ocular MZBCL is a novel finding and may constitute a crucial genetic alteration in the pathogenesis of ocular MZBCL. © 2007 Wiley-Liss, Inc.
Won Seog Kim - One of the best experts on this subject based on the ideXlab platform.
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waldeyer s ring Marginal Zone b cell lymphoma are the clinical and prognostic features nodal or extranodal a study by the consortium for improving survival of lymphoma cisl
International Journal of Hematology, 2012Co-Authors: Won Seog Kim, Jin Seok Kim, Seok Jin Kim, Suee Lee, Dae Ho Lee, Hye Jin Kang, Jinny Park, Soon Il Lee, Chul Won Choi, Moo Kon SongAbstract:There has been controversy surrounding Waldeyer’s ring (WR), especially focused on the question of whether it should be regarded as a nodal or an extranodal site. We conducted retrospective analyses of Marginal Zone B cell lymphomas involving WR (WR-MZLs) to observe their clinical features and prognosis, with specific regard to the nodal-or-extranodal question. A total of 52 patients with histological diagnosis of WR-MZL were retrospectively analyzed. The most common involvement site was the tonsil (40.4 %). Ann Arbor stage III/VI disease was present in 48.1 % (25 of 52). The response rate of the 27 stage I/II patients was 88.9 %, with 21 complete remissions and three partial remissions. The median time to progression (TTP) was 3.7 years (95 % CI 2.5–4.9 years). The estimated 5-year TTP and overall survival rates were 39.4 and 90.5 %, respectively. In a comparison with the historical data regarding extra-WR MALT lymphoma and nodal MZL (N-MZL), MALT lymphoma showed better TTP results than did WR-MZL and N-MZL (P < 0.001).
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primary thyroid Marginal Zone b cell lymphoma of the mucosa associated lymphoid tissue type clinical manifestation and outcome of a rare disease consortium for improving survival of lymphoma study
Acta Haematologica, 2012Co-Authors: Won Seog Kim, Jin Seok Kim, Seok Jin Kim, Suee Lee, Dae Ho Lee, Hye Jin Kang, Moo Kon Song, Hyo Jung Kim, Jung Hye Kwon, Jae Yong KwakAbstract:Purpose: Primary thyroid Marginal Zone B-Cell lymphoma of the mucosa-associated lymphoid tissue type (pTY-MZL) is an extremely uncommon form of lymphoma. Due to its rarity, the natu
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pulmonary Marginal Zone b cell lymphoma of malt type what is a prognostic factor and which is the optimal treatment operation or chemotherapy consortium for improving survival of lymphoma cisl study
Annals of Hematology, 2010Co-Authors: Won Seog Kim, Jin Seok Kim, Dae Ho Lee, Hyuk Chan Kwon, Minkyoung Kim, Soon Il Lee, Seok Kim, Jong Ho Won, In Gyu Hwang, Yee Soo ChaeAbstract:Pulmonary Marginal Zone B-Cell lymphoma of the MALT type (P-MZL) is a relatively rare form of lymphoma. We conducted a retrospective analysis of the clinical features and treatment outcomes of P-MZL for the evaluation of prognostic factors, and to collect information about the optimal treatment modality for this condition. From 1991 to 2008, a total of 61 patients with biopsy-confirmed P-MZL were retrospectively analyzed. The median age of our subjects was 60 (range, 34–79) years. Twenty-five of the patients (41%) were initially diagnosed without any symptoms. Video-assisted thoracic surgery was utilized for diagnosis in 19 patients (31%). Thirty-eight patients' conditions (62%) involved a single lobe. Lung lesions were bilateral in 15 patients (25%). Eleven patients evidenced synchronous involvement of extra-pulmonary site MZL. Overall, 56 of 61 patients were treated with surgery (n = 22), chemotherapy (n = 28), or radiotherapy (n = 6). Among them, 46 patients achieved complete or partial remission. The median time to progression (TTP) was 5.6 (95% CI, 2.6–8.6) years. Five patients died during follow-up. Extra-pulmonary MZL and LN involvement were shown to be poor prognostic factors for TTP. We noted no differences between the operation group and chemotherapy group in terms of TTP. P-MZL tends to be an indolent disease—characterized by prolonged survival with frequent relapses. This is similar to what is observed with other cases of MALT-type site MZL. In order to conserve lung function and reduce the risks of operation, chemotherapy should be considered as a first-line option for the treatment of P-MZL.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Won Seog Kim, Y D Kim, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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genome wide array based comparative genomic hybridization of ocular Marginal Zone b cell lymphoma comparison with pulmonary and nodal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2007Co-Authors: Won Seog Kim, Keiichiro Honma, Sivasundaram Karnan, Hiroyuki Tagawa, Yoon Duck Kim, Masao SetoAbstract:The genetic changes in Marginal Zone B cell lymphomas (MZBCL) vary according to the anatomical region. This study aimed to investigate genomic aberrations in ocular MZBCL and to compare them with those of tumors from other anatomical sites. The study population comprised 24 cases of primary ocular MZBCL, 11 pulmonary MZBCL, and seven nodal MZBCL. For array CGH, fresh tumor tissues were analyzed with a genome-wide scanning array containing 2,304 BAC/PAC clones which cover the whole human genome at a resolution of 1.3 Mb. FISH analysis for MALT1 gene alteration was performed for ocular and nodal MZBCL and RT-PCR for the detection of API2-MALT1 transcripts was performed for pulmonary MZBCL. The recurrent genomic alterations in ocular MZBCL were losses of chromosome bands 6q23.3 (9/24, 38%), 7q36.3 (2/24, 8%), and 13q34 (2/24, 8%), and gains of chromosomes 3 (9/24, 38%), and 15 (4/24, 16%), and chromosome arms 18q (4/24, 16%), and 6p (2/24, 8%). The t(11;18)(q21;q21) was not detected. The genomic alterations of pulmonary MZBCL included recurrent loss of 18q21 (2/11, 19%). A t(11;18)(q21;q21) fusion transcript was detected in five out of eight cases (63%). Nodal MZBCL showed neither recurrent genome alterations nor any change in MALT1 gene copy number. In conclusion, the array CGH profile of ocular MZBCL is distinct from those of pulmonary and nodal MZBCL. Deletion of chromosome band 6q23.3 in ocular MZBCL is a novel finding and may constitute a crucial genetic alteration in the pathogenesis of ocular MZBCL. © 2007 Wiley-Liss, Inc.
Sivasundaram Karnan - One of the best experts on this subject based on the ideXlab platform.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Won Seog Kim, Y D Kim, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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tnfaip3 is the target gene of chromosome band 6q23 3 q24 1 loss in ocular adnexal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2008Co-Authors: Keiichiro Honma, Shinobu Tsuzuki, Masao Nakagawa, Sivasundaram Karnan, Yoshifusa Aizawa, Younghyeh Ko, Masao SetoAbstract:The genomic aberrations in extra nodal Marginal Zone B cell lymphoma vary according to their anatomical origin. This polarization is a reflection of the participation of different genes in the lymphomagenesis of Marginal Zone B cell lymphoma. We previously demonstrated by means of genome-wide array comparative genomic hybridization (CGH) that the genomic profile of ocular adnexal Marginal Zone B cell lymphoma is distinct from that of pulmonary or nodal Marginal Zone B cell lymphoma. The novel finding was a recurrent deletion of a 2.9-Mb region at chromosome band 6q23.3-q24.1, including homozygous loss, in ocular adnexal Marginal Zone B cell lymphoma. For a more detailed examination of the deletions of 6q23.3-24.1, we used contig bacterial artificial chromosome (BAC) array CGH, containing 24 BAC clones covering the 2.9-Mb region, to analyze nine cases with 6q23.3-q24.1 loss. We narrowed the minimal common region down to a length of 586 kb with two genes and four expressed sequence tags (ESTs). All of these genes and ESTs were subjected to RT-PCR and real-time quantitative RT-PCR. Correlation between genomic loss and expression level was found only for TNFAIP3, demonstrating that TNFAIP3 is a target gene of 6q deletion in ocular adnexal Marginal Zone B cell lymphoma. TNFAIP3 is an inhibitor of NF-kB signaling so that loss of this gene may play an important role in lymphomagenesis and suggests that TNFAIP3 may act as a tumor suppressor gene in ocular adnexal Marginal Zone B cell lymphoma.
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genome wide array based comparative genomic hybridization of ocular Marginal Zone b cell lymphoma comparison with pulmonary and nodal Marginal Zone b cell lymphoma
Genes Chromosomes and Cancer, 2007Co-Authors: Won Seog Kim, Keiichiro Honma, Sivasundaram Karnan, Hiroyuki Tagawa, Yoon Duck Kim, Masao SetoAbstract:The genetic changes in Marginal Zone B cell lymphomas (MZBCL) vary according to the anatomical region. This study aimed to investigate genomic aberrations in ocular MZBCL and to compare them with those of tumors from other anatomical sites. The study population comprised 24 cases of primary ocular MZBCL, 11 pulmonary MZBCL, and seven nodal MZBCL. For array CGH, fresh tumor tissues were analyzed with a genome-wide scanning array containing 2,304 BAC/PAC clones which cover the whole human genome at a resolution of 1.3 Mb. FISH analysis for MALT1 gene alteration was performed for ocular and nodal MZBCL and RT-PCR for the detection of API2-MALT1 transcripts was performed for pulmonary MZBCL. The recurrent genomic alterations in ocular MZBCL were losses of chromosome bands 6q23.3 (9/24, 38%), 7q36.3 (2/24, 8%), and 13q34 (2/24, 8%), and gains of chromosomes 3 (9/24, 38%), and 15 (4/24, 16%), and chromosome arms 18q (4/24, 16%), and 6p (2/24, 8%). The t(11;18)(q21;q21) was not detected. The genomic alterations of pulmonary MZBCL included recurrent loss of 18q21 (2/11, 19%). A t(11;18)(q21;q21) fusion transcript was detected in five out of eight cases (63%). Nodal MZBCL showed neither recurrent genome alterations nor any change in MALT1 gene copy number. In conclusion, the array CGH profile of ocular MZBCL is distinct from those of pulmonary and nodal MZBCL. Deletion of chromosome band 6q23.3 in ocular MZBCL is a novel finding and may constitute a crucial genetic alteration in the pathogenesis of ocular MZBCL. © 2007 Wiley-Liss, Inc.
Masaru Kojima - One of the best experts on this subject based on the ideXlab platform.
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nodal Marginal Zone b cell lymphoma with prominent follicular colonization with deletion of chromosome 13
Pathology Research and Practice, 2012Co-Authors: Rie Tabata, Chiharu Tabata, Tomoko Nagai, Ryoji Yasumizu, Masaru KojimaAbstract:Nodal Marginal Zone B cell lymphoma is a rare type of malignant lymphoma and appears to be heterogeneous. Here we report a 60-year-old woman with stage I splenic type of nodal Marginal Zone B cell lymphoma with prominent follicular colonization. She was treated only by radiation therapy, and remained free of disease on examination for 4 years. The lymph node cells showed an abnormal chromosome of deletion 13, although neither bone marrow cells nor peripheral blood cells demonstrated the same abnormal chromosome. This type of chromosomal abnormality has not been previously reported and may be related to good prognosis in the present case.
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Marginal Zone b cell lymphoma among primary b cell lymphoma of waldeyer s ring histopathologic and immunohistochemical study of 16 tonsillectomy specimens
International Journal of Surgical Pathology, 2008Co-Authors: Masaru Kojima, Naoya Nakamura, Kazuhiko Shimizu, Yoshio Tamaki, Hideaki Itoh, Shigeo NakamuraAbstract:Two subtypes of Marginal Zone B-Cell lymphoma (eg, mucosa-associated lymphoid tissue [MALT] type and splenic type) have been reported in the lymph node. To determine the presence or absence of Marginal Zone B-Cell lymphoma of MALT type and the splenic type among Waldeyer's ring (WR) lymphomas, 16 tonsillectomy specimens were studied. Ten cases (63%) were Marginal Zone B-Cell lymphoma. Among Marginal Zone B-Cell lymphoma, 7 were the MALT type and the remaining 3 cases of Marginal Zone B-Cell lymphoma were the splenic type. Moreover, 4 cases of 7 MALT-type lymphomas contained numerous large cells (diffuse large B-Cell lymphoma arising from a low-grade Marginal Zone B-Cell lymphoma of MALT type). The low incidence of primary mucosa-associated lymphoid tissue type lymphoma of WR in previous reports may be because it is difficult to correctly identify the characteristic histologic findings of MALT-type lymphoma because of the small biopsy size.
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massive hyperplasia of Marginal Zone b cells with clear cytoplasm in the lymph node a case report
Pathology Research and Practice, 2003Co-Authors: Masaru Kojima, Shigeo Nakamura, Hiroshi Tanaka, Yuko Yamane, Shiro Sugihara, Nobuhide MasawaAbstract:Summary An enlarged axillary lymph node from a 63-year-old woman showed proliferating Marginal Zone B-Cells arranged in a vague nodular pattern or in band-forming aggregates throughout the cortex. Marginal Zone B-Cells, which also infiltrated the adjacent fatty tissue, had round or slightly indented nuclei of medium size and a moderate amount of clear cytoplasm. Immunohistochemically, these cells were CD20+, CD79a+, Bcl-2+, sIgD–, CD5–, CD10–, CD21–, CD23–, CD45RO–, Bcl-6–, and cyclin D–. A portion of the cells were sIgM- and CD43-positive. The polytypic nature of these cells was demonstrated by immunohistochemistry and polymerase chain reaction. Systemic bacterial infection appears to be the cause of Marginal Zone B-Cell hyperplasia. This unusual Marginal Zone B-Cell hyperplasia should be differentiated from low-grade B cell lymphomas, and particularly from nodal Marginal Zone B-Cell lymphomas.
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primary Marginal Zone b cell lymphoma of the lymph node resembling plasmacytoma arising from a plasma cell variant of castleman s disease a clinicopathological and immunohistochemical study of seven patients
Apmis, 2002Co-Authors: Masaru Kojima, Shigeo Nakamura, Shiro Sugihara, Kazuhiko Shimizu, Yoshio Tamaki, Tadashi Motoori, Shunichi Shimano, Kayako Murayama, Tetsunari Oyama, Noriyuki SakataAbstract:: Nodal Marginal Zone B-Cell lymphomas (NMZBL) occasionally represent prominent plasma cell differentiation. Recently, we presented a patient with NMZBL who exhibited histological features that resembled plasmacytoma arising from a localized plasma cell variant of Castleman's disease. To further clarify the clinicopathological, immunohistochemical, and genotypical findings, we studied seven such patients. Clinically, these patients were characterized by localized disease and an indolent clinical course with a slowly growing bulky mass in the affected lymph node. Only one patient exhibited paraproteinemia. Histologically, the lesions were characterized by numerous evenly distributed germinal centers in extensive sheets of plasma cells. Various numbers of centrocyte-like (CCL) cells arranged in a Marginal Zone distribution pattern occupied the peripheral region of the lymph node. The majority of the lymphoid follicles had atrophic or regressive germinal centers. A few lymphoid follicles were colonized by CCL cells. Immunohistochemistry showed that all of the lesions contained a monoclonal plasma cell population. In three tumors, a number of the CCL cells had a similar light chain restriction pattern to that observed in plasma cells. Two of the four patients evaluated exhibited clonal bands for the IgH gene by polymerase chain reaction assay. Moreover, the presence of surface IgM+, IgD- and CD27+ CCL- cells suggests that these tumors are derived from memory B-lymphocytes.
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nodal Marginal Zone b cell lymphoma resembling plasmacytoma arising from a plasma cell variant of localized castleman s disease a case report
Apmis, 2002Co-Authors: Masaru Kojima, Shigeo Nakamura, Shiro Sugihara, Kazuhiko Shimizu, Noriyuki Sakata, Yoshio Suda, Yoshio Kasuga, Nobuhide MasawaAbstract:: Nodal Marginal Zone B-Cell lymphoma (NMZBL) occasionally represents prominent plasma cell differentiation. Recently, primary lymph node plasmacytoma has been suggested to represent an extremely plasmacytic differentiation of NMZBL. We here report a case of NMZBL showing histological features resembling plasmacytoma arising from a plasma cell variant of localized Castleman's disease (PCLCD). The patient was a 69-year-old Japanese female with a 20-year history of a right inguinal mass. Histologically, a prominent proliferation of plasma cells occupied the interfollicular area of the central portion of the lymph node, whereas centrocyte-like (CCL) cells were the main cellular component in the peripheral portion of the lymph node. Although most of the plasma cells were mature 'Marshalko-type', occasional atypical forms with enlarged nuclei were also present. The majority of the lymphoid follicles had atrophic or regressive germinal centers. A few lymphoid follicles were colonized by CCL cells. Immunohistochemistry study revealed that both plasma cells and some CCL cells had a monotypic intracytoplasmic lambda light chain. When monoclonal plasma cell infiltration is observed in PCLCD, the light chains are mostly restricted to the lambda chain. This case suggests that some plasma cell-containing tumors arising from PCLCD may represent a variant of NMZBL.