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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.
Jens Pedersenbjergaard - One of the best experts on this subject based on the ideXlab platform.
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amplification or duplication of Chromosome Band 21q22 with multiple copies of the aml1 gene and mutation of the tp53 gene in therapy related mds and aml
Leukemia, 2005Co-Authors: Mette K Andersen, Debes H Christiansen, Jens PedersenbjergaardAbstract:Amplification or duplication of the AML1 gene at Chromosome Band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%). In two patients AML1 signals were located tandemly on derivative Chromosomes, in one patient on a dic(9;21) and in the the other patient on a derivative Chromosome 18 made up of interchanging layers of material from Chromosomes 9, 14, 18, and 21. In the third patient three single supernumerary copies of AML1 were located on derivatives of Chromosomes 19 and 21. All three patients were older, had previously received therapy with alkylating agents without topoisomerase II inhibitors, had complex karyotypes including abnormalities of Chromosomes 5 or 7, and presented acquired point mutations of the TP53 gene. No point mutations of the AML1 gene were observed. The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
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duplication or amplification of Chromosome Band 11q23 including the unrearranged mll gene is a recurrent abnormality in therapy related mds and aml and is closely related to mutation of the tp53 gene and to previous therapy with alkylating agents
Genes Chromosomes and Cancer, 2001Co-Authors: Mette K Andersen, Debes H Christiansen, Maria Kirchhoff, Jens PedersenbjergaardAbstract:Gene amplification is a rare phenomenon in acute leukemia, but recently amplification of specific Chromosome Bands containing genes rearranged in leukemia-specific balanced Chromosome translocations has been reported in a few cases. We detected duplication or amplification of Chromosome Band 11q23 with 3-7 copies of the MLL gene by fluorescence in situ hybridization in 12 out of 70 unselected patients with therapy-related myelodysplasia or acute myeloid leukemia (17%). In all but one case, the supernumerary copies of MLL were located to previously unidentified marker Chromosomes or unbalanced translocations. In 4 of the 12 patients, 2-6 copies were located together on the same Chromosome arm representing amplification, 7 patients had single, extra duplicated copies of MLL, whereas both amplification and duplication were observed in the same cell in 1 patient. Comparative genomic hybridization demonstrated gain of varying, often large parts of 11q in five patients. The MLL gene was shown to be unrearranged in all 12 patients. Seven out of eight patients with duplication or amplification of MLL had mutations of TP53. Patients with supernumerary copies of MLL were in general older (P = 0.007) and had a shorter survival (P < 0.001) compared to other patients. Duplication or amplification of MLL was significantly associated with a complex karyotype (P = 0.002), with deletion or loss of 5q (P = 0.001), and with prior therapy with alkylating agents. These results support the existence of a specific genetic pathway in t-MDS and t-AML with many previously unidentified Chromosome aberrations demonstrated to represent extra copies of parts of 11q, including the unrearranged MLL gene.
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duplication or amplification of Chromosome Band 11q23 including the unrearranged mll gene is a recurrent abnormality in therapy related mds and aml and is closely related to mutation of the tp53 gene and to previous therapy with alkylating agents
Genes Chromosomes and Cancer, 2001Co-Authors: Mette K Andersen, Debes H Christiansen, Maria Kirchhoff, Jens PedersenbjergaardAbstract:Gene amplification is a rare phenomenon in acute leukemia, but recently amplification of specific Chromosome Bands containing genes rearranged in leukemia-specific balanced Chromosome translocations has been reported in a few cases. We detected duplication or amplification of Chromosome Band 11q23 with 3–7 copies of the MLL gene by fluorescence in situ hybridization in 12 out of 70 unselected patients with therapy-related myelodysplasia or acute myeloid leukemia (17%). In all but one case, the supernumerary copies of MLL were located to previously unidentified marker Chromosomes or unbalanced translocations. In 4 of the 12 patients, 2–6 copies were located together on the same Chromosome arm representing amplification, 7 patients had single, extra duplicated copies of MLL, whereas both amplification and duplication were observed in the same cell in 1 patient. Comparative genomic hybridization demonstrated gain of varying, often large parts of 11q in five patients. The MLL gene was shown to be unrearranged in all 12 patients. Seven out of eight patients with duplication or amplification of MLL had mutations of TP53. Patients with supernumerary copies of MLL were in general older (P = 0.007) and had a shorter survival (P < 0.001) compared to other patients. Duplication or amplification of MLL was significantly associated with a complex karyotype (P = 0.002), with deletion or loss of 5q (P = 0.001), and with prior therapy with alkylating agents. These results support the existence of a specific genetic pathway in t-MDS and t-AML with many previously unidentified Chromosome aberrations demonstrated to represent extra copies of parts of 11q, including the unrearranged MLL gene. © 2001 Wiley-Liss, Inc.
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.
Mark P Sawicki - One of the best experts on this subject based on the ideXlab platform.
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deletion mapping of endocrine tumors localizes a second tumor suppressor gene on Chromosome Band 11q13
Genes Chromosomes and Cancer, 1998Co-Authors: Rita Chakrabarti, Thomas F Wood, Patricia J Eubanks, Sam A Ebrahimi, Edward Passaro, Richard A Gatti, Eri S. Srivatsan, Mark P SawickiAbstract:Multiple endocrine neoplasia type 1 syndrome (MEN1, MIM 131100), an autosomal dominant disease, is characterized by parathyroid hyperplasia, pancreatic endocrine tumors, and pituitary adenomas. These tumors also occur sporadically. Both the familial (MEN1) and the sporadic tumors reveal loss of heterozygosity (LOH) for Chromosome Band 11q13 sequences. Based on prior linkage and LOH analyses, the MEN1 gene was localized between PYGM and D11S460. Recently, the MEN1 gene (menin) has been cloned from sequences 30-kb distal to PYGM. We performed deletion mapping on 25 endocrine tumors (5 MEN1 and 20 sporadic) by using 21 polymorphic markers on Chromosome Band 11q13. Of these, two (137C7A, 137C7B) were derived from PYGM-containing BAC (bacterial artificial Chromosome-137C7) sequences, one from INT2-containing cosmid sequences and the marker D11S4748, a (CA)20 repeat marker that was developed by us. The LOH analysis shows that the markers close to the MEN1 (menin) gene were not deleted in three of the tumors. These tumors, however, showed LOH for distal markers. Thus, the data suggest the existence of a second tumor suppressor gene on Chromosome Band 11q13. Genes Chromosomes Cancer 22:130–137, 1998. © 1998 Wiley-Liss, Inc.
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deletion mapping of endocrine tumors localizes a second tumor suppressor gene on Chromosome Band 11q13
Genes Chromosomes and Cancer, 1998Co-Authors: Rita Chakrabarti, Thomas F Wood, Patricia J Eubanks, Sam A Ebrahimi, Edward Passaro, Richard A Gatti, Eri S. Srivatsan, Mark P SawickiAbstract:Multiple endocrine neoplasia type 1 syndrome (MEN1, MIM 131100), an autosomal dominant disease, is characterized by parathyroid hyperplasia, pancreatic endocrine tumors, and pituitary adenomas. These tumors also occur sporadically. Both the familial (MEN1) and the sporadic tumors reveal loss of heterozygosity (LOH) for Chromosome Band 11q13 sequences. Based on prior linkage and LOH analyses, the MEN1 gene was localized between PYGM and D11S460. Recently, the MEN1 gene (menin) has been cloned from sequences 30-kb distal to PYGM. We performed deletion mapping on 25 endocrine tumors (5 MEN1 and 20 sporadic) by using 21 polymorphic markers on Chromosome Band 11q13. Of these, two (137C7A, 137C7B) were derived from PYGM-containing BAC (bacterial artificial Chromosome-137C7) sequences, one from INT2-containing cosmid sequences and the marker D11S4748, a (CA)20 repeat marker that was developed by us. The LOH analysis shows that the markers close to the MEN1 (menin) gene were not deleted in three of the tumors. These tumors, however, showed LOH for distal markers. Thus, the data suggest the existence of a second tumor suppressor gene on Chromosome Band 11q13. Genes Chromosomes Cancer 22:130–137, 1998. © 1998 Wiley-Liss, Inc.
Mette K Andersen - One of the best experts on this subject based on the ideXlab platform.
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amplification or duplication of Chromosome Band 21q22 with multiple copies of the aml1 gene and mutation of the tp53 gene in therapy related mds and aml
Leukemia, 2005Co-Authors: Mette K Andersen, Debes H Christiansen, Jens PedersenbjergaardAbstract:Amplification or duplication of the AML1 gene at Chromosome Band 21q22 was detected by FISH using a locus-specific probe in three out of 171 unselected patients with therapy-related myelodysplasia (t-MDS) or t-AML (1.7%). In two patients AML1 signals were located tandemly on derivative Chromosomes, in one patient on a dic(9;21) and in the the other patient on a derivative Chromosome 18 made up of interchanging layers of material from Chromosomes 9, 14, 18, and 21. In the third patient three single supernumerary copies of AML1 were located on derivatives of Chromosomes 19 and 21. All three patients were older, had previously received therapy with alkylating agents without topoisomerase II inhibitors, had complex karyotypes including abnormalities of Chromosomes 5 or 7, and presented acquired point mutations of the TP53 gene. No point mutations of the AML1 gene were observed. The results support a pivotal role of impaired TP53 function in the development of gene amplification or duplication in t-MDS and t-AML.
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duplication or amplification of Chromosome Band 11q23 including the unrearranged mll gene is a recurrent abnormality in therapy related mds and aml and is closely related to mutation of the tp53 gene and to previous therapy with alkylating agents
Genes Chromosomes and Cancer, 2001Co-Authors: Mette K Andersen, Debes H Christiansen, Maria Kirchhoff, Jens PedersenbjergaardAbstract:Gene amplification is a rare phenomenon in acute leukemia, but recently amplification of specific Chromosome Bands containing genes rearranged in leukemia-specific balanced Chromosome translocations has been reported in a few cases. We detected duplication or amplification of Chromosome Band 11q23 with 3-7 copies of the MLL gene by fluorescence in situ hybridization in 12 out of 70 unselected patients with therapy-related myelodysplasia or acute myeloid leukemia (17%). In all but one case, the supernumerary copies of MLL were located to previously unidentified marker Chromosomes or unbalanced translocations. In 4 of the 12 patients, 2-6 copies were located together on the same Chromosome arm representing amplification, 7 patients had single, extra duplicated copies of MLL, whereas both amplification and duplication were observed in the same cell in 1 patient. Comparative genomic hybridization demonstrated gain of varying, often large parts of 11q in five patients. The MLL gene was shown to be unrearranged in all 12 patients. Seven out of eight patients with duplication or amplification of MLL had mutations of TP53. Patients with supernumerary copies of MLL were in general older (P = 0.007) and had a shorter survival (P < 0.001) compared to other patients. Duplication or amplification of MLL was significantly associated with a complex karyotype (P = 0.002), with deletion or loss of 5q (P = 0.001), and with prior therapy with alkylating agents. These results support the existence of a specific genetic pathway in t-MDS and t-AML with many previously unidentified Chromosome aberrations demonstrated to represent extra copies of parts of 11q, including the unrearranged MLL gene.
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duplication or amplification of Chromosome Band 11q23 including the unrearranged mll gene is a recurrent abnormality in therapy related mds and aml and is closely related to mutation of the tp53 gene and to previous therapy with alkylating agents
Genes Chromosomes and Cancer, 2001Co-Authors: Mette K Andersen, Debes H Christiansen, Maria Kirchhoff, Jens PedersenbjergaardAbstract:Gene amplification is a rare phenomenon in acute leukemia, but recently amplification of specific Chromosome Bands containing genes rearranged in leukemia-specific balanced Chromosome translocations has been reported in a few cases. We detected duplication or amplification of Chromosome Band 11q23 with 3–7 copies of the MLL gene by fluorescence in situ hybridization in 12 out of 70 unselected patients with therapy-related myelodysplasia or acute myeloid leukemia (17%). In all but one case, the supernumerary copies of MLL were located to previously unidentified marker Chromosomes or unbalanced translocations. In 4 of the 12 patients, 2–6 copies were located together on the same Chromosome arm representing amplification, 7 patients had single, extra duplicated copies of MLL, whereas both amplification and duplication were observed in the same cell in 1 patient. Comparative genomic hybridization demonstrated gain of varying, often large parts of 11q in five patients. The MLL gene was shown to be unrearranged in all 12 patients. Seven out of eight patients with duplication or amplification of MLL had mutations of TP53. Patients with supernumerary copies of MLL were in general older (P = 0.007) and had a shorter survival (P < 0.001) compared to other patients. Duplication or amplification of MLL was significantly associated with a complex karyotype (P = 0.002), with deletion or loss of 5q (P = 0.001), and with prior therapy with alkylating agents. These results support the existence of a specific genetic pathway in t-MDS and t-AML with many previously unidentified Chromosome aberrations demonstrated to represent extra copies of parts of 11q, including the unrearranged MLL gene. © 2001 Wiley-Liss, Inc.