Genomic segmental duplications on the basis of the t(9;22) rearrangement in chronic myeloid leukemia
A crucial role of segmental duplications (SDs) of the human genome has been shown in chromosomal rearrangements associated with several genomic disorders. Limited knowledge is yet available on the molecular processes resulting in chromosomal rearrangements in tumors. The t(9;22)(q34;q11) rearrangeme...
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| Veröffentlicht in: | Oncogene 2010-04, Vol.29 (17), p.2509-2516 |
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| creator | Albano, F Anelli, L Zagaria, A Coccaro, N D'Addabbo, P Liso, V Rocchi, M Specchia, G |
| description | A crucial role of segmental duplications (SDs) of the human genome has been shown in chromosomal rearrangements associated with several genomic disorders. Limited knowledge is yet available on the molecular processes resulting in chromosomal rearrangements in tumors. The t(9;22)(q34;q11) rearrangement causing the
5′BCR/3′ABL
gene formation has been detected in more than 90% of cases with chronic myeloid leukemia (CML). In 10–18% of patients with CML, genomic deletions were detected on der(9) chromosome next to translocation breakpoints. The molecular mechanism triggering the t(9;22) and deletions on der(9) is still speculative. Here we report a molecular cytogenetic analysis of a large series of patients with CML with der(9) deletions, revealing an evident breakpoint clustering in two regions located proximally to
ABL
and distally to
BCR
, containing an interchromosomal duplication block (SD_9/22). The deletions breakpoints distribution appeared to be strictly related to the distance from the SD_9/22. Moreover, bioinformatic analyses of the regions surrounding the SD_9/22 revealed a high Alu frequency and a poor gene density, reflecting genomic instability and susceptibility to rearrangements. On the basis of our results, we propose a three-step model for t(9;22) formation consisting of alignment of chromosomes 9 and 22 mediated by SD_9/22, spontaneous chromosome breakages and misjoining of DNA broken ends. |
| doi_str_mv | 10.1038/onc.2009.524 |
| format | Article |
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5′BCR/3′ABL
gene formation has been detected in more than 90% of cases with chronic myeloid leukemia (CML). In 10–18% of patients with CML, genomic deletions were detected on der(9) chromosome next to translocation breakpoints. The molecular mechanism triggering the t(9;22) and deletions on der(9) is still speculative. Here we report a molecular cytogenetic analysis of a large series of patients with CML with der(9) deletions, revealing an evident breakpoint clustering in two regions located proximally to
ABL
and distally to
BCR
, containing an interchromosomal duplication block (SD_9/22). The deletions breakpoints distribution appeared to be strictly related to the distance from the SD_9/22. Moreover, bioinformatic analyses of the regions surrounding the SD_9/22 revealed a high Alu frequency and a poor gene density, reflecting genomic instability and susceptibility to rearrangements. On the basis of our results, we propose a three-step model for t(9;22) formation consisting of alignment of chromosomes 9 and 22 mediated by SD_9/22, spontaneous chromosome breakages and misjoining of DNA broken ends.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2009.524</identifier><identifier>PMID: 20101201</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/420/2489/68 ; 692/699/67/1990/283/1896 ; Analysis ; Apoptosis ; BCR-ABL protein ; Biological and medical sciences ; Breakpoints ; Cell Biology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chromosome abnormalities ; Chromosome rearrangements ; Chromosomes ; Chromosomes, Human, Pair 22 ; Chromosomes, Human, Pair 9 ; Chronic myeloid leukemia ; Complications and side effects ; Computational Biology ; Cytogenetics ; Diverse techniques ; Fundamental and applied biological sciences. Psychology ; Gene Duplication ; Gene rearrangement ; Genetic aspects ; Genomic instability ; Genomics ; Hematologic and hematopoietic diseases ; Human Genetics ; Humans ; Internal Medicine ; Leukemia ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Medicine ; Medicine & Public Health ; Molecular and cellular biology ; Molecular biology ; Myeloid leukemia ; Oncology ; original-article ; Risk factors ; Translocation, Genetic ; Tumors</subject><ispartof>Oncogene, 2010-04, Vol.29 (17), p.2509-2516</ispartof><rights>Macmillan Publishers Limited 2010</rights><rights>2015 INIST-CNRS</rights><rights>COPYRIGHT 2010 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Apr 29, 2010</rights><rights>Macmillan Publishers Limited 2010.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c550t-cef1eeaa073a7a29fdee10a2370b583a1d174a88b96ce24abb0479999ccd47fd3</citedby><cites>FETCH-LOGICAL-c550t-cef1eeaa073a7a29fdee10a2370b583a1d174a88b96ce24abb0479999ccd47fd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2009.524$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2009.524$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,41469,42538,51300</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22770599$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20101201$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Albano, F</creatorcontrib><creatorcontrib>Anelli, L</creatorcontrib><creatorcontrib>Zagaria, A</creatorcontrib><creatorcontrib>Coccaro, N</creatorcontrib><creatorcontrib>D'Addabbo, P</creatorcontrib><creatorcontrib>Liso, V</creatorcontrib><creatorcontrib>Rocchi, M</creatorcontrib><creatorcontrib>Specchia, G</creatorcontrib><title>Genomic segmental duplications on the basis of the t(9;22) rearrangement in chronic myeloid leukemia</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>A crucial role of segmental duplications (SDs) of the human genome has been shown in chromosomal rearrangements associated with several genomic disorders. Limited knowledge is yet available on the molecular processes resulting in chromosomal rearrangements in tumors. The t(9;22)(q34;q11) rearrangement causing the
5′BCR/3′ABL
gene formation has been detected in more than 90% of cases with chronic myeloid leukemia (CML). In 10–18% of patients with CML, genomic deletions were detected on der(9) chromosome next to translocation breakpoints. The molecular mechanism triggering the t(9;22) and deletions on der(9) is still speculative. Here we report a molecular cytogenetic analysis of a large series of patients with CML with der(9) deletions, revealing an evident breakpoint clustering in two regions located proximally to
ABL
and distally to
BCR
, containing an interchromosomal duplication block (SD_9/22). The deletions breakpoints distribution appeared to be strictly related to the distance from the SD_9/22. Moreover, bioinformatic analyses of the regions surrounding the SD_9/22 revealed a high Alu frequency and a poor gene density, reflecting genomic instability and susceptibility to rearrangements. On the basis of our results, we propose a three-step model for t(9;22) formation consisting of alignment of chromosomes 9 and 22 mediated by SD_9/22, spontaneous chromosome breakages and misjoining of DNA broken ends.</description><subject>692/420/2489/68</subject><subject>692/699/67/1990/283/1896</subject><subject>Analysis</subject><subject>Apoptosis</subject><subject>BCR-ABL protein</subject><subject>Biological and medical sciences</subject><subject>Breakpoints</subject><subject>Cell Biology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. 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Action of oncogenes and antioncogenes</topic><topic>Chromosome abnormalities</topic><topic>Chromosome rearrangements</topic><topic>Chromosomes</topic><topic>Chromosomes, Human, Pair 22</topic><topic>Chromosomes, Human, Pair 9</topic><topic>Chronic myeloid leukemia</topic><topic>Complications and side effects</topic><topic>Computational Biology</topic><topic>Cytogenetics</topic><topic>Diverse techniques</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Duplication</topic><topic>Gene rearrangement</topic><topic>Genetic aspects</topic><topic>Genomic instability</topic><topic>Genomics</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Leukemia</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. 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Limited knowledge is yet available on the molecular processes resulting in chromosomal rearrangements in tumors. The t(9;22)(q34;q11) rearrangement causing the
5′BCR/3′ABL
gene formation has been detected in more than 90% of cases with chronic myeloid leukemia (CML). In 10–18% of patients with CML, genomic deletions were detected on der(9) chromosome next to translocation breakpoints. The molecular mechanism triggering the t(9;22) and deletions on der(9) is still speculative. Here we report a molecular cytogenetic analysis of a large series of patients with CML with der(9) deletions, revealing an evident breakpoint clustering in two regions located proximally to
ABL
and distally to
BCR
, containing an interchromosomal duplication block (SD_9/22). The deletions breakpoints distribution appeared to be strictly related to the distance from the SD_9/22. Moreover, bioinformatic analyses of the regions surrounding the SD_9/22 revealed a high Alu frequency and a poor gene density, reflecting genomic instability and susceptibility to rearrangements. On the basis of our results, we propose a three-step model for t(9;22) formation consisting of alignment of chromosomes 9 and 22 mediated by SD_9/22, spontaneous chromosome breakages and misjoining of DNA broken ends.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>20101201</pmid><doi>10.1038/onc.2009.524</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncogene, 2010-04, Vol.29 (17), p.2509-2516 |
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| subjects | 692/420/2489/68 692/699/67/1990/283/1896 Analysis Apoptosis BCR-ABL protein Biological and medical sciences Breakpoints Cell Biology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chromosome abnormalities Chromosome rearrangements Chromosomes Chromosomes, Human, Pair 22 Chromosomes, Human, Pair 9 Chronic myeloid leukemia Complications and side effects Computational Biology Cytogenetics Diverse techniques Fundamental and applied biological sciences. Psychology Gene Duplication Gene rearrangement Genetic aspects Genomic instability Genomics Hematologic and hematopoietic diseases Human Genetics Humans Internal Medicine Leukemia Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Medicine Medicine & Public Health Molecular and cellular biology Molecular biology Myeloid leukemia Oncology original-article Risk factors Translocation, Genetic Tumors |
| title | Genomic segmental duplications on the basis of the t(9;22) rearrangement in chronic myeloid leukemia |
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