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Analysis of balanced rearrangements of chromosome 6 in acute leukemia: clustered breakpoints in q22-q23 and possible involvement of c-MYB in a new recurrent translocation, t(6;7)(q23;q32 through 36)
P Sinclair, CJ Harrison, M Jarosova, L Foroni
Jazyk angličtina Země Itálie
Typ dokumentu práce podpořená grantem
Grantová podpora
NC7490
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Část
Zdroj
NLK
Directory of Open Access Journals
od 1994
Free Medical Journals
od 1994
Freely Accessible Science Journals
od 1994
Open Access Digital Library
od 1994-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1996
PubMed
15921375
Knihovny.cz E-zdroje
- MeSH
- adaptorové proteiny signální transdukční genetika MeSH
- akutní lymfatická leukemie * genetika patologie MeSH
- akutní nemoc MeSH
- akutní T-buněčná leukemie * genetika patologie MeSH
- buněčné klony patologie MeSH
- buňky kostní dřeně MeSH
- chromozomální inverze * genetika MeSH
- dítě MeSH
- fúzní onkogenní proteiny genetika MeSH
- geny myb * MeSH
- hybridizace in situ fluorescenční MeSH
- kojenec MeSH
- lidé MeSH
- lidské chromozomy, pár 6 * genetika ultrastruktura MeSH
- lidské chromozomy, pár 7 * genetika ultrastruktura MeSH
- mladiství MeSH
- myeloidní leukemie * genetika patologie MeSH
- pre-B-buněčná leukemie genetika patologie MeSH
- předškolní dítě MeSH
- pruhování chromozomů MeSH
- translokace genetická * genetika MeSH
- zlomy chromozomů * MeSH
- Check Tag
- dítě MeSH
- kojenec MeSH
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- předškolní dítě MeSH
- ženské pohlaví MeSH
- Publikační typ
- práce podpořená grantem MeSH
BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia. The contribution of sporadic rearrangements to malignancy is less clear and few have been mapped in detail. In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). DESIGN AND METHODS: Breakpoints of balanced 6q rearrangements were mapped in sequential fluorescent in situ hybridization (FISH) experiments with BAC and PAC clones in 11 patients. RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe. In two cases of childhood T-ALL, both carrying a t(6;7)(q23;q32 through 36), split FISH signals were produced by adjacent PAC, mapping the breakpoints to within an approximately 150 Kb region containing the genes c-MYB and AHI1. Five similar rearrangements, four also in pediatric T ALL were identified in the literature. Other 6q22-q23 translocations mapped in detail interrupted regions containing no recognized genes. 6q breakpoints outside the q22-q23 region were widely dispersed and in two were mapped to positions overlapping the cloned fragile sites FRA6E and FRA6F. The involvement of MLL was demonstrated in one case with t(6;11)(q15;q23). INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL. Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism. Key words; chromosome 6, translocation, c-Myb, AHI1.
Obsahuje tabulky
Bibliografie atd.Literatura
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- $a BACKGROUND AND OBJECTIVES: Many clinically important oncogenes and tumor suppressor genes have been identified through analysis of recurrent chromosomal rearrangements in acute leukemia. The contribution of sporadic rearrangements to malignancy is less clear and few have been mapped in detail. In this study we investigated the significance of novel translocations and inversions of 6q in acute lymphoblastic leukemia (ALL) and acute myeloid leukemia (AML). DESIGN AND METHODS: Breakpoints of balanced 6q rearrangements were mapped in sequential fluorescent in situ hybridization (FISH) experiments with BAC and PAC clones in 11 patients. RESULTS: Six of seven breakpoints in ALL and two in a single case of AML were localized to within a 10.5 Mb hotspot at 6q22-q23 with five analyzed to the level of a single probe. In two cases of childhood T-ALL, both carrying a t(6;7)(q23;q32 through 36), split FISH signals were produced by adjacent PAC, mapping the breakpoints to within an approximately 150 Kb region containing the genes c-MYB and AHI1. Five similar rearrangements, four also in pediatric T ALL were identified in the literature. Other 6q22-q23 translocations mapped in detail interrupted regions containing no recognized genes. 6q breakpoints outside the q22-q23 region were widely dispersed and in two were mapped to positions overlapping the cloned fragile sites FRA6E and FRA6F. The involvement of MLL was demonstrated in one case with t(6;11)(q15;q23). INTERPRETATION AND CONCLUSIONS: We identified a new primary recurrent translocation t(6;7) (q22;q23 through q26) in pediatric T-ALL. Other translocations interrupting the 6q22-q23 breakpoint cluster region did not appear to be recurrent and may contribute to leukemogenesis through a novel mechanism. Key words; chromosome 6, translocation, c-Myb, AHI1.
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