Search: WFRF:(Pession Andrea) > (2007) > Cytogenetic feature...
Fältnamn | Indikatorer | Metadata |
---|---|---|
000 | 03834naa a2200481 4500 | |
001 | oai:DiVA.org:umu-18036 | |
003 | SwePub | |
008 | 080112s2007 | |||||||||||000 ||eng| | |
009 | oai:lup.lub.lu.se:2aad6b30-bdea-460d-8cf9-dbc8651c5c8d | |
024 | 7 | a https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-180362 URI |
024 | 7 | a https://lup.lub.lu.se/record/11988372 URI |
024 | 7 | a https://doi.org/10.1182/blood-2007-09-1142312 DOI |
040 | a (SwePub)umud (SwePub)lu | |
041 | a engb eng | |
042 | 9 SwePub | |
072 | 7 | a ref2 swepub-contenttype |
072 | 7 | a art2 swepub-publicationtype |
100 | 1 | a Forestier, Eriku Umeå universitet,Pediatrik4 aut0 (Swepub:umu)erfo0007 |
245 | 1 0 | a Cytogenetic features of acute lymphoblastic and myeloid leukemias in pediatric patients with Down syndrome - an iBFM-SG study. |
264 | 1 | b American Society of Hematology,c 2007 |
338 | a print2 rdacarrier | |
520 | a Children with Down syndrome (DS) have a markedly increased risk of acute lymphoblastic and myeloid leukemias (ALL+AML). To identify chromosomal changes cooperating with +21 that may provide information on the pathogenesis of these leukemias, we analyzed 215 DS-ALL and 189 DS-AML. Unlike previous smaller series, a significant proportion of DS-ALL had the typical B-cell precursor ALL abnormalities high hyperdiploidy (HeH; 11%) and t(12;21)(p13;q22) (10%). The HeH DS-ALL were characterized by gains of the same chromosomes as non-DS-HeH, suggesting the same etiology/pathogenesis. In addition, specific genetic subtypes of DS-ALL were suggested by the significant overrepresentation of cases with +X, t(8;14)(q11;q32), and del(9p). Unlike DS-ALL, the common translocations associated with non-DS-AML were rare in DS-AML, which instead were characterized by the frequent presence of dup(1q), del(6q), del(7p), dup(7q), +8, +11, del(16q), and +21. This series of DS leukemias - the largest to date - reveals that DS-ALL is a heterogeneous disorder that comprises both t(12;21) and HeH as well as DS-related abnormalities. Furthermore, this analysis confirms that DS-AML is a distinct entity, originating through other genetic pathways than do non-DS-AML, and suggests that unbalanced changes such as dup(1q), +8, and +21 are involved in the leukemogenic process. | |
650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Hematologi0 (SwePub)302022 hsv//swe |
650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Hematology0 (SwePub)302022 hsv//eng |
653 | a Leukemia | |
653 | a Down syndrome | |
653 | a children | |
700 | 1 | a Izraeli, Shai4 aut |
700 | 1 | a Beverloo, Berna4 aut |
700 | 1 | a Haas, Oskar4 aut |
700 | 1 | a Pession, Andrea4 aut |
700 | 1 | a Michalova, Kyra4 aut |
700 | 1 | a Stark, Batia4 aut |
700 | 1 | a Harrison, Christine J4 aut |
700 | 1 | a Teigler-Schlegel, Andrea4 aut |
700 | 1 | a Johansson, Bertilu Lund University,Lunds universitet,Avdelningen för klinisk genetik,Institutionen för laboratoriemedicin,Medicinska fakulteten,Genetiska och epigenetiska studier av barnleukemi,Forskargrupper vid Lunds universitet,Division of Clinical Genetics,Department of Laboratory Medicine,Faculty of Medicine,Genetic and epigenetic studies of pediatric leukemia,Lund University Research Groups,Skåne University Hospital4 aut0 (Swepub:lu)kgen-bjo |
710 | 2 | a Umeå universitetb Pediatrik4 org |
773 | 0 | t Bloodd : American Society of Hematologyx 0006-4971x 1528-0020 |
856 | 4 | u http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Retrieve&list_uids=17971484&dopt=Citation |
856 | 4 | u http://dx.doi.org/10.1182/blood-2007-09-114231x freey FULLTEXT |
856 | 4 8 | u https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-18036 |
856 | 4 8 | u https://lup.lub.lu.se/record/1198837 |
856 | 4 8 | u https://doi.org/10.1182/blood-2007-09-114231 |
Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.