Research Topics
Species | K PaulssonSummaryAffiliation: University Hospital Country: Sweden Publications
| Collaborators
|
Detail Information
Publications
The incidence of trisomy 8 as a sole chromosomal aberration in myeloid malignancies varies in relation to gender, age, prior iatrogenic genotoxic exposure, and morphologyK Paulsson
Department of Clinical Genetics, Lund University Hospital, SE 221 85, Lund, Sweden
Cancer Genet Cytogenet 130:160-5. 2001....- Formation of trisomies and their parental origin in hyperdiploid childhood acute lymphoblastic leukemiaKajsa Paulsson
Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
Blood 102:3010-5. 2003..0703). Thus, the present results indicate that imprinting is not pathogenetically important in hyperdiploid childhood ALL, with the possible exception of the observed parental skewness of +8 and +14... - Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemiaKajsa Paulsson
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Genes Chromosomes Cancer 44:113-22. 2005..These data strongly suggest that hyperdiploidy in childhood ALL generally arises by a simultaneous gain of all additional chromosomes in a single abnormal mitosis... - Formation of der(19)t(1;19)(q23;p13) in acute lymphoblastic leukemiaKajsa Paulsson
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Genes Chromosomes Cancer 42:144-8. 2005.... - High-resolution genome-wide array-based comparative genome hybridization reveals cryptic chromosome changes in AML and MDS cases with trisomy 8 as the sole cytogenetic aberrationK Paulsson
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Leukemia 20:840-6. 2006..The present results show that cryptic genetic abnormalities are frequent in trisomy 8-positive AML/MDS cases and that +8 as the sole cytogenetic aberration is not always the primary genetic event... - Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemiaK Paulsson
Department of Clinical Genetics, Lund University Hospital, Sweden
Leukemia 20:2002-7. 2006..The detection and characterization of these additional genetic aberrations will most likely increase our understanding of the pathogenesis of high hyperdiploid childhood ALL... - A novel and cytogenetically cryptic t(7;21)(p22;q22) in acute myeloid leukemia results in fusion of RUNX1 with the ubiquitin-specific protease gene USP42K Paulsson
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Leukemia 20:224-9. 2006..Its involvement in the t(7;21) suggests that deregulation of ubiquitin-associated pathways may be pathogenetically important in AML... - Trisomy 8 as the sole chromosomal aberration in acute myeloid leukemia and myelodysplastic syndromesK Paulsson
Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
Pathol Biol (Paris) 55:37-48. 2007..Here, we summarize and review these various aspects of trisomy 8, focusing on AMLs and MDS harboring this abnormality as a single change... - Trisomy 8 as the sole chromosomal aberration in myelocytic malignancies: a multicolor and locus-specific fluorescence in situ hybridization studyKajsa Paulsson
Department of Clinical Genetics, University Hospital, SE 221 85, Lund, Sweden
Cancer Genet Cytogenet 140:66-9. 2003..No cryptic changes were detected, thus excluding the possibility of gross genetic rearrangements or aberrations involving these loci on chromosome 8... - Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutationsJ Davidsson
Department of Clinical Genetics, University and Regional Laboratories, Skane University Hospital, Lund University, Lund, Sweden
Leukemia 24:924-31. 2010..This ancestral clone was characterized by numerical changes only, with structural changes and RTK-RAS mutations being secondary to the high hyperdiploid pattern... - Identification of a commonly amplified 4.3 Mb region with overexpression of C8FW, but not MYC in MYC-containing double minutes in myeloid malignanciesClelia T Storlazzi
Department of Clinical Genetics, University Hospital, Lund, Sweden
Hum Mol Genet 13:1479-85. 2004..These results exclude MYC as the target gene and indicate that overexpression of C8FW may be the functionally important consequence of 8q24 amplicons in AML and MDS... - High hyperdiploid childhood acute lymphoblastic leukemiaKajsa Paulsson
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Genes Chromosomes Cancer 48:637-60. 2009..However, during the last few years, several studies have addressed some of these important issues, and these, as well as previous reports on high hyperdiploid childhood ALL, are reviewed herein... - Characterisation of genomic translocation breakpoints and identification of an alternative TCF3/PBX1 fusion transcript in t(1;19)(q23;p13)-positive acute lymphoblastic leukaemiasKajsa Paulsson
Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
Br J Haematol 138:196-201. 2007..The PBX1 breakpoints were more dispersed, although still clustered in two regions. This confirms that most t(1;19) rearrangements may arise by a combination of illegitimate V(D)J recombination and non-homologous end joining... - Multicolor fluorescence in situ hybridization characterization of cytogenetically polyclonal hematologic malignanciesJosef Davidsson
Department of Clinical Genetics, Lund University Hospital, SE 221 85 Lund, Sweden
Cancer Genet Cytogenet 163:180-3. 2005..Based on the present results, we conclude that M-FISH, in general, does not reveal primary cryptic aberrations supporting a monoclonal origin of cytogenetically polyclonal hematologic malignancies... - Tiling resolution array comparative genomic hybridization, expression and methylation analyses of dup(1q) in Burkitt lymphomas and pediatric high hyperdiploid acute lymphoblastic leukemias reveal clustered near-centromeric breakpoints and overexpression oJosef Davidsson
Department of Clinical Genetics, Lund University Hospital, Sweden
Hum Mol Genet 16:2215-25. 2007..However, involvement of these genes in dup(1q)-positive ALLs and BLs has previously not been reported... - Mutations of FLT3, NRAS, KRAS, and PTPN11 are frequent and possibly mutually exclusive in high hyperdiploid childhood acute lymphoblastic leukemiaKajsa Paulsson
Department of Clinical Genetics, University Hospital, Lund, Sweden
Genes Chromosomes Cancer 47:26-33. 2008..In total, one third of the cases harbored a FLT3, NRAS, KRAS, or PTPN11 mutation, identifying the RTK-RAS signaling pathway as a potential target for novel therapies of high hyperdiploid pediatric ALLs... - The idic(X)(q13) in myeloid malignancies: breakpoint clustering in segmental duplications and association with TET2 mutationsKajsa Paulsson
Department of Clinical Genetics, University and Regional Laboratories, Lund University Hospital, Lund University, Lund, Sweden
Hum Mol Genet 19:1507-14. 2010..In total, TET2 mutations were seen in 4/11 (36%) analyzed cases, thus constituting a common secondary event in idic(X)-positive malignancies... - Searching for cryptic chromosomal aberrations in high hyperdiploid childhood acute lymphoblastic leukaemiasJosef Davidsson
Eur J Haematol 76:449-50. 2006 - Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric diseaseKajsa Paulsson
Cancer Research UK Medical Oncology Centre, Barts and the London School of Medicine, Queen Mary College, London EC1M 6BQ, United Kingdom
Proc Natl Acad Sci U S A 105:6708-13. 2008..Most importantly, we report that microdeletions of key genes appear to be a common, characteristic feature of ALL that is shared among different clinical, morphological, and cytogenetic subgroups...