K Paulsson

Summary

Affiliation: University Hospital
Country: Sweden

Publications

  1. ncbi request reprint The incidence of trisomy 8 as a sole chromosomal aberration in myeloid malignancies varies in relation to gender, age, prior iatrogenic genotoxic exposure, and morphology
    K Paulsson
    Department of Clinical Genetics, Lund University Hospital, SE 221 85, Lund, Sweden
    Cancer Genet Cytogenet 130:160-5. 2001
  2. ncbi request reprint Formation of trisomies and their parental origin in hyperdiploid childhood acute lymphoblastic leukemia
    Kajsa Paulsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Blood 102:3010-5. 2003
  3. ncbi request reprint Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia
    Kajsa Paulsson
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 44:113-22. 2005
  4. ncbi request reprint Formation of der(19)t(1;19)(q23;p13) in acute lymphoblastic leukemia
    Kajsa Paulsson
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 42:144-8. 2005
  5. ncbi request reprint 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 aberration
    K Paulsson
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Leukemia 20:840-6. 2006
  6. ncbi request reprint Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemia
    K Paulsson
    Department of Clinical Genetics, Lund University Hospital, Sweden
    Leukemia 20:2002-7. 2006
  7. ncbi request reprint 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 USP42
    K Paulsson
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Leukemia 20:224-9. 2006
  8. ncbi request reprint Trisomy 8 as the sole chromosomal aberration in acute myeloid leukemia and myelodysplastic syndromes
    K Paulsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Pathol Biol (Paris) 55:37-48. 2007
  9. ncbi request reprint Trisomy 8 as the sole chromosomal aberration in myelocytic malignancies: a multicolor and locus-specific fluorescence in situ hybridization study
    Kajsa Paulsson
    Department of Clinical Genetics, University Hospital, SE 221 85, Lund, Sweden
    Cancer Genet Cytogenet 140:66-9. 2003
  10. doi request reprint Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations
    J Davidsson
    Department of Clinical Genetics, University and Regional Laboratories, Skane University Hospital, Lund University, Lund, Sweden
    Leukemia 24:924-31. 2010

Detail Information

Publications19

  1. ncbi request reprint The incidence of trisomy 8 as a sole chromosomal aberration in myeloid malignancies varies in relation to gender, age, prior iatrogenic genotoxic exposure, and morphology
    K Paulsson
    Department of Clinical Genetics, Lund University Hospital, SE 221 85, Lund, Sweden
    Cancer Genet Cytogenet 130:160-5. 2001
    ....
  2. ncbi request reprint Formation of trisomies and their parental origin in hyperdiploid childhood acute lymphoblastic leukemia
    Kajsa 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...
  3. ncbi request reprint Evidence for a single-step mechanism in the origin of hyperdiploid childhood acute lymphoblastic leukemia
    Kajsa 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...
  4. ncbi request reprint Formation of der(19)t(1;19)(q23;p13) in acute lymphoblastic leukemia
    Kajsa Paulsson
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 42:144-8. 2005
    ....
  5. ncbi request reprint 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 aberration
    K 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...
  6. ncbi request reprint Identification of cryptic aberrations and characterization of translocation breakpoints using array CGH in high hyperdiploid childhood acute lymphoblastic leukemia
    K 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...
  7. ncbi request reprint 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 USP42
    K 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...
  8. ncbi request reprint Trisomy 8 as the sole chromosomal aberration in acute myeloid leukemia and myelodysplastic syndromes
    K 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...
  9. ncbi request reprint Trisomy 8 as the sole chromosomal aberration in myelocytic malignancies: a multicolor and locus-specific fluorescence in situ hybridization study
    Kajsa 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...
  10. doi request reprint Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations
    J 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...
  11. ncbi request reprint Identification of a commonly amplified 4.3 Mb region with overexpression of C8FW, but not MYC in MYC-containing double minutes in myeloid malignancies
    Clelia 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...
  12. doi request reprint High hyperdiploid childhood acute lymphoblastic leukemia
    Kajsa 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...
  13. ncbi request reprint Characterisation of genomic translocation breakpoints and identification of an alternative TCF3/PBX1 fusion transcript in t(1;19)(q23;p13)-positive acute lymphoblastic leukaemias
    Kajsa 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...
  14. ncbi request reprint Multicolor fluorescence in situ hybridization characterization of cytogenetically polyclonal hematologic malignancies
    Josef 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...
  15. ncbi request reprint 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 o
    Josef 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...
  16. ncbi request reprint Mutations of FLT3, NRAS, KRAS, and PTPN11 are frequent and possibly mutually exclusive in high hyperdiploid childhood acute lymphoblastic leukemia
    Kajsa 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...
  17. doi request reprint The idic(X)(q13) in myeloid malignancies: breakpoint clustering in segmental duplications and association with TET2 mutations
    Kajsa 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...
  18. ncbi request reprint Searching for cryptic chromosomal aberrations in high hyperdiploid childhood acute lymphoblastic leukaemias
    Josef Davidsson
    Eur J Haematol 76:449-50. 2006
  19. pmc Microdeletions are a general feature of adult and adolescent acute lymphoblastic leukemia: Unexpected similarities with pediatric disease
    Kajsa 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...