David Gisselsson

Summary

Affiliation: University Hospital
Country: Sweden

Publications

  1. ncbi A case of dermatofibrosarcoma protuberans with a ring chromosome 5 and a rearranged chromosome 22 containing amplified COL1A1 and PDGFB sequences
    D Gisselsson
    Department of Clinical Genetics, Lund University Hospital, Sweden
    Cancer Lett 133:129-34. 1998
  2. ncbi Connecting mitotic instability and chromosome aberrations in cancer--can telomeres bridge the gap?
    David Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Semin Cancer Biol 15:13-23. 2005
  3. ncbi Telomere shortening and mitotic dysfunction generate cytogenetic heterogeneity in a subgroup of renal cell carcinomas
    D Gisselsson
    Department of Clinical Genetics, University Hospital, Lund SE 221 85, Sweden
    Br J Cancer 91:327-32. 2004
  4. ncbi Telomere-mediated mitotic disturbances in immortalized ovarian epithelial cells reproduce chromosomal losses and breakpoints from ovarian carcinoma
    David Gisselsson
    Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China
    Genes Chromosomes Cancer 42:22-33. 2005
  5. ncbi Centrosomal abnormalities, multipolar mitoses, and chromosomal instability in head and neck tumours with dysfunctional telomeres
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Br J Cancer 87:202-7. 2002
  6. ncbi Mitotic instability associated with late genomic changes in bone and soft tissue tumours
    David Gisselsson
    Department of Clinical Genetics, University Hospital, Lund SE 221 85, Sweden
    Cancer Lett 206:69-76. 2004
  7. ncbi Differentially amplified chromosome 12 sequences in low- and high-grade osteosarcoma
    David Gisselsson
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 33:133-40. 2002
  8. ncbi Refined characterisation of chromosome aberrations in tumours by multicolour banding and electronic mapping resources
    D Gisselsson
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Methods Cell Sci 23:23-8. 2001
  9. ncbi Telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Proc Natl Acad Sci U S A 98:12683-8. 2001
  10. ncbi Tumour morphology--interplay between chromosome aberrations and founder cell differentiation
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Histol Histopathol 17:1207-12. 2002

Detail Information

Publications66

  1. ncbi A case of dermatofibrosarcoma protuberans with a ring chromosome 5 and a rearranged chromosome 22 containing amplified COL1A1 and PDGFB sequences
    D Gisselsson
    Department of Clinical Genetics, Lund University Hospital, Sweden
    Cancer Lett 133:129-34. 1998
    ....
  2. ncbi Connecting mitotic instability and chromosome aberrations in cancer--can telomeres bridge the gap?
    David Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Semin Cancer Biol 15:13-23. 2005
    ..Even though many common cancers, such as breast, colorectal, and renal cell carcinomas adhere to this simple power-law dynamics, the underlying molecular mechanisms remain elusive...
  3. ncbi Telomere shortening and mitotic dysfunction generate cytogenetic heterogeneity in a subgroup of renal cell carcinomas
    D Gisselsson
    Department of Clinical Genetics, University Hospital, Lund SE 221 85, Sweden
    Br J Cancer 91:327-32. 2004
    ..Abnormalities of the cell division machinery may thus contribute to the evolution of complex karyotypes and genetic intratumour heterogeneity in a subgroup of RCC...
  4. ncbi Telomere-mediated mitotic disturbances in immortalized ovarian epithelial cells reproduce chromosomal losses and breakpoints from ovarian carcinoma
    David Gisselsson
    Department of Medicine, Queen Mary Hospital, University of Hong Kong, Hong Kong, China
    Genes Chromosomes Cancer 42:22-33. 2005
    ..That the model did not produce any of the whole-chromosome gains observed in OC indicates that these changes develop through a different mechanism...
  5. ncbi Centrosomal abnormalities, multipolar mitoses, and chromosomal instability in head and neck tumours with dysfunctional telomeres
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Br J Cancer 87:202-7. 2002
    ..In turn, this may cause an accumulation of centrosomes and mitotic multipolarity. Telomerase expression does not confer total stability to the tumour genome but could be crucial for moderating the rate of chromosomal evolution...
  6. ncbi Mitotic instability associated with late genomic changes in bone and soft tissue tumours
    David Gisselsson
    Department of Clinical Genetics, University Hospital, Lund SE 221 85, Sweden
    Cancer Lett 206:69-76. 2004
    ....
  7. ncbi Differentially amplified chromosome 12 sequences in low- and high-grade osteosarcoma
    David Gisselsson
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 33:133-40. 2002
    ..These findings indicate that gain of sequences from the short arm of chromosome 12 could be a possible genetic pathway in the development of aggressive osteosarcoma...
  8. ncbi Refined characterisation of chromosome aberrations in tumours by multicolour banding and electronic mapping resources
    D Gisselsson
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Methods Cell Sci 23:23-8. 2001
    ..The resulting colour-banding allows the characterisation of chromosome abnormalities in relation to expressed sequences, even in tumours exhibiting highly complex rearrangements...
  9. ncbi Telomere dysfunction triggers extensive DNA fragmentation and evolution of complex chromosome abnormalities in human malignant tumors
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Proc Natl Acad Sci U S A 98:12683-8. 2001
    ..Telomerase expression is not sufficient for completely stabilizing the chromosome complement but may be crucial for preventing complete genomic deterioration and maintaining cellular survival...
  10. ncbi Tumour morphology--interplay between chromosome aberrations and founder cell differentiation
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Histol Histopathol 17:1207-12. 2002
    ..Tumour morphology thus appears to be determined not only by the lineage of the transformed cell but also by its propensity for chromosomal instability...
  11. ncbi Variable stability of chromosomes containing amplified alpha-satellite sequences in human mesenchymal tumours
    D Gisselsson
    Department of Clinical Genetics, University Hospital, S 221 85 Lund, Sweden
    Chromosoma 108:271-7. 1999
    ..A propensity for additional kinetochore formation might thus be associated with the coamplification of alphoid DNA and pericentromeric sequences from chromosome 12...
  12. ncbi Hibernomas are characterized by homozygous deletions in the multiple endocrine neoplasia type I region. Metaphase fluorescence in situ hybridization reveals complex rearrangements not detected by conventional cytogenetics
    D Gisselsson
    Department of Clinical Genetics, University Hospital, Lund, Sweden University of Leuven, Leuven, Belgium
    Am J Pathol 155:61-6. 1999
    ..In addition to the MEN1 deletions, heterozygous loss of a second region, approximately 3 Mb distal to MEN1, was found in all five cases, adding to previous evidence for a second tumor suppressor locus in 11q13...
  13. ncbi Locus-specific multifluor FISH analysis allows physical characterization of complex chromosome abnormalities in neoplasia
    D Gisselsson
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 28:347-52. 2000
    ..Combinatorially labeled single-copy probes may thus simultaneously provide physical localization of breakpoints and an overview of complex structural rearrangements. Genes Chromosomes Cancer 28:347-352, 2000...
  14. ncbi The structure and dynamics of ring chromosomes in human neoplastic and non-neoplastic cells
    D Gisselsson
    Department of Clinical Genetics, Lund University Hospital, Sweden
    Hum Genet 104:315-25. 1999
    ..We conclude that it is not only the ring structure per se or the neoplastic nature of the host cell that determines ring instability, but probably also the functional role of the genes carried in the ring...
  15. ncbi Abnormal nuclear shape in solid tumors reflects mitotic instability
    D Gisselsson
    Departments of Clinical Genetics, Occupational and Environmental Medicine, and Pathology, University Hospital, Lund, Sweden
    Am J Pathol 158:199-206. 2001
    ..Abnormalities in nuclear shape may thus primarily be regarded as an indicator of genetic instability and intratumor heterogeneity, independent of cytogenetic complexity and the grade of malignancy...
  16. ncbi High-resolution molecular cytogenetic analysis of Wilms tumors highlights diagnostic difficulties among small round cell kidney tumors
    Ylva Stewénius
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 47:845-52. 2008
    ..The fact that no recurrent translocations were found in the WTs of this study argues against the presence of a frequent pathognomonic translocation in this disease entity...
  17. ncbi Structural and numerical chromosome changes in colon cancer develop through telomere-mediated anaphase bridges, not through mitotic multipolarity
    Ylva Stewénius
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Proc Natl Acad Sci U S A 102:5541-6. 2005
    ..Bridging of telomere-deficient chromosomes could thus be a major mutational mechanism in colorectal cancer, whereas mitotic multipolarity appears to be a secondary phenomenon that rarely, if ever, contributes to clonal evolution...
  18. ncbi Ovarian carcinoma develops through multiple modes of chromosomal evolution
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Cancer Res 63:3378-85. 2003
    ..This process was linked to the presence of imbalances characteristic for the 6q-/1q- pathway. The transition to Phase III involved triploidization and was also linked to the presence of the 6q-/1q- pathway...
  19. ncbi Dissecting karyotypic patterns in renal cell carcinoma: an analysis of the accumulated cytogenetic data
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Cancer Genet Cytogenet 153:1-9. 2004
    ..The analyses also revealed three possible cytogenetic subtypes of the papillary tumors, one characterized by the presence of +10, a second by +17 and +3q, and a third by +16, +20, and +12...
  20. ncbi Wilms tumors develop through two distinct karyotypic pathways
    Mattias Hoglund
    Department of Clinical Genetics, Lund University Hospital, SE 221 85 Lund, Sweden
    Cancer Genet Cytogenet 150:9-15. 2004
    ..We also show that these pathways are well separated and do not share a common set of late imbalances...
  21. ncbi Statistical analyses of karyotypic complexity in head and neck squamous cell carcinoma
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Cancer Genet Cytogenet 150:1-8. 2004
    ..Two major cytogenetic pathways, one dominated by gains and another by losses, were identified by means of principal component analysis. These were initiated by +7 and by any of the aberrations 1p-, 3p-, or 7q-, respectively...
  22. ncbi Alternative lengthening of telomeres--an enhanced chromosomal instability in aggressive non-MYCN amplified and telomere elongated neuroblastomas
    Gisela Lundberg
    Department of Clinical Genetics, Lund University, University and Regional Laboratories, Skane University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 50:250-62. 2011
    ..Thus, telomere-dependent chromosomal instability is highly prevalent in NB, and may contribute to the complexity of genomic alterations as well as therapy resistance in the absence of MYCN amplification and in this tumor type...
  23. ncbi Deletions of 16q in Wilms tumors localize to blastemal-anaplastic cells and are associated with reduced expression of the IRXB renal tubulogenesis gene cluster
    Linda Holmquist Mengelbier
    Department of Clinical Genetics, University and Regional Laboratories, Lund University, Skane University Hospital, SE 221 85 Lund, Sweden
    Am J Pathol 177:2609-21. 2010
    ..A disturbed balance between tubular differentiation and self-renewal of anaplastic-blastic elements may thus be one mechanism linking 16q deletion to adverse outcome in Wilms tumor...
  24. ncbi Binomial mitotic segregation of MYCN-carrying double minutes in neuroblastoma illustrates the role of randomness in oncogene amplification
    Gisela Lundberg
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    PLoS ONE 3:e3099. 2008
    ..Because DMs lack centromeric sequences it has been unclear how NB cells retain and amplify extrachromosomal MYCN copies during tumour development...
  25. ncbi Distinct mitotic segregation errors mediate chromosomal instability in aggressive urothelial cancers
    Yuesheng Jin
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Clin Cancer Res 13:1703-12. 2007
    ..The aim of this study was to evaluate whether disturbances of mitotic segregation contribute to CIN in UC, if these processes have any effect on the course of disease, and how deregulation of these mechanisms affects tumor cell growth...
  26. ncbi When the genome plays dice: circumvention of the spindle assembly checkpoint and near-random chromosome segregation in multipolar cancer cell mitoses
    David Gisselsson
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    PLoS ONE 3:e1871. 2008
    ..Such multipolar mitoses have been proposed to generate genetic diversity and thereby contribute to clonal evolution. However, this notion has been little validated experimentally...
  27. ncbi Statistical dissection of cytogenetic patterns in lung cancer reveals multiple modes of karyotypic evolution independent of histological classification
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Cancer Genet Cytogenet 154:99-109. 2004
    ..No marked differences between the karyotypic profiles were found among morphologic subtypes, suggesting that lung cancer morphology is independent of the particular cytogenetic pathway operating in the tumor cells...
  28. ncbi Statistical behavior of complex cancer karyotypes
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Genes Chromosomes Cancer 42:327-41. 2005
    ..The change in karyotypic orderliness at the transition from Phase I to Phase II/III was also shown by a drastic difference in karyotypic entropy...
  29. ncbi Generation of trisomies in cancer cells by multipolar mitosis and incomplete cytokinesis
    David Gisselsson
    Department of Clinical Genetics, Lund University, University and Regional Laboratories, University Hospital, SE 221 85 Lund, Sweden
    Proc Natl Acad Sci U S A 107:20489-93. 2010
    ....
  30. ncbi Molecular cytogenetic characterization of the 11q13 amplicon in head and neck squamous cell carcinoma
    C Jin
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Cytogenet Genome Res 115:99-106. 2006
    ....
  31. ncbi Coping with complexity. multivariate analysis of tumor karyotypes
    Mattias Hoglund
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Cancer Genet Cytogenet 135:103-9. 2002
    ..By applying these methods on the chromosomal changes presently known, distinct subgroups have been identified among breast, kidney, bladder, colon, and brain tumors...
  32. ncbi Ewing tumours and synovial sarcomas have critical features of karyotype evolution in common with epithelial tumours
    Mattias Hoglund
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Int J Cancer 116:401-6. 2005
    ....
  33. ncbi Defective chromosome segregation and telomere dysfunction in aggressive Wilms' tumors
    Ylva Stewénius
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Clin Cancer Res 13:6593-602. 2007
    ..As an alternative to cytogenetic classification, we therefore have evaluated whether the rate of telomere-dependent chromosomal instability could influence the clinical course in WT patients...
  34. ncbi A model for karyotypic evolution in testicular germ cell tumors
    Attila Frigyesi
    Center for Mathematical Sciences, Mathematical Statistics, Lund University, Lund, Sweden
    Genes Chromosomes Cancer 40:172-8. 2004
    ..The results suggest that whole-chromosome changes originate from a multipolar cell division of a tetraploid cell, whereas imbalances caused by structural changes accumulate in a stepwise manner...
  35. ncbi SIX1 protein expression selectively identifies blastemal elements in Wilms tumor
    Daniel Sehic
    Department of Clinical Genetics, Lund University, University and Regional Laboratories, Lund, Sweden
    Pediatr Blood Cancer 59:62-8. 2012
    ..However, there is currently no molecular marker for blastemal cells, and risk stratification for post-nephrectomy treatment is therefore often based on clinico-histological parameters alone...
  36. ncbi Dissecting karyotypic patterns in malignant melanomas: temporal clustering of losses and gains in melanoma karyotypic evolution
    Mattias Hoglund
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Int J Cancer 108:57-65. 2004
    ....
  37. ncbi Classification of chromosome segregation errors in cancer
    David Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Chromosoma 117:511-9. 2008
    ..Any morphology-based classification of chromosome segregation errors in cancer must therefore be taken as provisional, anticipating a satisfactory integration of morphology and molecular biology...
  38. ncbi Dissecting karyotypic patterns in colorectal tumors: two distinct but overlapping pathways in the adenoma-carcinoma transition
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Cancer Res 62:5939-46. 2002
    ..We also show that the adenoma-carcinoma transition in the 1p- pathway is strongly linked to karyoytypic evolution, whereas the +7 pathway is not, and that the cytogenetic pathways are separated at both early and late stages...
  39. ncbi Genetic bottlenecks and the hazardous game of population reduction in cell line based research
    David Gisselsson
    Department of Clinical Genetics, Lund University, University and Regional Laboratories, Lund, Sweden
    Exp Cell Res 316:3379-86. 2010
    ..Genetic bottlenecks should therefore be considered a potential caveat in all studies involving sub-cloning, transfection and other conditions leading to a temporary reduction in cell number...
  40. ncbi Cryptic terminal chromosome rearrangements in colorectal carcinoma cell lines detected by subtelomeric FISH analysis
    Y Stewénius
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Cytogenet Genome Res 114:257-62. 2006
    ..In particular, previously undetected terminal imbalances were found in the two cell lines not showing microsatellite instability...
  41. ncbi A novel fusion gene, SS18L1/SSX1, in synovial sarcoma
    Clelia Tiziana Storlazzi
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 37:195-200. 2003
    ..Thus, the existence of genetic heterogeneity has to be taken into account when RT-PCR is used for the diagnosis of synovial sarcoma...
  42. ncbi Telomeric associations correlate with telomere length reduction and clonal chromosome aberrations in giant cell tumor of bone
    S Gebre-Medhin
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Cytogenet Genome Res 124:121-7. 2009
    ..Thus, the present findings provide strong support for the notion that decreased telomere length is a prerequisite for tas in GCTBs and that the clonal changes occurring in GCTBs are derived from tas...
  43. ncbi Bone marrow multipotent mesenchymal stroma cells act as pericyte-like migratory vehicles in experimental gliomas
    Daniel Bexell
    The Rausing Laboratory, Division of Neurosurgery, Department of Clinical Sciences, Lund University, Lund, Sweden
    Mol Ther 17:183-90. 2009
    ..v. injections. Intratumorally grafted pericyte-like MSCs might represent a particularly well-suited vector system for delivering molecules to affect tumor angiogenesis and for targeting cancer stem cells within the perivascular niche...
  44. ncbi Glial progenitor-like phenotype in low-grade glioma and enhanced CD133-expression and neuronal lineage differentiation potential in high-grade glioma
    Johan Rebetz
    The Rausing Laboratory, Division of Neurosurgery, Lund University Hospital, Lund, Sweden
    PLoS ONE 3:e1936. 2008
    ....
  45. ncbi Multivariate analysis of chromosomal imbalances in breast cancer delineates cytogenetic pathways and reveals complex relationships among imbalances
    Mattias Hoglund
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Cancer Res 62:2675-80. 2002
    ..Although the cytogenetic pathways are well separated at earlier stages, they later converge and include a common set of late imbalances...
  46. ncbi Cytogenetic aberrations and their prognostic impact in chondrosarcoma
    Nils Mandahl
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 33:188-200. 2002
    ..Only -13q was an independent prognostic factor for metastasis, regardless of tumor grade or size...
  47. ncbi Concurrent gain of 17q and the MYC oncogene in a medullomyoblastoma
    Eva Lindberg
    Department of Pathology, University Hospital, Lund, Sweden
    Neuropathology 27:556-60. 2007
    ..Our findings support the notion that MMB and classical medulloblastoma arise through similar genetic mechanisms and that the two main tissue components in MMB are clonally related...
  48. ncbi [Sudanese cytogeneticists--vision of a new kind of assistance]
    Therese Nilsson
    Avdelningen för klinisk genetik, Universitetssjukhuset i Lund
    Lakartidningen 101:702-5. 2004
  49. ncbi Chromosomal breakage-fusion-bridge events cause genetic intratumor heterogeneity
    D Gisselsson
    Department of Clinical Genetics, University Hospital, SE 221 85 Lund, Sweden
    Proc Natl Acad Sci U S A 97:5357-62. 2000
    ....
  50. ncbi Retained heterodisomy for chromosome 12 in atypical lipomatous tumors: implications for ring chromosome formation
    F Mertens
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Cytogenet Genome Res 106:33-8. 2004
    ..The molecular genetic analyses showed that the tumor cells always retained both parental copies of chromosome 12, thus refuting the trisomy 12 and duplication hypotheses...
  51. ncbi Multivariate analyses of genomic imbalances in solid tumors reveal distinct and converging pathways of karyotypic evolution
    M Hoglund
    Department of Clinical Genetics, Lund University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 31:156-71. 2001
    ..It was found that the majority of the tumor types displayed more than one cytogenetic route, but, as the karyotypic evolution continued, these converged to a common pathway...
  52. ncbi Characterization of chromosome aberrations in salivary gland tumors by FISH, including multicolor COBRA-FISH
    C Jin
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Genes Chromosomes Cancer 30:161-7. 2001
    ....
  53. ncbi Interphase chromosomal abnormalities and mitotic missegregation of hypomethylated sequences in ICF syndrome cells
    David Gisselsson
    Department of Clinical Genetics, University Hospital, 22185 Lund, Sweden
    Chromosoma 114:118-26. 2005
    ..This can help explain why specific types of 1qh and 16qh rearrangements are not present at high frequencies in ICF lymphoid cells despite diverse 1qh and 16qh aberrations continuously being generated...
  54. ncbi Modeling the human 8p11-myeloproliferative syndrome in immunodeficient mice
    Helena Agerstam
    Department of Clinical Genetics, University and Regional Laboratories, Skane University Hospital, Lund University, Lund, Sweden
    Blood 116:2103-11. 2010
    ..The established in vivo EMS model should provide a valuable tool for future studies of this disorder...
  55. ncbi Distinct evolutionary mechanisms for genomic imbalances in high-risk and low-risk neuroblastomas
    David Gisselsson
    Department of Clinical Genetics, Lund University Hospital, SE 221 85 Lund, Sweden
    J Carcinog 6:15. 2007
    ..Little is known about the temporal sequence in which these imbalances occur during the carcinogenic process...
  56. ncbi Intratumor diversity and clonal evolution in cancer--a skeptical standpoint
    David Gisselsson
    Departments of Clinical Genetics and Pathology, Lund University, Lund, Sweden
    Adv Cancer Res 112:1-9. 2011
    ....
  57. ncbi Chromosome instability in cancer: how, when, and why?
    David Gisselsson
    Department of Clinical Genetics, University Hospital SE 221 85 Lund, Sweden
    Adv Cancer Res 87:1-29. 2003
    ..Also, overexpression of telomerase appears to play a crucial role for moderating the rate of chromosomal evolution...
  58. ncbi Telomere dysfunction and telomerase activation in cancer--a pathological paradox?
    O Calcagnile
    Department of Clinical Genetics, University Hospital, Lund, Sweden
    Cytogenet Genome Res 118:270-6. 2007
    ..Taken together, the available data on the role of telomerase in cancer strongly support that inhibition of this enzyme is a feasible strategy for cancer therapy...
  59. ncbi Genetic intratumour heterogeneity in high-grade brain tumours is associated with telomere-dependent mitotic instability
    C Glanz
    The Rausing Laboratory, Division of Neurosurgery, Lund University Hospital, Lund, Sweden
    Neuropathol Appl Neurobiol 33:440-54. 2007
    ..Telomere-dependent abnormal segregation of chromosomes at mitosis is thus a common phenomenon in high-grade brain tumours and may be one important factor behind cytogenetic intratumour diversity in GBM...
  60. ncbi Biphasic, hyperdiploid breast tumors in children: a distinct entity?
    Charles Walther
    Departments of Clinical Genetics Pathology Pediatric Surgery, University and Regional Laboratories, Skane University Hospital, Lund University, Lund, Sweden
    J Pediatr Hematol Oncol 35:64-8. 2013
    ..However, the distinction between the 2 lesions is important to make, especially since the latter can be malignant and consequently the prognoses differ...
  61. ncbi Array-based genotype-phenotype correlation in a case of supernumerary ring chromosome 12
    J Davidsson
    Department of Clinical Genetics, Lund University Hospital, Lund SE 221 85, Sweden
    Clin Genet 73:44-9. 2008
    ..Detailed genomic evaluation, by array CGH or similar techniques may thus be of importance to predict the clinical course in individual cases...
  62. ncbi Mitotic instability in cancer: is there method in the madness?
    David Gisselsson
    Department of Clinical Genetics University Hospital SE 221 85 Lund, Sweden
    Cell Cycle 4:1007-10. 2005
    ..The telomere-dependent instability can be partly counteracted by expression of telomerase during tumor progression, but genomic stabilisation is rarely, if ever, complete...
  63. ncbi Euploidy in somatic cells from R6/2 transgenic Huntington's disease mice
    Asa Petersen
    Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, Sweden
    BMC Cell Biol 6:34. 2005
    ..Aneuploidy is normally a feature closely connected to neoplastic disease. To further explore this unexpected aspect of HD, we studied cultures derived from 6- and 12-week-old R6/2 fibroblasts, skeletal muscle cells, and liver cells...
  64. ncbi Power law distribution of chromosome aberrations in cancer
    Attila Frigyesi
    Centre for Mathematical Sciences, Mathematical Statistics, Lund University, SE-221 85 Lund, Sweden
    Cancer Res 63:7094-7. 2003
    ..Because almost identical power law distributions are seen in breast, colorectal, and renal cell carcinomas we suggest that the obtained distributions are consequences of a common mechanism operating in malignant epithelial tumors...
  65. ncbi A case of Cornelia de Lange syndrome from Sudan
    Mona Ellaithi
    The Orchids Organization for Children with Special Needs, Khartoum, Sudan
    BMC Pediatr 7:6. 2007
    ....
  66. ncbi Cancer stem cells: differentiation block or developmental back-tracking?
    David Gisselsson
    Semin Cancer Biol 17:189-90. 2007