Jumping translocations are common in solid tumor cell lines and result in recurrent fusions of whole chromosome arms

被引:74
作者
Padilla-Nash, HM
Heselmeyer-Haddad, K
Wangsa, N
Zhang, HG
Ghadimi, BM
Macville, M
Augustus, M
Schröck, E
Hilgenfeld, E
Ried, T
机构
[1] NCI, Dept Genet, Div Clin Sci, NIH, Bethesda, MD 20892 USA
[2] NHGRI, Canc Genet Branch, NIH, Bethesda, MD 20892 USA
[3] Univ Nijmegen, Lab In Situ Hybridizat, Inst Pathol, Nijmegen, Netherlands
关键词
D O I
10.1002/gcc.1101
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Jumping translocations (JTs) and segmental jumping translocations (SJTs) are unbalanced translocations involving a donor chromosome arm or chromosome segment that has fused to multiple recipient chromosomes. In leukemia, where JTs have been predominantly observed. the donor segment (usually Iq) preferentially fuses to the telomere regions of recipient chromosomes. In this study, spectral karyotyping (SKY) and FISH analysis revealed 188 JTs and JJTs in 10 cell lines derived from carcinomas of the bladder, prostate, breast, cervix, and pancreas. Multiple JTs and SJTs were detected in each cell line and contributed to recurrent unbalanced whole-arm translocations involving chromosome arms 5p, 14q, 15q, 20q, and 21q. Sixty percent (113/188) of JT breakpoints occurred within centromere or pericentromeric regions of the recipient chromosomes, whereas only 12% of the breakpoints were located in the telomere regions. JT breakpoints of both donor and recipient chromosomes coincided with numerous fragile sites as well as viral integration sites for human DNA viruses. The JTs within each tumor cell line promoted clonal progression, leading to the acquisition of extra copies of the donated chromosome segments that often contained oncogenes (MYC, ABL, HER2/NEU, etc.), consequently resulting in tumor-specific genomic imbalances. Published 2001 Wiley-Liss, Inc.dagger.
引用
收藏
页码:349 / 363
页数:15
相关论文
共 47 条
  • [1] JUMPING TRANSLOCATION OF CHROMOSOME-14 IN A SKIN SQUAMOUS-CELL CARCINOMA FROM A XERODERMA PIGMENTOSUM PATIENT
    ALEDO, R
    AURIAS, A
    CHRETIEN, B
    DUTRILLAUX, B
    [J]. CANCER GENETICS AND CYTOGENETICS, 1988, 33 (01) : 29 - 33
  • [2] Molecular characterization of jumping translocations reveals spatial and temporal breakpoint heterogeneity
    Andreasson, P
    Höglund, M
    Jonson, T
    Békàssy, A
    Mitelman, F
    Johansson, B
    [J]. LEUKEMIA, 1998, 12 (09) : 1411 - 1416
  • [3] BARTOLI C, 1996, CANCER, V78, P1142
  • [4] Jumping translocation in acute leukemia of myelomonocytic lineage:: a case report and review of the literature
    Bernard, M
    Lemée, F
    Picard, F
    Ghandour, C
    Drenou, B
    Le Prise, PY
    Lamy, T
    [J]. LEUKEMIA, 2000, 14 (01) : 119 - 122
  • [5] Busson-Le Coniat M, 1999, LEUKEMIA, V13, P1975
  • [6] HERPES-SIMPLEX VIRUS AND HUMAN PAPILLOMAVIRUS SITES CORRELATE WITH CHROMOSOMAL BREAKPOINTS IN HUMAN CERVICAL-CARCINOMA
    DEBRAEKELEER, M
    SREEKANTAIAH, C
    HAAS, O
    [J]. CANCER GENETICS AND CYTOGENETICS, 1992, 59 (02) : 135 - 137
  • [7] Masquerading repeats: Paralogous pitfalls of the human genome
    Eichler, EE
    [J]. GENOME RESEARCH, 1998, 8 (08): : 758 - 762
  • [8] Specific destruction of kinetochore protein CENP-C and disruption of cell division by herpes simplex virus immediate-early protein Vmw110
    Everett, RD
    Earnshaw, WC
    Findlay, J
    Lomonte, P
    [J]. EMBO JOURNAL, 1999, 18 (06) : 1526 - 1538
  • [9] FANGLIN S, 2000, P NATL ACAD SCI USA, V97, P5340
  • [10] Genome screening by comparative genomic hybridization
    Forozan, F
    Karhu, R
    Kononen, J
    Kallioniemi, A
    Kallioniemi, OP
    [J]. TRENDS IN GENETICS, 1997, 13 (10) : 405 - 409