DNA double-strand break rejoining in human follicular lymphoma and glioblastoma tumor cells.

  • Authors:
    • A M Macann
    • R A Britten
    • S Poppema
    • R Pearcey
    • E Rosenberg
    • M J Allalunis-Turner
    • D Murray
  • View Affiliations

  • Published online on: March 1, 2000     https://doi.org/10.3892/or.7.2.299
  • Pages: 299-602
Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Follicle center cell lymphoma is among the most radioresponsive of human cancers. To assess whether this radioresponsiveness might be a result of a compromised ability of the tumor cells to accomplish the biologically-effective repair of DNA double-strand breaks (DSBs), we have measured i) the extent of the mechanical rejoining of radiation-induced DSBs in biopsy-derived follicle center cell lymphoma cells and ii) the fidelity with which nuclear protein extracts from these cells rejoin restriction enzyme-induced DSBs. Cell suspensions derived from two lymphoma biopsies, designated FCL1 and FCL2, as well as two established human glioblastoma cell lines, M059J and M059K, were exposed to 30 Gy of gamma-rays and evaluated for their ability to rejoin DSBs using a Southern transfer-pulsed-field gel electrophoresis assay. The fidelity of rejoining of restriction enzyme-induced DSBs was assessed using a cell-free plasmid reactivation assay. Both lymphoma suspensions rejoined DSBs relatively slowly and exhibited a similar phenotype to the known DSB-rejoining deficient M059J line. The level of DSB mis-rejoining in the cell-free plasmid reactivation assay was also similar in M059J and FCL2 cells and was considerably ( approximately 6-fold) higher than in M059K cells. Because of insufficient numbers of cells, we were unable to perform this assay with the FCL1 lymphoma. These limited data suggest that follicle center cell lymphoma cells may be intrinsically deficient in performing the biologically-effective rejoining of DSBs. Such a deficiency might contribute to the radioresponsiveness of this disease and may be exploitable in the development of improved treatment strategies, such as radioimmunotherapy.

Related Articles

Journal Cover

Mar-Apr 2000
Volume 7 Issue 2

Print ISSN: 1021-335X
Online ISSN:1791-2431

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Macann A, Britten R, Poppema S, Pearcey R, Rosenberg E, Allalunis-Turner M and Murray D: DNA double-strand break rejoining in human follicular lymphoma and glioblastoma tumor cells.. Oncol Rep 7: 299-602, 2000
APA
Macann, A., Britten, R., Poppema, S., Pearcey, R., Rosenberg, E., Allalunis-Turner, M., & Murray, D. (2000). DNA double-strand break rejoining in human follicular lymphoma and glioblastoma tumor cells.. Oncology Reports, 7, 299-602. https://doi.org/10.3892/or.7.2.299
MLA
Macann, A., Britten, R., Poppema, S., Pearcey, R., Rosenberg, E., Allalunis-Turner, M., Murray, D."DNA double-strand break rejoining in human follicular lymphoma and glioblastoma tumor cells.". Oncology Reports 7.2 (2000): 299-602.
Chicago
Macann, A., Britten, R., Poppema, S., Pearcey, R., Rosenberg, E., Allalunis-Turner, M., Murray, D."DNA double-strand break rejoining in human follicular lymphoma and glioblastoma tumor cells.". Oncology Reports 7, no. 2 (2000): 299-602. https://doi.org/10.3892/or.7.2.299