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Figure 3 | Genome Integrity

Figure 3

From: Dysfunctional telomeres in primary cells from Fanconi anemia FANCD2 patients

Figure 3

Results of analyses in FANCD2 and control lymphocytes. a Average telomere length (arbitrary units of RTLU ± SD) measured by Q-FISH in FANCD2 (1823, 1866, 1879 and 2093) and control (C1-C4) cells. Cells originated from FANCD2 patients display shorter telomeres than the age-matched controls (p = 0.024). b The distribution of telomere length indicated that control lymphocytes displayed typical Poisson distributions for individual chromosome telomere length, whereas the peak of Poisson distribution was shifted leftward in FANCD2 lymphocytes. c The percentage of fragile and long extended telomeres: in FANCD2 lymphocytes the percentage of cells displaying fragile telomeres is 18.45% on the average, wheras percentage of cells displaying long-extended telomeres is 17.83%. d SCE analysis. The incidence of spontaneous SCE in FANCD2 lymphocytes was significantly reduced when compared to control (p < 0.05). In response to DEB, almost two-fold increase of SCEs was observed in FANCD2 lymphocytes relative to the baseline state before treatment (p = 0.04). Metaphase spread showing DEB treated FANCD2 lymphocytes with 13 SCE and two chromosomes with dSCE . f CO-FISH analysis. The incidence of spontaneously occurring T-SCEs in FANCD2 lymphocytes was significantly higher than that in control cells (p = 0.026), and further increased in response to DEB. g Apoptosis assay showed a significant difference between FANCD2 and control leucocytes in percentage of spontaneously dying cells as well as in percentage of apoptotic cells induced by ionizing radiation. The data are presented as mean ± SD. h Apotosis of FANCD2 and control fibroblasts: FANCD2 cells spontaneously die with higher rate than controls and exhibit a mild delay in entering apoptosis. The data are presented as mean ± SD.

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