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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of <t>γH2AX</t> and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of <t>γH2AX</t> and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
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Effect of monoHER (M) combined with radiation (RT) on γ-H2AX immunofluorescence staining (at 24 h post-irradiation time point) in breast cancer and normal cells. Data are presented as mean ± SEM from three independent experiments (20 cells/experiment). *p < 0.05, **p < 0.01.
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Parameters associated with high ferritin were assessed in patients with non-elevated (≤ 275 µg/L), moderately elevated (> 275 and < 1000 µg/L), and highly elevated SF (≥ 1000 µg/L). Shown are a bone marrow blasts; markers for early-stage genetic instability such as b average number of <t>γH2AX-foci</t> in CD34+ peripheral blood cells, c age-adjusted telomere length in peripheral blood granulocytes (kilo base pairs, kb), d age-adjusted telomere length in peripheral blood lymphocytes (kb); and markers for advanced-stage genetic aberrations such as e total number of genetic alterations (molecular and cytogenetic), f number of cytogenetic aberrations, g number of molecularly mutated genes, and h total genomic alteration size (mega base pairs, Mb). Black points indicate patients with bone marrow blasts ≥ 10% and grey points those with bone marrow blasts < 10%
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( A ) Genetic profiling of matched CTRL-GSCs and IR-GSCs using the NGS GBM-target panel; p TERT mutations were assessed by ddPCR. Samples are ordered by primary and secondary radioresistance. *Significant increase in MYCN copy number; see also A Table EV4. ( B ) Ploidy (n) of matched CTRL-GSCs e IR-GSCs assessed by chromosome G-banding. ( C ) Cumulative chromosomal aberration number in all IR-GSCs vs. matched CTRL-GSCs, assessed by G-banding and M-FISH. Median number is indicated. Data are shown as delta relative to the corresponding CTRL-GSC; median is indicated. One-sample Wilcoxon test. *p = 0.0313. ( D ) Western blots showing phospho-H2AX <t>(γH2AX),</t> phospho-CHK2 (pCHK2; Tyr68), total CHK2 and p21 in GBM95 CTRL-GSC and IR-GSC in a representative time-course experiment after a single 5 Gy dose. Calnexin: loading control. ( E-F ) Immunofluorescence for phospho-H2AX (γH2AX) in GBM95 CTRL-GSC and IR-GSC in a time-course experiment after a single 5 Gy dose. ( E ) Quantification of γH2AX-positive cell nuclei. n = 4 technical replicates, Student’s paired t test. * p<0.000001. ( F ) Representative images. Scale bar, 25 μm. ( G ) Fraction of GBM95 CTRL-GSC and IR-GSC cells in G2 and M phases, measured by flow cytometry using phospho-Histone 3 (pH3; Ser10) staining at 6 and 24 h after a single 5 Gy dose, shown as fold change vs. mock. Mock: no IR. n = 2 independent experiments, Student’s paired t test. ( H ) Schematic of adaptive mechanisms of secondary radioresistance in GBM95 GSC family. In (E, G), data are presented as mean ± SEM.
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Cell Signaling Technology Inc dna damage marker γh2ax
( A ) Genetic profiling of matched CTRL-GSCs and IR-GSCs using the NGS GBM-target panel; p TERT mutations were assessed by ddPCR. Samples are ordered by primary and secondary radioresistance. *Significant increase in MYCN copy number; see also A Table EV4. ( B ) Ploidy (n) of matched CTRL-GSCs e IR-GSCs assessed by chromosome G-banding. ( C ) Cumulative chromosomal aberration number in all IR-GSCs vs. matched CTRL-GSCs, assessed by G-banding and M-FISH. Median number is indicated. Data are shown as delta relative to the corresponding CTRL-GSC; median is indicated. One-sample Wilcoxon test. *p = 0.0313. ( D ) Western blots showing phospho-H2AX <t>(γH2AX),</t> phospho-CHK2 (pCHK2; Tyr68), total CHK2 and p21 in GBM95 CTRL-GSC and IR-GSC in a representative time-course experiment after a single 5 Gy dose. Calnexin: loading control. ( E-F ) Immunofluorescence for phospho-H2AX (γH2AX) in GBM95 CTRL-GSC and IR-GSC in a time-course experiment after a single 5 Gy dose. ( E ) Quantification of γH2AX-positive cell nuclei. n = 4 technical replicates, Student’s paired t test. * p<0.000001. ( F ) Representative images. Scale bar, 25 μm. ( G ) Fraction of GBM95 CTRL-GSC and IR-GSC cells in G2 and M phases, measured by flow cytometry using phospho-Histone 3 (pH3; Ser10) staining at 6 and 24 h after a single 5 Gy dose, shown as fold change vs. mock. Mock: no IR. n = 2 independent experiments, Student’s paired t test. ( H ) Schematic of adaptive mechanisms of secondary radioresistance in GBM95 GSC family. In (E, G), data are presented as mean ± SEM.
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Image Search Results


Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

Journal: Biochemistry and Biophysics Reports

Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

doi: 10.1016/j.bbrep.2026.102568

Figure Lengend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

Article Snippet: Ferrostatin-1 and Liproxstatin-1 were purchased from Cayman, and the GSH/GSSG Quantification Kit and Cell Counting WST-8 were purchased from Dojindo. γH2AX antibody and β-Actin were purchased from Cell Signaling Technology.

Techniques: Inhibition, Expressing, Control

Effect of monoHER (M) combined with radiation (RT) on γ-H2AX immunofluorescence staining (at 24 h post-irradiation time point) in breast cancer and normal cells. Data are presented as mean ± SEM from three independent experiments (20 cells/experiment). *p < 0.05, **p < 0.01.

Journal: Clinical and Translational Radiation Oncology

Article Title: MonoHER selectively enhances the radiotherapy response in p53 wild-type breast cancer via stabilization of p53

doi: 10.1016/j.ctro.2026.101147

Figure Lengend Snippet: Effect of monoHER (M) combined with radiation (RT) on γ-H2AX immunofluorescence staining (at 24 h post-irradiation time point) in breast cancer and normal cells. Data are presented as mean ± SEM from three independent experiments (20 cells/experiment). *p < 0.05, **p < 0.01.

Article Snippet: Cells were incubated with a rabbit anti-human γH2AX primary antibody (1:500, Merck, JBW301), followed by detection using goat anti-rabbit Alexa Fluor 488 (1:500, Invitrogen, 11001).

Techniques: Immunofluorescence, Staining, Irradiation

Parameters associated with high ferritin were assessed in patients with non-elevated (≤ 275 µg/L), moderately elevated (> 275 and < 1000 µg/L), and highly elevated SF (≥ 1000 µg/L). Shown are a bone marrow blasts; markers for early-stage genetic instability such as b average number of γH2AX-foci in CD34+ peripheral blood cells, c age-adjusted telomere length in peripheral blood granulocytes (kilo base pairs, kb), d age-adjusted telomere length in peripheral blood lymphocytes (kb); and markers for advanced-stage genetic aberrations such as e total number of genetic alterations (molecular and cytogenetic), f number of cytogenetic aberrations, g number of molecularly mutated genes, and h total genomic alteration size (mega base pairs, Mb). Black points indicate patients with bone marrow blasts ≥ 10% and grey points those with bone marrow blasts < 10%

Journal: Journal of Cancer Research and Clinical Oncology

Article Title: High serum ferritin is associated with genetic instability in myelodysplastic neoplasms

doi: 10.1007/s00432-026-06457-1

Figure Lengend Snippet: Parameters associated with high ferritin were assessed in patients with non-elevated (≤ 275 µg/L), moderately elevated (> 275 and < 1000 µg/L), and highly elevated SF (≥ 1000 µg/L). Shown are a bone marrow blasts; markers for early-stage genetic instability such as b average number of γH2AX-foci in CD34+ peripheral blood cells, c age-adjusted telomere length in peripheral blood granulocytes (kilo base pairs, kb), d age-adjusted telomere length in peripheral blood lymphocytes (kb); and markers for advanced-stage genetic aberrations such as e total number of genetic alterations (molecular and cytogenetic), f number of cytogenetic aberrations, g number of molecularly mutated genes, and h total genomic alteration size (mega base pairs, Mb). Black points indicate patients with bone marrow blasts ≥ 10% and grey points those with bone marrow blasts < 10%

Article Snippet: To detect double-strand breaks, immunomagnetically enriched CD34+ PB cells were stained using a primary γH2AX antibody (Phospho-Histone H2A.X (Ser139) (20E3) Rabbit mAB, Cell Signaling Technologies, Danvers, MA, USA) and a secondary fluorescent antibody (Anti-rabbit IgG Fab2 Alexa Fluor (R) 555 Molecular Probe, Cell Signaling Technologies, Danvers, MA, USA).

Techniques:

( A ) Genetic profiling of matched CTRL-GSCs and IR-GSCs using the NGS GBM-target panel; p TERT mutations were assessed by ddPCR. Samples are ordered by primary and secondary radioresistance. *Significant increase in MYCN copy number; see also A Table EV4. ( B ) Ploidy (n) of matched CTRL-GSCs e IR-GSCs assessed by chromosome G-banding. ( C ) Cumulative chromosomal aberration number in all IR-GSCs vs. matched CTRL-GSCs, assessed by G-banding and M-FISH. Median number is indicated. Data are shown as delta relative to the corresponding CTRL-GSC; median is indicated. One-sample Wilcoxon test. *p = 0.0313. ( D ) Western blots showing phospho-H2AX (γH2AX), phospho-CHK2 (pCHK2; Tyr68), total CHK2 and p21 in GBM95 CTRL-GSC and IR-GSC in a representative time-course experiment after a single 5 Gy dose. Calnexin: loading control. ( E-F ) Immunofluorescence for phospho-H2AX (γH2AX) in GBM95 CTRL-GSC and IR-GSC in a time-course experiment after a single 5 Gy dose. ( E ) Quantification of γH2AX-positive cell nuclei. n = 4 technical replicates, Student’s paired t test. * p<0.000001. ( F ) Representative images. Scale bar, 25 μm. ( G ) Fraction of GBM95 CTRL-GSC and IR-GSC cells in G2 and M phases, measured by flow cytometry using phospho-Histone 3 (pH3; Ser10) staining at 6 and 24 h after a single 5 Gy dose, shown as fold change vs. mock. Mock: no IR. n = 2 independent experiments, Student’s paired t test. ( H ) Schematic of adaptive mechanisms of secondary radioresistance in GBM95 GSC family. In (E, G), data are presented as mean ± SEM.

Journal: bioRxiv

Article Title: Ex vivo stem-like cell families model evolution of glioblastoma therapeutic resistance

doi: 10.64898/2026.04.02.716158

Figure Lengend Snippet: ( A ) Genetic profiling of matched CTRL-GSCs and IR-GSCs using the NGS GBM-target panel; p TERT mutations were assessed by ddPCR. Samples are ordered by primary and secondary radioresistance. *Significant increase in MYCN copy number; see also A Table EV4. ( B ) Ploidy (n) of matched CTRL-GSCs e IR-GSCs assessed by chromosome G-banding. ( C ) Cumulative chromosomal aberration number in all IR-GSCs vs. matched CTRL-GSCs, assessed by G-banding and M-FISH. Median number is indicated. Data are shown as delta relative to the corresponding CTRL-GSC; median is indicated. One-sample Wilcoxon test. *p = 0.0313. ( D ) Western blots showing phospho-H2AX (γH2AX), phospho-CHK2 (pCHK2; Tyr68), total CHK2 and p21 in GBM95 CTRL-GSC and IR-GSC in a representative time-course experiment after a single 5 Gy dose. Calnexin: loading control. ( E-F ) Immunofluorescence for phospho-H2AX (γH2AX) in GBM95 CTRL-GSC and IR-GSC in a time-course experiment after a single 5 Gy dose. ( E ) Quantification of γH2AX-positive cell nuclei. n = 4 technical replicates, Student’s paired t test. * p<0.000001. ( F ) Representative images. Scale bar, 25 μm. ( G ) Fraction of GBM95 CTRL-GSC and IR-GSC cells in G2 and M phases, measured by flow cytometry using phospho-Histone 3 (pH3; Ser10) staining at 6 and 24 h after a single 5 Gy dose, shown as fold change vs. mock. Mock: no IR. n = 2 independent experiments, Student’s paired t test. ( H ) Schematic of adaptive mechanisms of secondary radioresistance in GBM95 GSC family. In (E, G), data are presented as mean ± SEM.

Article Snippet: Cells were then washed with PBS 3 times for 5 min, permeabilized with HEPES-Triton for 5 min, washed with PBS for 5 min and saturated with PBS-BSA 5% for 1 h. Primary antibody γH2AX (Cell Signaling Technology, cat#9718), diluted 1:200 in PBS-BSA 0.5%, was incubated for 2 h RT.

Techniques: Western Blot, Control, Immunofluorescence, Flow Cytometry, Staining