Journal: Blood Advances

Article Title: Inhibition of NAMPT targets DNA damage response to sensitize alkylating chemotherapy in TP53 mutant mantle cell lymphoma ∗

doi: 10.1182/bloodadvances.2025016765

Figure Lengend Snippet: Inhibition of NAMPT function via KPT-9274 inhibits tumor growth in vivo. (A) NOG mice were injected subcutaneously with Mino cells. After detection of the tumor, the mice were randomized and treated orally with either KPT-9274 or the vehicle for 5 consecutive days per week for 3 weeks. Tumor volume was evaluated via caliper measurement. Differences between the 2 groups were evaluated using the standard t test. (B) Tumor cells collected from mice were lysed in radio-immunoprecipitation assay buffer, and the whole-cell lysate was subjected to WB analysis and probed with antibodies against Cl-PARP, FANCD2, RAD51, and γ-H2AX. GAPDH was used as the loading control. ns > .05; ∗∗ P ≤ .01; ∗∗∗ P ≤ .001; ∗∗∗∗ P ≤ .0001.

Article Snippet: Western blotting (WB) was performed to evaluate the expression levels of total protein and phospho-specific isoforms using the following antibodies: FANCD2 (Santa Cruz Biotechnology, sc-20022), RAD51 (Santa Cruz Biotechnology, sc-398587), PBEF (Santa Cruz Biotechnology, sc-166946), cleaved Caspase3 (Cell Signaling Technology, 9664s), PARP (Cell Signaling Technology, 9532s), cleaved PARP (Cell Signaling Technology, 5625s), γ-H2AX (Ser139; Cell Signaling Technology, 9718s), p-CHK1 (Ser345; Cell Signaling Technology, 2341s), p53 (Cell Signaling Technology, 2527s), p-ATR (Ser428; Cell Signaling Technology, 2853s), p-ATM (Ser1981; Cell Signaling Technology, 4526s), and p-CHK2 (Thr68; Cell Signaling Technology, 2197s).

Techniques: Inhibition, In Vivo, Injection, Radio Immunoprecipitation, Control

Journal: Blood Advances

Article Title: Inhibition of NAMPT targets DNA damage response to sensitize alkylating chemotherapy in TP53 mutant mantle cell lymphoma ∗

doi: 10.1182/bloodadvances.2025016765

Figure Lengend Snippet: Inhibition of NAMPT function via KPT-9274 inhibits tumor growth in vivo. (A) NOG mice were injected subcutaneously with Mino cells. After detection of the tumor, the mice were randomized and treated orally with either KPT-9274 or the vehicle for 5 consecutive days per week for 3 weeks. Tumor volume was evaluated via caliper measurement. Differences between the 2 groups were evaluated using the standard t test. (B) Tumor cells collected from mice were lysed in radio-immunoprecipitation assay buffer, and the whole-cell lysate was subjected to WB analysis and probed with antibodies against Cl-PARP, FANCD2, RAD51, and γ-H2AX. GAPDH was used as the loading control. ns > .05; ∗∗ P ≤ .01; ∗∗∗ P ≤ .001; ∗∗∗∗ P ≤ .0001.

Article Snippet: Western blotting (WB) was performed to evaluate the expression levels of total protein and phospho-specific isoforms using the following antibodies: FANCD2 (Santa Cruz Biotechnology, sc-20022), RAD51 (Santa Cruz Biotechnology, sc-398587), PBEF (Santa Cruz Biotechnology, sc-166946), cleaved Caspase3 (Cell Signaling Technology, 9664s), PARP (Cell Signaling Technology, 9532s), cleaved PARP (Cell Signaling Technology, 5625s), γ-H2AX (Ser139; Cell Signaling Technology, 9718s), p-CHK1 (Ser345; Cell Signaling Technology, 2341s), p53 (Cell Signaling Technology, 2527s), p-ATR (Ser428; Cell Signaling Technology, 2853s), p-ATM (Ser1981; Cell Signaling Technology, 4526s), and p-CHK2 (Thr68; Cell Signaling Technology, 2197s).

Techniques: Inhibition, In Vivo, Injection, Radio Immunoprecipitation, Control

Journal: iScience

Article Title: CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

doi: 10.1016/j.isci.2026.114646

Figure Lengend Snippet: Replication stress and DNA damage response at CTCF/cohesin-binding sites in normal cells (A–D) ChIP-seq signal profile and heatmap of (A) MRE11, (B) STN1+HU 3h, (C) γH2AX (normalized with H2AX), and (D) RAD51 in the Mid S phase of HeLa cells plotted at CBSs shared between HeLa and normal cells (H1, IMR90, and RPE1 cells) (12,517 sites) and HeLa-specific CBSs (2,293 sites) and normal-specific sites (13,702). For the γH2AX signal ±10 kb flanks were considered, while for others the signal is plotted at ±5 kb regions. (E–H) ChIP-qPCR plots of (E) MRE11, (F) FANCD2, (G) γH2AX, and (H) RAD51 in Mid S synchronized hTERT RPE-1 cells at CBSs and CTCF-unbound sites. The y axis (fold enrichment over beads) indicates the % input in immunoprecipitation divided by that of beads. The bar represents the mean value from three replicates, and the error bar represents the standard error of the mean. Statistical significance was determined by using a two-sided Mann-Whitney U test.

Article Snippet: Antibodies used are: CTCF (3418: Cell Signaling Technology, 1 μg), RAD21 (ab992: Abcam, 1 μg), MRE11 (ab208020: Abcam, 2 μg), γH2AX (ab81299: Abcam, 2 μg), H2AX (ab11175: Abcam, 2 μg), RAD51 (ab176458: Abcam, 2 μg), ATM (ab201022: Abcam, 2 μg) and FANCD2 (NB100-182: Novus Biologicals, 2 μg).

Techniques: Binding Assay, ChIP-sequencing, ChIP-qPCR, Immunoprecipitation, MANN-WHITNEY

Journal: bioRxiv

Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

doi: 10.64898/2026.02.04.703705

Figure Lengend Snippet: (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of FANCD2 monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.

Article Snippet: Cells were then incubated with the primary antibody for 1 hour at RT, rabbit anti-FANCD2 antibody (Novus Biologicals, NB100-182, 1:500 in SB) or mouse anti-FANCD2 antibody (Novus Biologicals, NB100-316, 1:500 in SB).

Techniques: Western Blot, Activation Assay

Journal: bioRxiv

Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

doi: 10.64898/2026.02.04.703705

Figure Lengend Snippet: Cells were exposed to 1 µM MMC for 24 hours vs control conditions (DMSO) and imaged via confocal microscopy using Zeiss LSM 710 or Zeiss LSM 980 (63x). (A,C,E) Representative immunofluorescence images for CCH-SCC-FA1 ( FANCA Compl ) vs CCH-SCC-FA1 ( FANCA -/- ) (A), DU145 WT vs DU145_ FANCA KO (C), and RPE1 WT vs RPE1_ FANCA KD (E); scale represents 20 µm. (B, D, F) FANCD2 foci quantification for the same FANCA-deficient vs proficient cell lines. The number of foci per cell are represented, and statistical significance was calculated with the unpaired t-test.

Article Snippet: Cells were then incubated with the primary antibody for 1 hour at RT, rabbit anti-FANCD2 antibody (Novus Biologicals, NB100-182, 1:500 in SB) or mouse anti-FANCD2 antibody (Novus Biologicals, NB100-316, 1:500 in SB).

Techniques: Control, Confocal Microscopy, Immunofluorescence

Journal: bioRxiv

Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

doi: 10.64898/2026.02.04.703705

Figure Lengend Snippet: (A) Western blot illustrating FANCA protein loss in FANCA-deficient cell lines. (B,C) Lack of FANCD2 monoubiquitination, a hallmark of FA pathway activation, in FANCA-deficient cells. (D,E) FANCA-deficient cells show increased vulnerability to MMC: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (D) and DU145 WT vs DU145_ FANCA KO (E) are illustrated. (F,G) FANCA-deficient cells show increased vulnerability to cisplatin: drug response curves for CCH-SCC-FA1 ( FANCA -/- ) vs CCH-SCC-FA1 ( FANCA Compl ) (F) and DU145 WT vs DU145_ FANCA KO (G) are illustrated.

Article Snippet: Cells were then incubated with the primary antibody for 1 hour at RT, rabbit anti-FANCD2 antibody (Novus Biologicals, NB100-182, 1:500 in SB) or mouse anti-FANCD2 antibody (Novus Biologicals, NB100-316, 1:500 in SB).

Techniques: Western Blot, Activation Assay

Journal: bioRxiv

Article Title: Aurora kinase A is a synthetic lethal target in FANCA-deficient cancers

doi: 10.64898/2026.02.04.703705

Figure Lengend Snippet: Cells were exposed to 1 µM MMC for 24 hours vs control conditions (DMSO) and imaged via confocal microscopy using Zeiss LSM 710 or Zeiss LSM 980 (63x). (A,C,E) Representative immunofluorescence images for CCH-SCC-FA1 ( FANCA Compl ) vs CCH-SCC-FA1 ( FANCA -/- ) (A), DU145 WT vs DU145_ FANCA KO (C), and RPE1 WT vs RPE1_ FANCA KD (E); scale represents 20 µm. (B, D, F) FANCD2 foci quantification for the same FANCA-deficient vs proficient cell lines. The number of foci per cell are represented, and statistical significance was calculated with the unpaired t-test.

Article Snippet: Cells were then incubated with the primary antibody for 1 hour at RT, rabbit anti-FANCD2 antibody (Novus Biologicals, NB100-182, 1:500 in SB) or mouse anti-FANCD2 antibody (Novus Biologicals, NB100-316, 1:500 in SB).

Techniques: Control, Confocal Microscopy, Immunofluorescence