binding protein 1 53bp1  (Bio-Techne corporation)

Journal: Frontiers in endocrinology

Article Title: MIEAP and ATG5 are tumor suppressors in a mouse model of BRAF V600E -positive thyroid cancer.

doi: 10.3389/fendo.2022.932754

Figure Lengend Snippet: FIGURE 3 IHC staining for Ki67, TUNEL, 53BP1, and MIEAP expression (A) and quantification of Ki67–positive cells (B), TUNEL–positive cells (C), and 53BP1 foci (D) in the thyroids from control, MieapKO/KO, Atg5thyr–KO/KO, Brafthyr–V600E, Brafthyr–V600E,MieapKO/KO, and Brafthyr–V600E, Atg5thyr–KO/KO mice at 12 months. The thyroid tissues obtained in Figure 1 were used for IHC as described in Materials and methods. The original magnifications were ×400. Data are shown as black circles for individual mice and as means ± SE. *P < 0.05, **P < 0.01. M, months.

Article Snippet: Sections (4 mm thick) were prepared and stained with hematoxylin and eosin (H&E) or immunostained with primary antibodies: rabbit monoclonal anti–Tg (ab156008, Abcam, Cambridge, UK, dilution of 1:250), rabbit monoclonal anti–Ki–67 (ab66155, Abcam, dilution of 1:100), rabbit polyclonal anti–tumor suppressor P53–binding protein 1 (53BP1) (A300–272A, Bethyl Laboratories, Montgomery, TX, USA, dilution of 1:200), rabbit monoclonal anti–MIEAP (ab180154, Abcam, dilution of 1:400), and rabbit polyclonal anti–TOMM20 (translocase of outer mitochondrial membrane 20) (11802–1–AP, Proteintech, Tokyo, Japan, dilution of 1:250).

Techniques: Immunohistochemistry, TUNEL Assay, Expressing, Control

Journal: Oncology and Therapy

Article Title: Liposomal Irinotecan Shows a Larger Therapeutic Index than Non-liposomal Irinotecan in Patient-Derived Xenograft Models of Pancreatic Cancer

doi: 10.1007/s40487-022-00215-2

Figure Lengend Snippet: Antitumor activity and toxicity after three treatment cycles at the MTD (IM-PAN-001 model). Analyses were performed during the third treatment cycle: at 24 and 168 h after the dose of liposomal irinotecan; at 1 h after the second dose and 168 h after the first dose of non-liposomal irinotecan. a Tumor growth profiles and survival analysis (TTRV600) in the IM-PAN-001 model treated at the MTD (mice per group, n = 8); charts are Fig. sub-plots. b Heat map visualization of BWL in individual mice in the IM-PAN-001 model compared with their first day of treatment. Mice were weighed at least twice a week. Color grading represents the intensity of BWL (mice per group, n = 8); ‘x’ represents mouse euthanasia. c pH2AX immunostaining in tumor samples and H&E staining to show representative tumor regression (magnification, × 400, scale bars: 50 µm). d pH2AX immunostaining in intestine samples (magnification, × 1000, scale bars : 20 µm). During the third treatment cycle, e tumoral H-scores of pH2AX, 53BP1, and RAD51 immunostaining, and tumor regression grading were assessed in parallel with f jejunum and bone marrow toxicity (assessed by pH2AX immunostaining). g Plasma CPT-11, plasma SN-38 and tumor SN-38 levels (mice per group, n = 4). Plasma CPT-11 LLOQ = 1 nmol/l; plasma SN-38 LLOQ = 13 nmol/l; tumor SN-38 LLOQ = 3 nmol/kg. 53BP1 p53 binding protein 1, BLQ below the limit of quantification, BWL body weight loss, CPT-11 irinotecan, H-score histological score, H&E hematoxylin–eosin, LLOQ lower limit of quantification, MTD maximum tolerated dose, pH2AX phospho-histone gamma H2AX, SD standard deviation, SEM standard error of the mean, TTRV600 time (days) to reach a TV of 600 mm 3 , TV tumor volume

Article Snippet: DNA damage was assessed through immunohistochemical staining for p53 binding protein 1 (53BP1 [Novus Biologicals]), phospho-histone gamma-H2AX protein (pH2AX [Abcam]) and RAD51 (Abcam) (further details in Supplementary methods).

Techniques: Activity Assay, Immunostaining, Staining, Clinical Proteomics, Binding Assay, Standard Deviation