Additional file 10 of Replication catastrophe is responsible for intrinsic PAR glycohydrolase inhibitor-sensitivity in patient-derived ovarian cancer models
Creators: name: Coulson-Gilmer, Camilla
name: Morgan, Robert D.
name: Nelson, Louisa
name: Barnes, Bethany M.
name: Tighe, Anthony
name: Wardenaar, René
name: Spierings, Diana C. J.
name: Schlecht, Helene
name: Burghel, George J.
name: Foijer, Floris
name: Desai, Sudha
name: McGrail, Joanne C.
name: Taylor, Stephen S.
Publisher: name: figshare
Year: 2021
Subjects: subject: Biophysics
subject: Biochemistry
subject: Cell Biology
subject: Genetics
subject: FOS: Biological sciences
subject: Molecular Biology
subject: Pharmacology
subject: Biotechnology
subject: 39999 Chemical Sciences not elsewhere classified
subject: FOS: Chemical sciences
subject: 69999 Biological Sciences not elsewhere classified
subject: Cancer
subject: Hematology

description: Additional file 10: Supplementary Table 1. Clinical data, OCMs and primary tumour blocks. The table outlines the clinical data for the 25 new HGSOC OCMs screened for PARPi and PARGi sensitivity. Key: dx, diagnosis; FIGO, International Federation of Gynecology and Obstetrics; gBRCAm, germline BRCA1/2 mutation; VUS, variant of uncertain clinical significance; CTx, chemotherapy; Ref, platinum-refractory disease (tumour progression during or within 4 weeks of completing platinum therapy); Res, platinum-resistant (tumour progression between 4 weeks and 6 months from completing platinum therapy); Sens, platinum-sensitive (tumour progression ≥6 months from completing platinum therapy). CN, chemonaïve; OS, overall survival; mo, months; WT, wild-type; FR, frameshift; NS, nonsense; IF, immunofluorescence; IHC, immunohistochemistry; For IF and IHC: CK7 and PAX8, coloured box (present), white box (absent), S, strong; P, patchy; F, focal; W, weak. p53 is either mutant-type (strong/diffuse nuclear staining; darker coloured box), wild-type (lighter colour box) or absent nuclear staining (white box). NE, not evaluable (antibody failed); block unavailable (grey box). IB, immunoblotting; For IB: +(sm), band present but at lower than 53 kDa; +(S), strong band present; *At the time of the research biopsy; †Histologically re-classified from HGSOC to intermediate grade (grade 2/moderately differentiated) serous adenocarcinoma following tumour block analysis; ‡cell agar block only, histologically re-classified from HGSOC to suspicion of adenocarcinoma arising from the gynaecological tract. Clinical data for previously characterised OCMs are published [13], and not repeated here. Supplementary Table 2. BRCA1/2 variants detected in OCMs. The table outlines the BRCA1/2 variants detected in the panel of 7 OCMs screened for PARGi and PARPi sensitivity using colony survival and cell proliferation assays. Variants are described using Human Genome Variation Society (HGVS) nomenclature. Key: FR, frameshift; MS, missense; NS, nonsense; VAF, variant allele frequency; VUS, variant of uncertain clinical significance; WT, wild-type. All OCMs underwent both NGS and MLPA testing for BRCA1/2 variants. Supplementary Table 3. EC50 values for OCMs for the inhibitors/compounds tested. The table outlines the EC50 values for the inhibitors/compounds tested in the cell proliferation assay for the panel of 7 OCMs assessed. See Fig. 5C and D for Log EC50 values. Data are mean ± SEM from 3 biological replicates. PRISM could not accurately calculate EC50 for PARGi-resistant cells, therefore for resistant OCMs, the EC50 was approximated as 50 μM (half the maximal concentration tested) and described in the table as not calculable (NC).