C. Lord
Molecular Biology · 2005–2019
A researcher in the Science corpus: 10 papers; trusts 9 researchers and is trusted by 3 researchers here, as inferred from the citation graph.
Subfields
- Molecular Biology — 117 citations into it; #10,539 of 17,773 by trust here, #2,053 by citations
- Oncology — 101 citations into it; #826 of 1,698 by trust here, #167 by citations
- Genetics — 50 citations into it
- Cancer Research — 44 citations into it
- Cell Biology — 10 citations into it
Whom C. Lord trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
- M. Moynahan
- Jan H. J. Hoeijmakers
- N. Turner
- Michael Weller
- Alan Ashworth
- Andrew Tutt
- M. Jasin
- Yves Pommier
- Jonathan A. Ledermann
- S. Artandi
Who trusts C. Lord overall
- D. Fruman
- Alan Ashworth
- Andrew N. Blackford
- Honyin Chiu
- Ruixue Huang
- T. Niccoli
- Mark J. O'Connor
- Guocan Wang
- J. Prat
Papers from C. Lord's perspective
Ordered by how strongly the researchers C. Lord trusts endorse each paper. Same corpus, a different order for every researcher.
- Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy (Nature)
- Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors (EMBO Molecular Medicine)
- 53BP1 inhibits homologous recombination in Brca1-deficient cells by blocking resection of DNA breaks (Cell)
- The Breast Cancer Susceptibility Gene BRCA1 Is Required for Subnuclear Assembly of Rad51 and Survival following Treatment with the DNA Cross-linking Agent Cisplatin*
- A synthetic lethal therapeutic approach: poly(ADP) ribose polymerase inhibitors for the treatment of cancers deficient in DNA double-strand break repair. (Journal of Clinical Oncology)
- The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair (Nature Cell Biology)
- Olaparib in patients with recurrent high-grade serous or poorly differentiated ovarian carcinoma or triple-negative breast cancer: a phase 2, multicentre, open-label, non-randomised study. (The Lancet Oncology)
- BRCA2 is required for homology-directed repair of chromosomal breaks. (Molecules and Cells)
- Hallmarks of cancer: the next generation. (Cell)
- Signatures of mutational processes in human cancer (Nature)
Their papers
- Targeting the DNA repair defect in BRCA mutant cells as a therapeutic strategy (2005) — 6,462 citations
- Resistance to therapy caused by intragenic deletion in BRCA2 (2008) — 1,036 citations
- The DNA damage response and cancer therapy (2012) — 1,734 citations
- BRCAness revisited (2016) — 1,160 citations
- Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors (2009) — 674 citations
- Deficiency in the repair of DNA damage by homologous recombination and sensitivity to poly(ADP-ribose) polymerase inhibition. (2006) — 1,299 citations
- A decade of clinical development of PARP inhibitors in perspective (2019) — 625 citations
- PARP Inhibitors: The First Synthetic Lethal Targeted Therapy (2017) — 2,440 citations
- DNA-Repair Defects and Olaparib in Metastatic Prostate Cancer (2015) — 1,991 citations
- Rethinking Ovarian Cancer: Recommendations for Improving Outcomes (2011) — 1,276 citations