Thomas Helleday
Molecular Biology · 2005–2014
A researcher in the Science corpus: 11 papers; trusts 6 researchers and is trusted by 4 researchers here, as inferred from the citation graph.
Subfields
- Molecular Biology — 139 citations into it; #7,516 of 17,773 by trust here, #1,854 by citations
- Oncology — 64 citations into it; #501 of 1,698 by trust here, #221 by citations
Whom Thomas Helleday trusts overall
Their strongest outbound trust, strongest first, inferred from their citations.
- K. Caldecott
- Leonard Wu
- M. Moynahan
- M. Jasin
- J. Falck
- James C. Wang
- Ian D. Hickson
- K. Rothkamm
- S. West
Who trusts Thomas Helleday overall
Papers from Thomas Helleday's perspective
Ordered by how strongly the researchers Thomas Helleday 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)
- Functional interaction between PARP‐1 and PARP‐2 in chromosome stability and embryonic development in mouse (EMBO Journal)
- Review Cancer Susceptibility and the Functions of BRCA1 and BRCA2
- Sensing DNA Damage Through ATRIP Recognition of RPA-ssDNA Complexes (Science)
- Human CtIP promotes DNA end resection (Nature)
- A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage. (Current Biology)
- Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. (New England Journal of Medicine)
- Functional uncoupling of MCM helicase and DNA polymerase activities activates the ATR-dependent checkpoint. (Genes & Development)
- DNA repair pathways as targets for cancer therapy (Nature Reviews. Cancer)
- Single-strand break repair and genetic disease (Nature reviews genetics)
Their papers
- Specific killing of BRCA2-deficient tumours with inhibitors of poly(ADP-ribose) polymerase (2005) — 4,680 citations
- Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints (2006) — 2,043 citations
- Hydroxyurea-Stalled Replication Forks Become Progressively Inactivated and Require Two Different RAD51-Mediated Pathways for Restart and Repair (2010) — 840 citations
- DNA repair pathways as targets for cancer therapy (2008) — 1,734 citations
- The cell-cycle checkpoint kinase Chk1 is required for mammalian homologous recombination repair (2005) — 682 citations
- PARP is activated at stalled forks to mediate Mre11‐dependent replication restart and recombination (2009) — 627 citations
- DNA double-strand break repair: from mechanistic understanding to cancer treatment. (2007) — 690 citations
- Chk1 promotes replication fork progression by controlling replication initiation (2010) — 298 citations
- Mechanisms underlying mutational signatures in human cancers (2014) — 793 citations
- The underlying mechanism for the PARP and BRCA synthetic lethality: Clearing up the misunderstandings (2011) — 830 citations
- Replication stress links structural and numerical cancer chromosomal instability (2013) — 840 citations