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John A. Hartley

Researcher at University College London

Publications -  336
Citations -  17105

John A. Hartley is an academic researcher from University College London. The author has contributed to research in topics: DNA & DNA damage. The author has an hindex of 61, co-authored 316 publications receiving 14655 citations. Previous affiliations of John A. Hartley include University of Texas at Austin & National Institutes of Health.

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Tracking the Evolution of Non–Small-Cell Lung Cancer

Mariam Jamal-Hanjani, +82 more
TL;DR: Intratumor heterogeneity mediated through chromosome instability was associated with an increased risk of recurrence or death, a finding that supports the potential value of chromosome instability as a prognostic predictor.
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Phylogenetic ctDNA analysis depicts early-stage lung cancer evolution

Christopher Abbosh, +119 more
- 25 May 2017 - 
TL;DR: It is shown that phylogenetic ct DNA profiling tracks the subclonal nature of lung cancer relapse and metastasis, providing a new approach for ctDNA-driven therapeutic studies.
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Allele-Specific HLA Loss and Immune Escape in Lung Cancer Evolution

Nicholas McGranahan, +219 more
- 30 Nov 2017 - 
TL;DR: It is found that HLA LOH occurs in 40% of non-small-cell lung cancers (NSCLCs) and is associated with a high subclonal neoantigen burden, APOBEC-mediated mutagenesis, upregulation of cytolytic activity, and PD-L1 positivity.
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Defining the roles of nucleotide excision repair and recombination in the repair of DNA interstrand cross-links in mammalian cells.

TL;DR: A role for XPF and ERCC1 is defined in the excision of ICLs, but not in the recombinational components of cross-link repair, and homologous recombination but not nonhomologous end joining appears to play an important role in the repair of DSBs resulting from nitrogen mustard treatment.
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Repair of DNA interstrand crosslinks: molecular mechanisms and clinical relevance

TL;DR: It is now clear that cells from bacteria and yeast to mammals eliminate interstrand ICLs through the coordinated action of several DNA repair pathways, and this new knowledge may permit the development of screens for tumour response to crosslinking agents, and should also aid the design of more effective crossl linking agents that evade DNA repair.