Author

L. D. Samson

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 1 Cell Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:human· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1

Frequent Co-Authors

A. L. Armijo· 1 shared A. M. H. Boots· 1 shared A. Nohturfft· 1 shared A.-M. Buisman· 1 shared B. P. Engelward· 1 shared C. F. Charlier· 1 shared D. K. Torous· 1 shared D. N. Wadduwage· 1 shared

Activity by Year

2021-2021 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperCancer Biology

A. L. Armijo

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A DNA repair-independent role for alkyladenine DNA glycosylase in alkylation-induced unfolded protein response

L. Milano, C. F. Charlier, R. Andreguetti, T. Cox, E. Healing, M. P. Thome, R. M. Elliott, L. D. Samson, J.-Y. Masson, G. Lenz, J. A. P. Henriques, A. Nohturfft, L. B. Meira

This paper shows that alkyladenine DNA glycosylase (AAG) is required for alkylation-induced unfolded protein response (UPR) in mouse liver and human cancer cells, independent of its DNA repair activity.

bioRxiv · Mar 31, 2021Cell Biology

Relation of inflammatory marker trajectories with frailty and aging in a 20-year longitudinal study

L. D. Samson, A.-M. Buisman, J. A. Ferreira, H. S. J. Picavet, W. M. M. Verschuren, A. M. H. Boots, P. Engelfriet

This study examines 20-year changes in inflammatory markers and their links to frailty and aging in a longitudinal cohort.

bioRxiv · Feb 10, 2021 · PreprintImmunology

Excision of mutagenic replication-blocking lesions suppresses cancer but promotes cytotoxicity and lethality in nitrosamine-exposed mice

J. E. Kay, J. J. Corrigan, A. L. Armijo, I. S. Nazari, I. N. Kohale, D. K. Torous, S. L. Avlasevich, R. G. Croy, D. N. Wadduwage, S. E. Carrasco, S. D. Dertinger, F. M. White, J. M. Essigmann, L. D. Samson, B. P. Engelward

The paper shows that altering AAG levels in mice changes the outcome of NDMA exposure from cancer to lethality by shifting the balance between replication-blocking lesions and strand breaks.

bioRxiv · Jan 12, 2021Cancer Biology