Author

F. M. Riemers

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· 4

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 3 Organism:human· 3 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Approach:genetic perturbation / CRISPR· 2 Approach:statistical model· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

B. Westendorp· 3 shared A. de Bruin· 2 shared E. A. van Liere· 2 shared H. A. Segeren· 2 shared A. Slob· 1 shared A. Veldhuizen· 1 shared B. P. Meij· 1 shared E. Moreno· 1 shared

Activity by Year

2020-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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3 shared papersCancer Biology

B. Westendorp

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4 papers

Recent·Most cited

Stochastic variation in the FOXM1 transcription program mediates replication stress tolerance.

H. A. Segeren, K. Wierenga, F. M. Riemers, E. A. van Liere, B. Westendorp

The paper identifies FOXM1 expression levels as a factor in replication stress tolerance in oncogenic RAS-expressing cells using single-cell RNA sequencing and drug combination experiments.

bioRxiv · Mar 26, 2024Cancer Biology

Circulating microRNAs as noninvasive biomarkers for canine Cushing's syndrome

K. Sanders, A. Veldhuizen, H. S. Kooistra, A. Slob, E. P. M. Timmermans-Sprang, F. M. Riemers, S. Daminet, F. Fracassi, S. A. van Nimwegen, B. P. Meij, S. Galac

This study identifies circulating microRNAs as potential noninvasive biomarkers for canine Cushing's syndrome, showing differential expression in pituitary-dependent and adrenal tumors and recurrence prediction.

bioRxiv · Aug 17, 2021 · PreprintCancer Biology

Oncogenic RAS sensitizes cells to drug-induced replication stress via transcriptional silencing of P53

H. A. Segeren, E. A. van Liere, F. M. Riemers, A. de Bruin, B. Westendorp

This study shows that oncogenic RAS increases sensitivity to ATR/CHK1 inhibitors by suppressing P53 transcriptional responses to replication stress.

bioRxiv · Jun 14, 2021Cancer Biology

Excessive E2F transcription in single cancer cells precludes transient cell cycle exit after DNA damage.

H. S. Segeren, L. M. van Rijnberk, E. Moreno, F. M. Riemers, R. Yuan, R. Wubbolts, A. de Bruin, B. Westendorp

The paper shows that high E2F transcription in cancer cells prevents cell cycle exit after DNA damage, leading to genomic instability and reduced drug sensitivity.

bioRxiv · Mar 19, 2020Cancer Biology