Author

A. Dolnik

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· 2

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Assay:scRNA-seq· 1

Frequent Co-Authors

L. Bullinger· 2 shared A. Oestlund· 1 shared A. Riedel· 1 shared A. Touzart· 1 shared A. Waraky· 1 shared B. Schlegelberger· 1 shared C. Nilsson· 1 shared C. Plass· 1 shared

Activity by Year

2022-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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2 shared papersCancer Biology

L. Bullinger

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2 papers

Recent·Most cited

Altered enhancer-promoter interaction leads to MNX1 expression in pediatric acute myeloid leukemia with t(7;12)(q36;p13)

D. Weichenhan, A. Riedel, E. Sollier, U. H. Toprak, J. Hey, K. Breuer, J. A. Wierzbinska, A. Touzart, P. Lutsik, M. Baehr, A. Oestlund, C. Nilsson, S. Jacobsson, M. Edler, A. Waraky, , C. Plass

The paper shows MNX1 overexpression in t(7;12)(q36;p13) AML is due to enhancer hijacking, not oncofusion, and is common in pediatric cases.

bioRxiv · Sep 13, 2023 · PreprintCancer Biology

Longitudinal single-cell transcriptomics reveals distinct patterns of recurrence in acute myeloid leukemia

Y. Zhai, P. Singh, A. Dolnik, P. Brazda, N. Atlasy, N. del Gaudio, K. Dohner, H. Dohner, S. Minucci, J. Martens, L. Altucci, W. Megchelenbrink, L. Bullinger, H. G. Stunnenberg

This study uses longitudinal single-cell transcriptomics to analyze AML recurrence patterns, finding varying transcriptional changes between diagnosis and relapse that challenge the clonal evolution model.

bioRxiv · Jan 4, 2022 · PreprintCancer Biology